[{"publisher":"Springer Nature","_id":"9009","acknowledgement":"This work was supported by National Institute of Health grants R01 EY030123, P30 EY016665, and T32 GM081061, an unrestricted research grant from Research to Prevent Blindness, Inc., and the Frederick A. Davis Endowment from the Department of Ophthalmology and Visual Sciences at the University of Wisconsin-Madison.","doi":"10.1007/s10495-020-01654-w","title":"Characteristics of intracellular propagation of mitochondrial BAX recruitment during apoptosis","year":"2021","day":"01","article_type":"original","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","month":"02","fulldoi":"https://doi.org/10.1007/s10495-020-01654-w","quality_controlled":"1","publication_identifier":{"eissn":["1573-675X"],"issn":["1360-8185"]},"date_updated":"2023-08-07T13:32:40Z","volume":26,"oa_version":"Submitted Version","isi":1,"scopus_import":"1","publication":"Apoptosis","status":"public","article_processing_charge":"No","oa":1,"external_id":{"pmid":["33426618"],"isi":["000606722600001"]},"language":[{"iso":"eng"}],"date_published":"2021-02-01T00:00:00Z","department":[{"_id":"SaSi"}],"intvolume":"        26","abstract":[{"text":"Recent advancements in live cell imaging technologies have identified the phenomenon of intracellular propagation of late apoptotic events, such as cytochrome c release and caspase activation. The mechanism, prevalence, and speed of apoptosis propagation remain unclear. Additionally, no studies have demonstrated propagation of the pro-apoptotic protein, BAX. To evaluate the role of BAX in intracellular apoptotic propagation, we used high speed live-cell imaging to visualize fluorescently tagged-BAX recruitment to mitochondria in four immortalized cell lines. We show that propagation of mitochondrial BAX recruitment occurs in parallel to cytochrome c and SMAC/Diablo release and is affected by cellular morphology, such that cells with processes are more likely to exhibit propagation. The initiation of propagation events is most prevalent in the distal tips of processes, while the rate of propagation is influenced by the 2-dimensional width of the process. Propagation was rarely observed in the cell soma, which exhibited near synchronous recruitment of BAX. Propagation velocity is not affected by mitochondrial volume in segments of processes, but is negatively affected by mitochondrial density. There was no evidence of a propagating wave of increased levels of intracellular calcium ions. Alternatively, we did observe a uniform increase in superoxide build-up in cellular mitochondria, which was released as a propagating wave simultaneously with the propagating recruitment of BAX to the mitochondrial outer membrane.","lang":"eng"}],"pmid":1,"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8082518/","open_access":"1"}],"author":[{"first_name":"Joshua A.","full_name":"Grosser, Joshua A.","last_name":"Grosser"},{"last_name":"Maes","id":"3838F452-F248-11E8-B48F-1D18A9856A87","full_name":"Maes, Margaret E","orcid":"0000-0001-9642-1085","first_name":"Margaret E"},{"first_name":"Robert W.","full_name":"Nickells, Robert W.","last_name":"Nickells"}],"issue":"2","type":"journal_article","date_created":"2021-01-17T23:01:11Z","page":"132-145","publication_status":"published","citation":{"short":"J.A. Grosser, M.E. Maes, R.W. Nickells, Apoptosis 26 (2021) 132–145.","apa":"Grosser, J. A., Maes, M. E., &#38; Nickells, R. W. (2021). Characteristics of intracellular propagation of mitochondrial BAX recruitment during apoptosis. <i>Apoptosis</i>. Springer Nature. <a href=\"https://doi.org/10.1007/s10495-020-01654-w\">https://doi.org/10.1007/s10495-020-01654-w</a>","ista":"Grosser JA, Maes ME, Nickells RW. 2021. Characteristics of intracellular propagation of mitochondrial BAX recruitment during apoptosis. Apoptosis. 26(2), 132–145.","chicago":"Grosser, Joshua A., Margaret E Maes, and Robert W. Nickells. “Characteristics of Intracellular Propagation of Mitochondrial BAX Recruitment during Apoptosis.” <i>Apoptosis</i>. Springer Nature, 2021. <a href=\"https://doi.org/10.1007/s10495-020-01654-w\">https://doi.org/10.1007/s10495-020-01654-w</a>.","mla":"Grosser, Joshua A., et al. “Characteristics of Intracellular Propagation of Mitochondrial BAX Recruitment during Apoptosis.” <i>Apoptosis</i>, vol. 26, no. 2, Springer Nature, 2021, pp. 132–45, doi:<a href=\"https://doi.org/10.1007/s10495-020-01654-w\">10.1007/s10495-020-01654-w</a>.","ieee":"J. A. Grosser, M. E. Maes, and R. W. Nickells, “Characteristics of intracellular propagation of mitochondrial BAX recruitment during apoptosis,” <i>Apoptosis</i>, vol. 26, no. 2. Springer Nature, pp. 132–145, 2021.","ama":"Grosser JA, Maes ME, Nickells RW. Characteristics of intracellular propagation of mitochondrial BAX recruitment during apoptosis. <i>Apoptosis</i>. 2021;26(2):132-145. doi:<a href=\"https://doi.org/10.1007/s10495-020-01654-w\">10.1007/s10495-020-01654-w</a>"}},{"ec_funded":1,"article_processing_charge":"No","oa":1,"language":[{"iso":"eng"}],"external_id":{"pmid":["34233180"],"isi":["000670188500004"]},"department":[{"_id":"SaSi"}],"date_published":"2021-07-06T00:00:00Z","abstract":[{"text":"Perineuronal nets (PNNs), components of the extracellular matrix, preferentially coat parvalbumin-positive interneurons and constrain critical-period plasticity in the adult cerebral cortex. Current strategies to remove PNN are long-lasting, invasive, and trigger neuropsychiatric symptoms. Here, we apply repeated anesthetic ketamine as a method with minimal behavioral effect. We find that this paradigm strongly reduces PNN coating in the healthy adult brain and promotes juvenile-like plasticity. Microglia are critically involved in PNN loss because they engage with parvalbumin-positive neurons in their defined cortical layer. We identify external 60-Hz light-flickering entrainment to recapitulate microglia-mediated PNN removal. Importantly, 40-Hz frequency, which is known to remove amyloid plaques, does not induce PNN loss, suggesting microglia might functionally tune to distinct brain frequencies. Thus, our 60-Hz light-entrainment strategy provides an alternative form of PNN intervention in the healthy adult brain.","lang":"eng"}],"intvolume":"        36","pmid":1,"has_accepted_license":"1","scopus_import":"1","ddc":["570"],"status":"public","publication":"Cell Reports","acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"publication_status":"published","project":[{"name":"International IST Doctoral Program","grant_number":"665385","call_identifier":"H2020","_id":"2564DBCA-B435-11E9-9278-68D0E5697425"},{"_id":"260C2330-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"754411","name":"ISTplus - Postdoctoral Fellowships"},{"name":"Microglia action towards neuronal circuit formation and function in health and disease","call_identifier":"H2020","_id":"25D4A630-B435-11E9-9278-68D0E5697425","grant_number":"715571"}],"file":[{"date_updated":"2021-07-19T13:32:17Z","file_id":"9693","checksum":"f056255f6d01fd9a86b5387635928173","date_created":"2021-07-19T13:32:17Z","relation":"main_file","content_type":"application/pdf","file_name":"2021_CellReports_Venturino.pdf","file_size":56388540,"success":1,"access_level":"open_access","creator":"cziletti"}],"citation":{"short":"A. Venturino, R. Schulz, H. De Jesús-Cortés, M.E. Maes, B. Nagy, F. Reilly-Andújar, G. Colombo, R.J. Cubero, F.E. Miteva, M.F. Bear, S. Siegert, Cell Reports 36 (2021).","apa":"Venturino, A., Schulz, R., De Jesús-Cortés, H., Maes, M. E., Nagy, B., Reilly-Andújar, F., … Siegert, S. (2021). Microglia enable mature perineuronal nets disassembly upon anesthetic ketamine exposure or 60-Hz light entrainment in the healthy brain. <i>Cell Reports</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.celrep.2021.109313\">https://doi.org/10.1016/j.celrep.2021.109313</a>","ista":"Venturino A, Schulz R, De Jesús-Cortés H, Maes ME, Nagy B, Reilly-Andújar F, Colombo G, Cubero RJ, Miteva FE, Bear MF, Siegert S. 2021. Microglia enable mature perineuronal nets disassembly upon anesthetic ketamine exposure or 60-Hz light entrainment in the healthy brain. Cell Reports. 36(1), 109313.","ama":"Venturino A, Schulz R, De Jesús-Cortés H, et al. Microglia enable mature perineuronal nets disassembly upon anesthetic ketamine exposure or 60-Hz light entrainment in the healthy brain. <i>Cell Reports</i>. 2021;36(1). doi:<a href=\"https://doi.org/10.1016/j.celrep.2021.109313\">10.1016/j.celrep.2021.109313</a>","mla":"Venturino, Alessandro, et al. “Microglia Enable Mature Perineuronal Nets Disassembly upon Anesthetic Ketamine Exposure or 60-Hz Light Entrainment in the Healthy Brain.” <i>Cell Reports</i>, vol. 36, no. 1, 109313, Elsevier, 2021, doi:<a href=\"https://doi.org/10.1016/j.celrep.2021.109313\">10.1016/j.celrep.2021.109313</a>.","ieee":"A. Venturino <i>et al.</i>, “Microglia enable mature perineuronal nets disassembly upon anesthetic ketamine exposure or 60-Hz light entrainment in the healthy brain,” <i>Cell Reports</i>, vol. 36, no. 1. Elsevier, 2021.","chicago":"Venturino, Alessandro, Rouven Schulz, Héctor De Jesús-Cortés, Margaret E Maes, Balint Nagy, Francis Reilly-Andújar, Gloria Colombo, et al. “Microglia Enable Mature Perineuronal Nets Disassembly upon Anesthetic Ketamine Exposure or 60-Hz Light Entrainment in the Healthy Brain.” <i>Cell Reports</i>. Elsevier, 2021. <a href=\"https://doi.org/10.1016/j.celrep.2021.109313\">https://doi.org/10.1016/j.celrep.2021.109313</a>."},"file_date_updated":"2021-07-19T13:32:17Z","issue":"1","author":[{"full_name":"Venturino, Alessandro","orcid":"0000-0003-2356-9403","first_name":"Alessandro","last_name":"Venturino","id":"41CB84B2-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0001-5297-733X","full_name":"Schulz, Rouven","first_name":"Rouven","last_name":"Schulz","id":"4C5E7B96-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Héctor","full_name":"De Jesús-Cortés, Héctor","last_name":"De Jesús-Cortés"},{"orcid":"0000-0001-9642-1085","full_name":"Maes, Margaret E","first_name":"Margaret E","last_name":"Maes","id":"3838F452-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Nagy","id":"93C65ECC-A6F2-11E9-8DF9-9712E6697425","full_name":"Nagy, Balint","first_name":"Balint"},{"last_name":"Reilly-Andújar","full_name":"Reilly-Andújar, Francis","first_name":"Francis"},{"last_name":"Colombo","id":"3483CF6C-F248-11E8-B48F-1D18A9856A87","full_name":"Colombo, Gloria","orcid":"0000-0001-9434-8902","first_name":"Gloria"},{"last_name":"Cubero","id":"850B2E12-9CD4-11E9-837F-E719E6697425","orcid":"0000-0003-0002-1867","full_name":"Cubero, Ryan J","first_name":"Ryan J"},{"last_name":"Schoot Uiterkamp","id":"3526230C-F248-11E8-B48F-1D18A9856A87","full_name":"Schoot Uiterkamp, Florianne E","first_name":"Florianne E"},{"last_name":"Bear","full_name":"Bear, Mark F.","first_name":"Mark F."},{"last_name":"Siegert","id":"36ACD32E-F248-11E8-B48F-1D18A9856A87","full_name":"Siegert, Sandra","orcid":"0000-0001-8635-0877","first_name":"Sandra"}],"type":"journal_article","date_created":"2021-07-11T22:01:16Z","article_number":"109313","article_type":"original","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","month":"07","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"related_material":{"link":[{"description":"News on IST Homepage","relation":"press_release","url":"https://ist.ac.at/en/news/the-twinkle-and-the-brain/"}]},"_id":"9642","publisher":"Elsevier","acknowledgement":"We thank the scientific service units at IST Austria, especially the IST bioimaging facility, the preclinical facility, and, specifically, Michael Schunn and Sonja Haslinger for excellent support; Plexxikon for the PLX food; the Csicsvari group for advice and equipment for in vivo recording; Jürgen Siegert for the light-entrainment design; Marco Benevento, Soledad Gonzalo Cogno, Pat King, and all Siegert group members for constant feedback on the project and manuscript; Lorena Pantano (PILM Bioinformatics Core) for assisting with sample-size determination for OD plasticity experiments; and Ana Morello from MIT for technical assistance with VEPs recordings. This research was supported by a DOC Fellowship from the Austrian Academy of Sciences at the Institute of Science and Technology Austria to R.S., from the European Union Horizon 2020 research and innovation program under the Marie Skłodowska-Curie Actions program (grants 665385 to G.C.; 754411 to R.J.A.C.), the European Research Council (grant 715571 to S.S.), and the National Eye Institute of the National Institutes of Health under award numbers R01EY029245 (to M.F.B.) and R01EY023037 (diversity supplement to H.D.J-C.).","doi":"10.1016/j.celrep.2021.109313","title":"Microglia enable mature perineuronal nets disassembly upon anesthetic ketamine exposure or 60-Hz light entrainment in the healthy brain","year":"2021","day":"06","oa_version":"Published Version","isi":1,"fulldoi":"https://doi.org/10.1016/j.celrep.2021.109313","publication_identifier":{"eissn":["2211-1247"]},"quality_controlled":"1","date_updated":"2026-04-03T09:46:05Z","volume":36},{"type":"journal_article","author":[{"last_name":"Muench","full_name":"Muench, Nicole A.","first_name":"Nicole A."},{"last_name":"Patel","full_name":"Patel, Sonia","first_name":"Sonia"},{"first_name":"Margaret E","orcid":"0000-0001-9642-1085","full_name":"Maes, Margaret E","id":"3838F452-F248-11E8-B48F-1D18A9856A87","last_name":"Maes"},{"last_name":"Donahue","full_name":"Donahue, Ryan J.","first_name":"Ryan J."},{"last_name":"Ikeda","full_name":"Ikeda, Akihiro","first_name":"Akihiro"},{"full_name":"Nickells, Robert W.","first_name":"Robert W.","last_name":"Nickells"}],"issue":"7","article_number":"1593","date_created":"2021-08-01T22:01:22Z","file_date_updated":"2021-08-04T14:01:30Z","citation":{"short":"N.A. Muench, S. Patel, M.E. Maes, R.J. Donahue, A. Ikeda, R.W. Nickells, Cells 10 (2021).","apa":"Muench, N. A., Patel, S., Maes, M. E., Donahue, R. J., Ikeda, A., &#38; Nickells, R. W. (2021). The influence of mitochondrial dynamics and function on retinal ganglion cell susceptibility in optic nerve disease. <i>Cells</i>. MDPI. <a href=\"https://doi.org/10.3390/cells10071593\">https://doi.org/10.3390/cells10071593</a>","ista":"Muench NA, Patel S, Maes ME, Donahue RJ, Ikeda A, Nickells RW. 2021. The influence of mitochondrial dynamics and function on retinal ganglion cell susceptibility in optic nerve disease. Cells. 10(7), 1593.","mla":"Muench, Nicole A., et al. “The Influence of Mitochondrial Dynamics and Function on Retinal Ganglion Cell Susceptibility in Optic Nerve Disease.” <i>Cells</i>, vol. 10, no. 7, 1593, MDPI, 2021, doi:<a href=\"https://doi.org/10.3390/cells10071593\">10.3390/cells10071593</a>.","chicago":"Muench, Nicole A., Sonia Patel, Margaret E Maes, Ryan J. Donahue, Akihiro Ikeda, and Robert W. Nickells. “The Influence of Mitochondrial Dynamics and Function on Retinal Ganglion Cell Susceptibility in Optic Nerve Disease.” <i>Cells</i>. MDPI, 2021. <a href=\"https://doi.org/10.3390/cells10071593\">https://doi.org/10.3390/cells10071593</a>.","ama":"Muench NA, Patel S, Maes ME, Donahue RJ, Ikeda A, Nickells RW. The influence of mitochondrial dynamics and function on retinal ganglion cell susceptibility in optic nerve disease. <i>Cells</i>. 2021;10(7). doi:<a href=\"https://doi.org/10.3390/cells10071593\">10.3390/cells10071593</a>","ieee":"N. A. Muench, S. Patel, M. E. Maes, R. J. Donahue, A. Ikeda, and R. W. Nickells, “The influence of mitochondrial dynamics and function on retinal ganglion cell susceptibility in optic nerve disease,” <i>Cells</i>, vol. 10, no. 7. MDPI, 2021."},"file":[{"file_name":"2021_Cells_Muench.pdf","content_type":"application/pdf","access_level":"open_access","success":1,"file_size":4555611,"creator":"cziletti","date_updated":"2021-08-04T14:01:30Z","date_created":"2021-08-04T14:01:30Z","relation":"main_file","checksum":"e0497ce5c77fa3b65a538c7d6e0f6c66","file_id":"9768"}],"publication_status":"published","publication":"Cells","status":"public","ddc":["570"],"has_accepted_license":"1","scopus_import":"1","pmid":1,"oa":1,"external_id":{"pmid":["34201955"],"isi":["000678193300001"]},"language":[{"iso":"eng"}],"article_processing_charge":"Yes","abstract":[{"text":"The important roles of mitochondrial function and dysfunction in the process of neurodegeneration are widely acknowledged. Retinal ganglion cells (RGCs) appear to be a highly vulnerable neuronal cell type in the central nervous system with respect to mitochondrial dysfunction but the actual reasons for this are still incompletely understood. These cells have a unique circumstance where unmyelinated axons must bend nearly 90° to exit the eye and then cross a translaminar pressure gradient before becoming myelinated in the optic nerve. This region, the optic nerve head, contains some of the highest density of mitochondria present in these cells. Glaucoma represents a perfect storm of events occurring at this location, with a combination of changes in the translaminar pressure gradient and reassignment of the metabolic support functions of supporting glia, which appears to apply increased metabolic stress to the RGC axons leading to a failure of axonal transport mechanisms. However, RGCs themselves are also extremely sensitive to genetic mutations, particularly in genes affecting mitochondrial dynamics and mitochondrial clearance. These mutations, which systemically affect the mitochondria in every cell, often lead to an optic neuropathy as the sole pathologic defect in affected patients. This review summarizes knowledge of mitochondrial structure and function, the known energy demands of neurons in general, and places these in the context of normal and pathological characteristics of mitochondria attributed to RGCs. ","lang":"eng"}],"intvolume":"        10","department":[{"_id":"SaSi"}],"date_published":"2021-06-25T00:00:00Z","date_updated":"2026-04-02T13:56:24Z","volume":10,"fulldoi":"https://doi.org/10.3390/cells10071593","publication_identifier":{"eissn":["2073-4409"]},"quality_controlled":"1","isi":1,"oa_version":"Published Version","title":"The influence of mitochondrial dynamics and function on retinal ganglion cell susceptibility in optic nerve disease","day":"25","year":"2021","doi":"10.3390/cells10071593","acknowledgement":"The authors are grateful to Kazuya Oikawa and Gillian McLellan for generously sharing some of their data for this review, and to Janis Eells for helpful comments on the manuscript.","_id":"9761","publisher":"MDPI","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"article_type":"original","month":"06","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd"},{"citation":{"short":"A. Raso, E. Dirkx, V. Sampaio-Pinto, H. el Azzouzi, R.J. Cubero, D.W. Sorensen, L. Ottaviani, S. Olieslagers, M.M. Huibers, R. de Weger, S. Siddiqi, S. Moimas, C. Torrini, L. Zentillin, L. Braga, D.S. Nascimento, P.A. da Costa Martins, J.H. van Berlo, S. Zacchigna, M. Giacca, L.J. De Windt, Nature Communications 12 (2021).","apa":"Raso, A., Dirkx, E., Sampaio-Pinto, V., el Azzouzi, H., Cubero, R. J., Sorensen, D. W., … De Windt, L. J. (2021). A microRNA program regulates the balance between cardiomyocyte hyperplasia and hypertrophy and stimulates cardiac regeneration. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-021-25211-4\">https://doi.org/10.1038/s41467-021-25211-4</a>","ista":"Raso A, Dirkx E, Sampaio-Pinto V, el Azzouzi H, Cubero RJ, Sorensen DW, Ottaviani L, Olieslagers S, Huibers MM, de Weger R, Siddiqi S, Moimas S, Torrini C, Zentillin L, Braga L, Nascimento DS, da Costa Martins PA, van Berlo JH, Zacchigna S, Giacca M, De Windt LJ. 2021. A microRNA program regulates the balance between cardiomyocyte hyperplasia and hypertrophy and stimulates cardiac regeneration. Nature Communications. 12, 4808.","ama":"Raso A, Dirkx E, Sampaio-Pinto V, et al. A microRNA program regulates the balance between cardiomyocyte hyperplasia and hypertrophy and stimulates cardiac regeneration. <i>Nature Communications</i>. 2021;12. doi:<a href=\"https://doi.org/10.1038/s41467-021-25211-4\">10.1038/s41467-021-25211-4</a>","chicago":"Raso, Andrea, Ellen Dirkx, Vasco Sampaio-Pinto, Hamid el Azzouzi, Ryan J Cubero, Daniel W. Sorensen, Lara Ottaviani, et al. “A MicroRNA Program Regulates the Balance between Cardiomyocyte Hyperplasia and Hypertrophy and Stimulates Cardiac Regeneration.” <i>Nature Communications</i>. Springer Nature, 2021. <a href=\"https://doi.org/10.1038/s41467-021-25211-4\">https://doi.org/10.1038/s41467-021-25211-4</a>.","ieee":"A. Raso <i>et al.</i>, “A microRNA program regulates the balance between cardiomyocyte hyperplasia and hypertrophy and stimulates cardiac regeneration,” <i>Nature Communications</i>, vol. 12. Springer Nature, 2021.","mla":"Raso, Andrea, et al. “A MicroRNA Program Regulates the Balance between Cardiomyocyte Hyperplasia and Hypertrophy and Stimulates Cardiac Regeneration.” <i>Nature Communications</i>, vol. 12, 4808, Springer Nature, 2021, doi:<a href=\"https://doi.org/10.1038/s41467-021-25211-4\">10.1038/s41467-021-25211-4</a>."},"file":[{"checksum":"48d8562e8229e4282f3f354b329722c5","file_id":"9876","date_created":"2021-08-10T12:29:59Z","relation":"main_file","date_updated":"2021-08-10T12:29:59Z","file_name":"2021_NatureCommunications_Raso.pdf","content_type":"application/pdf","creator":"asandaue","file_size":4364333,"success":1,"access_level":"open_access"}],"publication_status":"published","type":"journal_article","author":[{"full_name":"Raso, Andrea","first_name":"Andrea","last_name":"Raso"},{"last_name":"Dirkx","first_name":"Ellen","full_name":"Dirkx, Ellen"},{"last_name":"Sampaio-Pinto","full_name":"Sampaio-Pinto, Vasco","first_name":"Vasco"},{"first_name":"Hamid","full_name":"el Azzouzi, Hamid","last_name":"el Azzouzi"},{"orcid":"0000-0003-0002-1867","full_name":"Cubero, Ryan J","first_name":"Ryan J","last_name":"Cubero","id":"850B2E12-9CD4-11E9-837F-E719E6697425"},{"first_name":"Daniel W.","full_name":"Sorensen, Daniel W.","last_name":"Sorensen"},{"first_name":"Lara","full_name":"Ottaviani, Lara","last_name":"Ottaviani"},{"first_name":"Servé","full_name":"Olieslagers, Servé","last_name":"Olieslagers"},{"last_name":"Huibers","first_name":"Manon M.","full_name":"Huibers, Manon M."},{"last_name":"de Weger","full_name":"de Weger, Roel","first_name":"Roel"},{"last_name":"Siddiqi","full_name":"Siddiqi, Sailay","first_name":"Sailay"},{"last_name":"Moimas","first_name":"Silvia","full_name":"Moimas, Silvia"},{"last_name":"Torrini","full_name":"Torrini, Consuelo","first_name":"Consuelo"},{"last_name":"Zentillin","full_name":"Zentillin, Lorena","first_name":"Lorena"},{"first_name":"Luca","full_name":"Braga, Luca","last_name":"Braga"},{"last_name":"Nascimento","first_name":"Diana S.","full_name":"Nascimento, Diana S."},{"last_name":"da Costa Martins","full_name":"da Costa Martins, Paula A.","first_name":"Paula A."},{"full_name":"van Berlo, Jop H.","first_name":"Jop H.","last_name":"van Berlo"},{"first_name":"Serena","full_name":"Zacchigna, Serena","last_name":"Zacchigna"},{"first_name":"Mauro","full_name":"Giacca, Mauro","last_name":"Giacca"},{"full_name":"De Windt, Leon J.","first_name":"Leon J.","last_name":"De Windt"}],"date_created":"2021-08-10T11:49:20Z","article_number":"4808","file_date_updated":"2021-08-10T12:29:59Z","pmid":1,"language":[{"iso":"eng"}],"external_id":{"pmid":["34376683"],"isi":["000683910200042"]},"oa":1,"article_processing_charge":"Yes","abstract":[{"text":"Myocardial regeneration is restricted to early postnatal life, when mammalian cardiomyocytes still retain the ability to proliferate. The molecular cues that induce cell cycle arrest of neonatal cardiomyocytes towards terminally differentiated adult heart muscle cells remain obscure. Here we report that the miR-106b~25 cluster is higher expressed in the early postnatal myocardium and decreases in expression towards adulthood, especially under conditions of overload, and orchestrates the transition of cardiomyocyte hyperplasia towards cell cycle arrest and hypertrophy by virtue of its targetome. In line, gene delivery of miR-106b~25 to the mouse heart provokes cardiomyocyte proliferation by targeting a network of negative cell cycle regulators including E2f5, Cdkn1c, Ccne1 and Wee1. Conversely, gene-targeted miR-106b~25 null mice display spontaneous hypertrophic remodeling and exaggerated remodeling to overload by derepression of the prohypertrophic transcription factors Hand2 and Mef2d. Taking advantage of the regulatory function of miR-106b~25 on cardiomyocyte hyperplasia and hypertrophy, viral gene delivery of miR-106b~25 provokes nearly complete regeneration of the adult myocardium after ischemic injury. Our data demonstrate that exploitation of conserved molecular programs can enhance the regenerative capacity of the injured heart.","lang":"eng"}],"intvolume":"        12","department":[{"_id":"SaSi"}],"date_published":"2021-08-10T00:00:00Z","publication":"Nature Communications","status":"public","ddc":["610","570"],"scopus_import":"1","has_accepted_license":"1","isi":1,"oa_version":"Published Version","date_updated":"2023-08-11T10:27:03Z","volume":12,"fulldoi":"https://doi.org/10.1038/s41467-021-25211-4","genbank":["GSE178867"],"quality_controlled":"1","publication_identifier":{"eissn":["2041-1723"]},"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"article_type":"original","month":"08","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","title":"A microRNA program regulates the balance between cardiomyocyte hyperplasia and hypertrophy and stimulates cardiac regeneration","day":"10","year":"2021","doi":"10.1038/s41467-021-25211-4","_id":"9874","related_material":{"link":[{"url":"https://doi.org/10.1038/s41467-022-32785-0","relation":"erratum"}]},"acknowledgement":"E.D. is supported by a VENI award 916-150-16 from the Netherlands Organization for Health Research and Development (ZonMW), an EMBO Long-term Fellowship (EMBO ALTF 848-2013) and a FP7 Marie Curie Intra-European Fellowship (Project number 627539). V.S.P. was funded by a fellowship from the FCT/ Ministério da Ciência, Tecnologia e Inovação SFRH/BD/111799/2015. P.D.C.M. is an Established Investigator of the Dutch Heart Foundation. L.D.W. acknowledges support from the Dutch CardioVascular Alliance (ARENA-PRIME). L.D.W. was further supported by grant 311549 from the European Research Council (ERC), a VICI award 918-156-47 from the Dutch Research Council and Marie Sklodowska-Curie grant agreement no. 813716 (TRAIN-HEART).","publisher":"Springer Nature"},{"date_updated":"2026-08-12T11:15:05Z","volume":62,"fulldoi":"https://doi.org/10.1167/IOVS.62.10.14","publication_identifier":{"issn":["0146-0404"],"eissn":["1552-5783"]},"quality_controlled":"1","isi":1,"oa_version":"Published Version","title":"Increased susceptibility and intrinsic apoptotic signaling in neurons by induced HDAC3 expression","year":"2021","day":"16","acknowledgement":"The authors thank Joel Dietz for maintaining the mice used in this study, Satoshi Kinoshita and the Translational Research Initiative in Pathology Laboratory at the University of Wisconsin-Madison for cutting retinal sections analyzed in this study, and Mark Banghart for statistical review of the data analysis. Supported by National Eye Institute Grants R01 EY012223 (RWN), R01 EY030123 (RWN), R01 EY029809 (LWG), R01 EY029809 (LWG) and a Vision Research CORE grant P30 EY016665, NRSA grant T32 GM081061, by an unrestricted research grant from Research to Prevent Blindness, Inc., and by a University of Wisconsin-Madison Vilas Life Cycle award and the Frederick A. Davis Research Chair (RWN). ","_id":"10000","publisher":"Association for Research in Vision and Ophthalmology","doi":"10.1167/IOVS.62.10.14","tmp":{"short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)"},"article_type":"original","month":"08","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"full_name":"Schmitt, Heather M.","first_name":"Heather M.","last_name":"Schmitt"},{"first_name":"Rachel L.","full_name":"Fehrman, Rachel L.","last_name":"Fehrman"},{"orcid":"0000-0001-9642-1085","full_name":"Maes, Margaret E","first_name":"Margaret E","last_name":"Maes","id":"3838F452-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Yang","full_name":"Yang, Huan","first_name":"Huan"},{"last_name":"Guo","full_name":"Guo, Lian Wang","first_name":"Lian Wang"},{"last_name":"Schlamp","first_name":"Cassandra L.","full_name":"Schlamp, Cassandra L."},{"last_name":"Pelzel","full_name":"Pelzel, Heather R.","first_name":"Heather R."},{"first_name":"Robert W.","full_name":"Nickells, Robert W.","last_name":"Nickells"}],"issue":"10","type":"journal_article","article_number":"14","date_created":"2021-09-12T22:01:23Z","file_date_updated":"2022-05-13T07:40:15Z","file":[{"content_type":"application/pdf","file_name":"2021_IOVS_Schmitt.pdf","success":1,"access_level":"open_access","file_size":19707796,"creator":"dernst","date_updated":"2022-05-13T07:40:15Z","relation":"main_file","date_created":"2022-05-13T07:40:15Z","file_id":"11369","checksum":"c430967746f653aa1ae84ee617f62b73"}],"citation":{"ieee":"H. M. Schmitt <i>et al.</i>, “Increased susceptibility and intrinsic apoptotic signaling in neurons by induced HDAC3 expression,” <i>Investigative Ophthalmology &#38; Visual Science</i>, vol. 62, no. 10. Association for Research in Vision and Ophthalmology, 2021.","ama":"Schmitt HM, Fehrman RL, Maes ME, et al. Increased susceptibility and intrinsic apoptotic signaling in neurons by induced HDAC3 expression. <i>Investigative Ophthalmology &#38; Visual Science</i>. 2021;62(10). doi:<a href=\"https://doi.org/10.1167/IOVS.62.10.14\">10.1167/IOVS.62.10.14</a>","chicago":"Schmitt, Heather M., Rachel L. Fehrman, Margaret E Maes, Huan Yang, Lian Wang Guo, Cassandra L. Schlamp, Heather R. Pelzel, and Robert W. Nickells. “Increased Susceptibility and Intrinsic Apoptotic Signaling in Neurons by Induced HDAC3 Expression.” <i>Investigative Ophthalmology &#38; Visual Science</i>. Association for Research in Vision and Ophthalmology, 2021. <a href=\"https://doi.org/10.1167/IOVS.62.10.14\">https://doi.org/10.1167/IOVS.62.10.14</a>.","mla":"Schmitt, Heather M., et al. “Increased Susceptibility and Intrinsic Apoptotic Signaling in Neurons by Induced HDAC3 Expression.” <i>Investigative Ophthalmology &#38; Visual Science</i>, vol. 62, no. 10, 14, Association for Research in Vision and Ophthalmology, 2021, doi:<a href=\"https://doi.org/10.1167/IOVS.62.10.14\">10.1167/IOVS.62.10.14</a>.","ista":"Schmitt HM, Fehrman RL, Maes ME, Yang H, Guo LW, Schlamp CL, Pelzel HR, Nickells RW. 2021. Increased susceptibility and intrinsic apoptotic signaling in neurons by induced HDAC3 expression. Investigative Ophthalmology &#38; Visual Science. 62(10), 14.","apa":"Schmitt, H. M., Fehrman, R. L., Maes, M. E., Yang, H., Guo, L. W., Schlamp, C. L., … Nickells, R. W. (2021). Increased susceptibility and intrinsic apoptotic signaling in neurons by induced HDAC3 expression. <i>Investigative Ophthalmology &#38; Visual Science</i>. Association for Research in Vision and Ophthalmology. <a href=\"https://doi.org/10.1167/IOVS.62.10.14\">https://doi.org/10.1167/IOVS.62.10.14</a>","short":"H.M. Schmitt, R.L. Fehrman, M.E. Maes, H. Yang, L.W. Guo, C.L. Schlamp, H.R. Pelzel, R.W. Nickells, Investigative Ophthalmology &#38; Visual Science 62 (2021)."},"publication_status":"published","publication":"Investigative Ophthalmology & Visual Science","status":"public","scopus_import":"1","has_accepted_license":"1","ddc":["570"],"pmid":1,"article_processing_charge":"Yes","language":[{"iso":"eng"}],"external_id":{"isi":["000695230000014"],"pmid":["34398198"]},"oa":1,"date_published":"2021-08-16T00:00:00Z","department":[{"_id":"SaSi"}],"intvolume":"        62","abstract":[{"lang":"eng","text":"Inhibition or targeted deletion of histone deacetylase 3 (HDAC3) is neuroprotective in a variety neurodegenerative conditions, including retinal ganglion cells (RGCs) after acute optic nerve damage. Consistent with this, induced HDAC3 expression in cultured cells shows selective toxicity to neurons. Despite an established role for HDAC3 in neuronal pathology, little is known regarding the mechanism of this pathology."}]},{"isi":1,"oa_version":"Published Version","volume":10,"date_updated":"2026-04-02T14:23:52Z","quality_controlled":"1","publication_identifier":{"eissn":["2045-2322"]},"fulldoi":"https://doi.org/10.1038/s41598-020-62089-6","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"month":"03","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","article_type":"original","year":"2020","day":"27","title":"Action representation in the mouse parieto-frontal network","_id":"7632","publisher":"Springer Nature","doi":"10.1038/s41598-020-62089-6","file":[{"file_size":2621249,"access_level":"open_access","creator":"dernst","file_name":"2020_ScientificReports_Tombaz.pdf","content_type":"application/pdf","date_updated":"2020-07-14T12:48:01Z","checksum":"e6cfaaaf7986532132934400038b824a","file_id":"7644","date_created":"2020-04-06T10:44:23Z","relation":"main_file"}],"citation":{"chicago":"Tombaz, Tuce, Benjamin A. Dunn, Karoline Hovde, Ryan J Cubero, Bartul Mimica, Pranav Mamidanna, Yasser Roudi, and Jonathan R. Whitlock. “Action Representation in the Mouse Parieto-Frontal Network.” <i>Scientific Reports</i>. Springer Nature, 2020. <a href=\"https://doi.org/10.1038/s41598-020-62089-6\">https://doi.org/10.1038/s41598-020-62089-6</a>.","ama":"Tombaz T, Dunn BA, Hovde K, et al. Action representation in the mouse parieto-frontal network. <i>Scientific reports</i>. 2020;10(1). doi:<a href=\"https://doi.org/10.1038/s41598-020-62089-6\">10.1038/s41598-020-62089-6</a>","mla":"Tombaz, Tuce, et al. “Action Representation in the Mouse Parieto-Frontal Network.” <i>Scientific Reports</i>, vol. 10, no. 1, 5559, Springer Nature, 2020, doi:<a href=\"https://doi.org/10.1038/s41598-020-62089-6\">10.1038/s41598-020-62089-6</a>.","ieee":"T. Tombaz <i>et al.</i>, “Action representation in the mouse parieto-frontal network,” <i>Scientific reports</i>, vol. 10, no. 1. Springer Nature, 2020.","ista":"Tombaz T, Dunn BA, Hovde K, Cubero RJ, Mimica B, Mamidanna P, Roudi Y, Whitlock JR. 2020. Action representation in the mouse parieto-frontal network. Scientific reports. 10(1), 5559.","apa":"Tombaz, T., Dunn, B. A., Hovde, K., Cubero, R. J., Mimica, B., Mamidanna, P., … Whitlock, J. R. (2020). Action representation in the mouse parieto-frontal network. <i>Scientific Reports</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41598-020-62089-6\">https://doi.org/10.1038/s41598-020-62089-6</a>","short":"T. Tombaz, B.A. Dunn, K. Hovde, R.J. Cubero, B. Mimica, P. Mamidanna, Y. Roudi, J.R. Whitlock, Scientific Reports 10 (2020)."},"publication_status":"published","article_number":"5559","date_created":"2020-04-05T22:00:47Z","author":[{"last_name":"Tombaz","first_name":"Tuce","full_name":"Tombaz, Tuce"},{"last_name":"Dunn","full_name":"Dunn, Benjamin A.","first_name":"Benjamin A."},{"first_name":"Karoline","full_name":"Hovde, Karoline","last_name":"Hovde"},{"last_name":"Cubero","id":"850B2E12-9CD4-11E9-837F-E719E6697425","full_name":"Cubero, Ryan J","orcid":"0000-0003-0002-1867","first_name":"Ryan J"},{"last_name":"Mimica","first_name":"Bartul","full_name":"Mimica, Bartul"},{"last_name":"Mamidanna","first_name":"Pranav","full_name":"Mamidanna, Pranav"},{"last_name":"Roudi","first_name":"Yasser","full_name":"Roudi, Yasser"},{"first_name":"Jonathan R.","full_name":"Whitlock, Jonathan R.","last_name":"Whitlock"}],"issue":"1","type":"journal_article","file_date_updated":"2020-07-14T12:48:01Z","date_published":"2020-03-27T00:00:00Z","department":[{"_id":"SaSi"}],"intvolume":"        10","abstract":[{"text":"The posterior parietal cortex (PPC) and frontal motor areas comprise a cortical network supporting goal-directed behaviour, with functions including sensorimotor transformations and decision making. In primates, this network links performed and observed actions via mirror neurons, which fire both when individuals perform an action and when they observe the same action performed by a conspecific. Mirror neurons are believed to be important for social learning, but it is not known whether mirror-like neurons occur in similar networks in other social species, such as rodents, or if they can be measured in such models using paradigms where observers passively view a demonstrator. Therefore, we imaged Ca2+ responses in PPC and secondary motor cortex (M2) while mice performed and observed pellet-reaching and wheel-running tasks, and found that cell populations in both areas robustly encoded several naturalistic behaviours. However, neural responses to the same set of observed actions were absent, although we verified that observer mice were attentive to performers and that PPC neurons responded reliably to visual cues. Statistical modelling also indicated that executed actions outperformed observed actions in predicting neural responses. These results raise the possibility that sensorimotor action recognition in rodents could take place outside of the parieto-frontal circuit, and underscore that detecting socially-driven neural coding depends critically on the species and behavioural paradigm used.","lang":"eng"}],"article_processing_charge":"No","external_id":{"isi":["000560406800007"]},"oa":1,"language":[{"iso":"eng"}],"status":"public","publication":"Scientific reports","scopus_import":"1","has_accepted_license":"1","ddc":["570"]},{"issue":"16","author":[{"first_name":"Rita R.","full_name":"Fagan, Rita R.","last_name":"Fagan"},{"first_name":"Patrick J.","full_name":"Kearney, Patrick J.","last_name":"Kearney"},{"last_name":"Sweeney","first_name":"Carolyn G.","full_name":"Sweeney, Carolyn G."},{"first_name":"Dino","full_name":"Luethi, Dino","last_name":"Luethi"},{"last_name":"Schoot Uiterkamp","id":"3526230C-F248-11E8-B48F-1D18A9856A87","full_name":"Schoot Uiterkamp, Florianne E","first_name":"Florianne E"},{"full_name":"Schicker, Klaus","first_name":"Klaus","last_name":"Schicker"},{"first_name":"Brian S.","full_name":"Alejandro, Brian S.","last_name":"Alejandro"},{"full_name":"O'Connor, Lauren C.","first_name":"Lauren C.","last_name":"O'Connor"},{"last_name":"Sitte","first_name":"Harald H.","full_name":"Sitte, Harald H."},{"last_name":"Melikian","first_name":"Haley E.","full_name":"Melikian, Haley E."}],"type":"journal_article","date_created":"2020-05-24T22:00:59Z","page":"5229-5244","citation":{"apa":"Fagan, R. R., Kearney, P. J., Sweeney, C. G., Luethi, D., Schoot Uiterkamp, F. E., Schicker, K., … Melikian, H. E. (2020). Dopamine transporter trafficking and Rit2 GTPase: Mechanism of action and in vivo impact. <i>Journal of Biological Chemistry</i>. ASBMB Publications. <a href=\"https://doi.org/10.1074/jbc.RA120.012628\">https://doi.org/10.1074/jbc.RA120.012628</a>","short":"R.R. Fagan, P.J. Kearney, C.G. Sweeney, D. Luethi, F.E. Schoot Uiterkamp, K. Schicker, B.S. Alejandro, L.C. O’Connor, H.H. Sitte, H.E. Melikian, Journal of Biological Chemistry 295 (2020) 5229–5244.","ista":"Fagan RR, Kearney PJ, Sweeney CG, Luethi D, Schoot Uiterkamp FE, Schicker K, Alejandro BS, O’Connor LC, Sitte HH, Melikian HE. 2020. Dopamine transporter trafficking and Rit2 GTPase: Mechanism of action and in vivo impact. Journal of Biological Chemistry. 295(16), 5229–5244.","mla":"Fagan, Rita R., et al. “Dopamine Transporter Trafficking and Rit2 GTPase: Mechanism of Action and in Vivo Impact.” <i>Journal of Biological Chemistry</i>, vol. 295, no. 16, ASBMB Publications, 2020, pp. 5229–44, doi:<a href=\"https://doi.org/10.1074/jbc.RA120.012628\">10.1074/jbc.RA120.012628</a>.","ieee":"R. R. Fagan <i>et al.</i>, “Dopamine transporter trafficking and Rit2 GTPase: Mechanism of action and in vivo impact,” <i>Journal of Biological Chemistry</i>, vol. 295, no. 16. ASBMB Publications, pp. 5229–5244, 2020.","ama":"Fagan RR, Kearney PJ, Sweeney CG, et al. Dopamine transporter trafficking and Rit2 GTPase: Mechanism of action and in vivo impact. <i>Journal of Biological Chemistry</i>. 2020;295(16):5229-5244. doi:<a href=\"https://doi.org/10.1074/jbc.RA120.012628\">10.1074/jbc.RA120.012628</a>","chicago":"Fagan, Rita R., Patrick J. Kearney, Carolyn G. Sweeney, Dino Luethi, Florianne E Schoot Uiterkamp, Klaus Schicker, Brian S. Alejandro, Lauren C. O’Connor, Harald H. Sitte, and Haley E. Melikian. “Dopamine Transporter Trafficking and Rit2 GTPase: Mechanism of Action and in Vivo Impact.” <i>Journal of Biological Chemistry</i>. ASBMB Publications, 2020. <a href=\"https://doi.org/10.1074/jbc.RA120.012628\">https://doi.org/10.1074/jbc.RA120.012628</a>."},"publication_status":"published","status":"public","publication":"Journal of Biological Chemistry","scopus_import":"1","pmid":1,"main_file_link":[{"open_access":"1","url":"https://escholarship.umassmed.edu/oapubs/4187"}],"article_processing_charge":"No","external_id":{"isi":["000530288000006"],"pmid":["32132171"]},"language":[{"iso":"eng"}],"oa":1,"date_published":"2020-04-17T00:00:00Z","department":[{"_id":"SaSi"}],"intvolume":"       295","abstract":[{"text":"Following its evoked release, dopamine (DA) signaling is rapidly terminated by presynaptic reuptake, mediated by the cocaine-sensitive DA transporter (DAT). DAT surface availability is dynamically regulated by endocytic trafficking, and direct protein kinase C (PKC) activation acutely diminishes DAT surface expression by accelerating DAT internalization. Previous cell line studies demonstrated that PKC-stimulated DAT endocytosis requires both Ack1 inactivation, which releases a DAT-specific endocytic brake, and the neuronal GTPase, Rit2, which binds DAT. However, it is unknown whether Rit2 is required for PKC-stimulated DAT endocytosis in DAergic terminals or whether there are region- and/or sex-dependent differences in PKC-stimulated DAT trafficking. Moreover, the mechanisms by which Rit2 controls PKC-stimulated DAT endocytosis are unknown. Here, we directly examined these important questions. Ex vivo studies revealed that PKC activation acutely decreased DAT surface expression selectively in ventral, but not dorsal, striatum. AAV-mediated, conditional Rit2 knockdown in DAergic neurons impacted baseline DAT surface:intracellular distribution in DAergic terminals from female ventral, but not dorsal, striatum. Further, Rit2 was required for PKC-stimulated DAT internalization in both male and female ventral striatum. FRET and surface pulldown studies in cell lines revealed that PKC activation drives DAT-Rit2 surface dissociation and that the DAT N terminus is required for both PKC-mediated DAT-Rit2 dissociation and DAT internalization. Finally, we found that Rit2 and Ack1 independently converge on DAT to facilitate PKC-stimulated DAT endocytosis. Together, our data provide greater insight into mechanisms that mediate PKC-regulated DAT internalization and reveal unexpected region-specific differences in PKC-stimulated DAT trafficking in bona fide DAergic terminals. ","lang":"eng"}],"date_updated":"2025-07-10T11:54:48Z","volume":295,"fulldoi":"https://doi.org/10.1074/jbc.RA120.012628","quality_controlled":"1","publication_identifier":{"issn":["0021-9258"],"eissn":["1083-351X"]},"isi":1,"oa_version":"Submitted Version","title":"Dopamine transporter trafficking and Rit2 GTPase: Mechanism of action and in vivo impact","year":"2020","day":"17","_id":"7880","publisher":"ASBMB Publications","doi":"10.1074/jbc.RA120.012628","article_type":"original","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","month":"04"},{"citation":{"apa":"Donahue, R., Maes, M. E., Grosser, J., &#38; Nickells, R. (2020). BAX-depleted retinal ganglion cells survive and become quiescent following optic nerve damage. <i>Molecular Neurobiology</i>. Springer Nature. <a href=\"https://doi.org/10.1007/s12035-019-01783-7\">https://doi.org/10.1007/s12035-019-01783-7</a>","short":"R. Donahue, M.E. Maes, J. Grosser, R. Nickells, Molecular Neurobiology 57 (2020) 1070–1084.","ista":"Donahue R, Maes ME, Grosser J, Nickells R. 2020. BAX-depleted retinal ganglion cells survive and become quiescent following optic nerve damage. Molecular Neurobiology. 57(2), 1070–1084.","mla":"Donahue, RJ, et al. “BAX-Depleted Retinal Ganglion Cells Survive and Become Quiescent Following Optic Nerve Damage.” <i>Molecular Neurobiology</i>, vol. 57, no. 2, Springer Nature, 2020, pp. 1070–1084, doi:<a href=\"https://doi.org/10.1007/s12035-019-01783-7\">10.1007/s12035-019-01783-7</a>.","chicago":"Donahue, RJ, Margaret E Maes, JA Grosser, and RW Nickells. “BAX-Depleted Retinal Ganglion Cells Survive and Become Quiescent Following Optic Nerve Damage.” <i>Molecular Neurobiology</i>. Springer Nature, 2020. <a href=\"https://doi.org/10.1007/s12035-019-01783-7\">https://doi.org/10.1007/s12035-019-01783-7</a>.","ama":"Donahue R, Maes ME, Grosser J, Nickells R. BAX-depleted retinal ganglion cells survive and become quiescent following optic nerve damage. <i>Molecular Neurobiology</i>. 2020;57(2):1070–1084. doi:<a href=\"https://doi.org/10.1007/s12035-019-01783-7\">10.1007/s12035-019-01783-7</a>","ieee":"R. Donahue, M. E. Maes, J. Grosser, and R. Nickells, “BAX-depleted retinal ganglion cells survive and become quiescent following optic nerve damage,” <i>Molecular Neurobiology</i>, vol. 57, no. 2. Springer Nature, pp. 1070–1084, 2020."},"publication_status":"published","issue":"2","author":[{"last_name":"Donahue","first_name":"RJ","full_name":"Donahue, RJ"},{"id":"3838F452-F248-11E8-B48F-1D18A9856A87","last_name":"Maes","first_name":"Margaret E","orcid":"0000-0001-9642-1085","full_name":"Maes, Margaret E"},{"full_name":"Grosser, JA","first_name":"JA","last_name":"Grosser"},{"first_name":"RW","full_name":"Nickells, RW","last_name":"Nickells"}],"type":"journal_article","date_created":"2019-11-18T14:18:39Z","page":"1070–1084","pmid":1,"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7035206/","open_access":"1"}],"article_processing_charge":"No","external_id":{"pmid":["31673950"],"isi":["000493754200001"]},"language":[{"iso":"eng"}],"oa":1,"department":[{"_id":"SaSi"}],"date_published":"2020-02-01T00:00:00Z","intvolume":"        57","abstract":[{"text":"Removal of the Bax gene from mice completely protects the somas of retinal ganglion cells (RGCs) from apoptosis following optic nerve injury. This makes BAX a promising therapeutic target to prevent neurodegeneration. In this study, Bax+/− mice were used to test the hypothesis that lowering the quantity of BAX in RGCs would delay apoptosis following optic nerve injury. RGCs were damaged by performing optic nerve crush (ONC) and then immunostaining for phospho-cJUN, and quantitative PCR were used to monitor the status of the BAX activation mechanism in the months following injury. The apoptotic susceptibility of injured cells was directly tested by virally introducing GFP-BAX into Bax−/− RGCs after injury. The competency of quiescent RGCs to reactivate their BAX activation mechanism was tested by intravitreal injection of the JNK pathway agonist, anisomycin. Twenty-four weeks after ONC, Bax+/− mice had significantly less cell loss in their RGC layer than Bax+/+ mice 3 weeks after ONC. Bax+/− and Bax+/+ RGCs exhibited similar patterns of nuclear phospho-cJUN accumulation immediately after ONC, which persisted in Bax+/− RGCs for up to 7 weeks before abating. The transcriptional activation of BAX-activating genes was similar in Bax+/− and Bax+/+ RGCs following ONC. Intriguingly, cells deactivated their BAX activation mechanism between 7 and 12 weeks after crush. Introduction of GFP-BAX into Bax−/− cells at 4 weeks after ONC showed that these cells had a nearly normal capacity to activate this protein, but this capacity was lost 8 weeks after crush. Collectively, these data suggest that 8–12 weeks after crush, damaged cells no longer displayed increased susceptibility to BAX activation relative to their naïve counterparts. In this same timeframe, retinal glial activation and the signaling of the pro-apoptotic JNK pathway also abated. Quiescent RGCs did not show a timely reactivation of their JNK pathway following intravitreal injection with anisomycin. These findings demonstrate that lowering the quantity of BAX in RGCs is neuroprotective after acute injury. Damaged RGCs enter a quiescent state months after injury and are no longer responsive to an apoptotic stimulus. Quiescent RGCs will require rejuvenation to reacquire functionality.","lang":"eng"}],"status":"public","publication":"Molecular Neurobiology","scopus_import":"1","isi":1,"oa_version":"Submitted Version","date_updated":"2023-08-17T14:05:48Z","volume":57,"fulldoi":"https://doi.org/10.1007/s12035-019-01783-7","publication_identifier":{"issn":["0893-7648"],"eissn":["1559-1182"]},"quality_controlled":"1","article_type":"original","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","month":"02","title":"BAX-depleted retinal ganglion cells survive and become quiescent following optic nerve damage","year":"2020","day":"01","publisher":"Springer Nature","_id":"7033","acknowledgement":"This work was supported by National Eye Institute grants R01 EY012223 (RWN), R01 EY030123 (RWN), T32 EY027721 (Department of Ophthalmology and Visual Sciences, University of Wisconsin-Madison), and a Vision Science Core grant P30 EY016665 (Department of Ophthalmology and Visual Sciences, University of Wisconsin-Madison), an unrestricted funding grant from Research to Prevent Blindness (Department of Ophthalmology and Visual Sciences, University of Wisconsin-Madison), the Frederick A. Davis Endowment (RWN), and the Mr. and Mrs. George Taylor Foundation (RWN).","doi":"10.1007/s12035-019-01783-7"},{"volume":48,"date_updated":"2025-04-14T07:44:02Z","publication_identifier":{"issn":["0929-5313"],"eissn":["1573-6873"]},"quality_controlled":"1","fulldoi":"https://doi.org/10.1007/s10827-020-00740-x","isi":1,"oa_version":"Published Version","day":"01","year":"2020","corr_author":"1","title":"Multiscale relevance and informative encoding in neuronal spike trains","doi":"10.1007/s10827-020-00740-x","acknowledgement":"This research was supported by the Kavli Foundation and the Centre of Excellence scheme of the Research Council of Norway (Centre for Neural Computation). RJC is currently receiving funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie Grant Agreement No. 754411.","_id":"7369","publisher":"Springer Nature","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"month":"02","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","article_type":"original","page":"85-102","date_created":"2020-01-28T10:34:00Z","keyword":["Time series analysis","Multiple time scale analysis","Spike train data","Information theory","Bayesian decoding"],"type":"journal_article","author":[{"last_name":"Cubero","id":"850B2E12-9CD4-11E9-837F-E719E6697425","orcid":"0000-0003-0002-1867","full_name":"Cubero, Ryan J","first_name":"Ryan J"},{"last_name":"Marsili","first_name":"Matteo","full_name":"Marsili, Matteo"},{"full_name":"Roudi, Yasser","first_name":"Yasser","last_name":"Roudi"}],"file_date_updated":"2020-07-14T12:47:56Z","citation":{"apa":"Cubero, R. J., Marsili, M., &#38; Roudi, Y. (2020). Multiscale relevance and informative encoding in neuronal spike trains. <i>Journal of Computational Neuroscience</i>. Springer Nature. <a href=\"https://doi.org/10.1007/s10827-020-00740-x\">https://doi.org/10.1007/s10827-020-00740-x</a>","short":"R.J. Cubero, M. Marsili, Y. Roudi, Journal of Computational Neuroscience 48 (2020) 85–102.","ista":"Cubero RJ, Marsili M, Roudi Y. 2020. Multiscale relevance and informative encoding in neuronal spike trains. Journal of Computational Neuroscience. 48, 85–102.","chicago":"Cubero, Ryan J, Matteo Marsili, and Yasser Roudi. “Multiscale Relevance and Informative Encoding in Neuronal Spike Trains.” <i>Journal of Computational Neuroscience</i>. Springer Nature, 2020. <a href=\"https://doi.org/10.1007/s10827-020-00740-x\">https://doi.org/10.1007/s10827-020-00740-x</a>.","ama":"Cubero RJ, Marsili M, Roudi Y. Multiscale relevance and informative encoding in neuronal spike trains. <i>Journal of Computational Neuroscience</i>. 2020;48:85-102. doi:<a href=\"https://doi.org/10.1007/s10827-020-00740-x\">10.1007/s10827-020-00740-x</a>","mla":"Cubero, Ryan J., et al. “Multiscale Relevance and Informative Encoding in Neuronal Spike Trains.” <i>Journal of Computational Neuroscience</i>, vol. 48, Springer Nature, 2020, pp. 85–102, doi:<a href=\"https://doi.org/10.1007/s10827-020-00740-x\">10.1007/s10827-020-00740-x</a>.","ieee":"R. J. Cubero, M. Marsili, and Y. Roudi, “Multiscale relevance and informative encoding in neuronal spike trains,” <i>Journal of Computational Neuroscience</i>, vol. 48. Springer Nature, pp. 85–102, 2020."},"file":[{"file_name":"10827_2020_740_MOESM1_ESM.pdf","content_type":"application/pdf","creator":"rcubero","access_level":"open_access","file_size":1941355,"date_created":"2020-01-28T09:31:09Z","relation":"supplementary_material","checksum":"036e9451d6cd0c190ad25791bf82393b","file_id":"7380","date_updated":"2020-07-14T12:47:56Z"},{"file_size":3257880,"access_level":"open_access","creator":"rcubero","content_type":"application/pdf","file_name":"Cubero2020_Article_MultiscaleRelevanceAndInformat.pdf","date_updated":"2020-07-14T12:47:56Z","file_id":"7381","checksum":"4dd8b1fd4b54486f79d82ac7b2a412b2","relation":"main_file","date_created":"2020-01-28T09:31:09Z"}],"project":[{"call_identifier":"H2020","_id":"260C2330-B435-11E9-9278-68D0E5697425","grant_number":"754411","name":"ISTplus - Postdoctoral Fellowships"}],"publication_status":"published","status":"public","publication":"Journal of Computational Neuroscience","ddc":["004","519","570"],"has_accepted_license":"1","scopus_import":"1","intvolume":"        48","abstract":[{"lang":"eng","text":"Neuronal responses to complex stimuli and tasks can encompass a wide range of time scales. Understanding these responses requires measures that characterize how the information on these response patterns are represented across multiple temporal resolutions. In this paper we propose a metric – which we call multiscale relevance (MSR) – to capture the dynamical variability of the activity of single neurons across different time scales. The MSR is a non-parametric, fully featureless indicator in that it uses only the time stamps of the firing activity without resorting to any a priori covariate or invoking any specific structure in the tuning curve for neural activity. When applied to neural data from the mEC and from the ADn and PoS regions of freely-behaving rodents, we found that neurons having low MSR tend to have low mutual information and low firing sparsity across the correlates that are believed to be encoded by the region of the brain where the recordings were made. In addition, neurons with high MSR contain significant information on spatial navigation and allow to decode spatial position or head direction as efficiently as those neurons whose firing activity has high mutual information with the covariate to be decoded and significantly better than the set of neurons with high local variations in their interspike intervals. Given these results, we propose that the MSR can be used as a measure to rank and select neurons for their information content without the need to appeal to any a priori covariate."}],"department":[{"_id":"SaSi"}],"date_published":"2020-02-01T00:00:00Z","external_id":{"isi":["000515321800006"]},"oa":1,"language":[{"iso":"eng"}],"ec_funded":1,"article_processing_charge":"Yes (via OA deal)"},{"scopus_import":"1","has_accepted_license":"1","ddc":["570"],"status":"public","publication":"Nature Communications","article_processing_charge":"No","external_id":{"isi":["000466118700002"]},"oa":1,"language":[{"iso":"eng"}],"date_published":"2019-04-29T00:00:00Z","department":[{"_id":"SaSi"}],"abstract":[{"text":"Polycomb group (PcG) proteins play critical roles in the epigenetic inheritance of cell fate. The Polycomb Repressive Complexes PRC1 and PRC2 catalyse distinct chromatin modifications to enforce gene silencing, but how transcriptional repression is propagated through mitotic cell divisions remains a key unresolved question. Using reversible tethering of PcG proteins to ectopic sites in mouse embryonic stem cells, here we show that PRC1 can trigger transcriptional repression and Polycomb-dependent chromatin modifications. We find that canonical PRC1 (cPRC1), but not variant PRC1, maintains gene silencing through cell division upon reversal of tethering. Propagation of gene repression is sustained by cis-acting histone modifications, PRC2-mediated H3K27me3 and cPRC1-mediated H2AK119ub1, promoting a sequence-independent feedback mechanism for PcG protein recruitment. Thus, the distinct PRC1 complexes present in vertebrates can differentially regulate epigenetic maintenance of gene silencing, potentially enabling dynamic heritable responses to complex stimuli. Our findings reveal how PcG repression is potentially inherited in vertebrates.","lang":"eng"}],"intvolume":"        10","file_date_updated":"2020-07-14T12:47:29Z","issue":"1","author":[{"first_name":"Hagar F.","full_name":"Moussa, Hagar F.","last_name":"Moussa"},{"first_name":"Daniel","full_name":"Bsteh, Daniel","last_name":"Bsteh"},{"last_name":"Yelagandula","full_name":"Yelagandula, Ramesh","first_name":"Ramesh"},{"last_name":"Pribitzer","full_name":"Pribitzer, Carina","first_name":"Carina"},{"full_name":"Stecher, Karin","first_name":"Karin","last_name":"Stecher"},{"last_name":"Bartalska","id":"4D883232-F248-11E8-B48F-1D18A9856A87","full_name":"Bartalska, Katarina","first_name":"Katarina"},{"first_name":"Luca","full_name":"Michetti, Luca","last_name":"Michetti"},{"full_name":"Wang, Jingkui","first_name":"Jingkui","last_name":"Wang"},{"last_name":"Zepeda-Martinez","full_name":"Zepeda-Martinez, Jorge A.","first_name":"Jorge A."},{"full_name":"Elling, Ulrich","first_name":"Ulrich","last_name":"Elling"},{"last_name":"Stuckey","first_name":"Jacob I.","full_name":"Stuckey, Jacob I."},{"last_name":"James","full_name":"James, Lindsey I.","first_name":"Lindsey I."},{"full_name":"Frye, Stephen V.","first_name":"Stephen V.","last_name":"Frye"},{"first_name":"Oliver","full_name":"Bell, Oliver","last_name":"Bell"}],"type":"journal_article","date_created":"2019-05-13T07:58:35Z","article_number":"1931","publication_status":"published","file":[{"access_level":"open_access","file_size":1223647,"creator":"dernst","content_type":"application/pdf","file_name":"2019_NatureComm_Moussa.pdf","date_updated":"2020-07-14T12:47:29Z","relation":"main_file","date_created":"2019-05-14T08:45:51Z","checksum":"6550a328335396c856db4cbdda7d2994","file_id":"6448"}],"citation":{"ista":"Moussa HF, Bsteh D, Yelagandula R, Pribitzer C, Stecher K, Bartalska K, Michetti L, Wang J, Zepeda-Martinez JA, Elling U, Stuckey JI, James LI, Frye SV, Bell O. 2019. Canonical PRC1 controls sequence-independent propagation of Polycomb-mediated gene silencing. Nature Communications. 10(1), 1931.","ama":"Moussa HF, Bsteh D, Yelagandula R, et al. Canonical PRC1 controls sequence-independent propagation of Polycomb-mediated gene silencing. <i>Nature Communications</i>. 2019;10(1). doi:<a href=\"https://doi.org/10.1038/s41467-019-09628-6\">10.1038/s41467-019-09628-6</a>","mla":"Moussa, Hagar F., et al. “Canonical PRC1 Controls Sequence-Independent Propagation of Polycomb-Mediated Gene Silencing.” <i>Nature Communications</i>, vol. 10, no. 1, 1931, Springer Nature, 2019, doi:<a href=\"https://doi.org/10.1038/s41467-019-09628-6\">10.1038/s41467-019-09628-6</a>.","ieee":"H. F. Moussa <i>et al.</i>, “Canonical PRC1 controls sequence-independent propagation of Polycomb-mediated gene silencing,” <i>Nature Communications</i>, vol. 10, no. 1. Springer Nature, 2019.","chicago":"Moussa, Hagar F., Daniel Bsteh, Ramesh Yelagandula, Carina Pribitzer, Karin Stecher, Katarina Bartalska, Luca Michetti, et al. “Canonical PRC1 Controls Sequence-Independent Propagation of Polycomb-Mediated Gene Silencing.” <i>Nature Communications</i>. Springer Nature, 2019. <a href=\"https://doi.org/10.1038/s41467-019-09628-6\">https://doi.org/10.1038/s41467-019-09628-6</a>.","short":"H.F. Moussa, D. Bsteh, R. Yelagandula, C. Pribitzer, K. Stecher, K. Bartalska, L. Michetti, J. Wang, J.A. Zepeda-Martinez, U. Elling, J.I. Stuckey, L.I. James, S.V. Frye, O. Bell, Nature Communications 10 (2019).","apa":"Moussa, H. F., Bsteh, D., Yelagandula, R., Pribitzer, C., Stecher, K., Bartalska, K., … Bell, O. (2019). Canonical PRC1 controls sequence-independent propagation of Polycomb-mediated gene silencing. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-019-09628-6\">https://doi.org/10.1038/s41467-019-09628-6</a>"},"publisher":"Springer Nature","_id":"6412","doi":"10.1038/s41467-019-09628-6","title":"Canonical PRC1 controls sequence-independent propagation of Polycomb-mediated gene silencing","year":"2019","day":"29","month":"04","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"fulldoi":"https://doi.org/10.1038/s41467-019-09628-6","quality_controlled":"1","publication_identifier":{"eissn":["2041-1723"]},"date_updated":"2026-04-03T09:38:23Z","volume":10,"oa_version":"Published Version","isi":1},{"isi":1,"oa_version":"Published Version","date_updated":"2025-03-31T16:01:17Z","volume":707,"fulldoi":"https://doi.org/10.1016/j.neulet.2019.134310","quality_controlled":"1","publication_identifier":{"issn":["0304-3940"]},"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"article_type":"original","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","month":"08","corr_author":"1","title":"Targeting microglia with lentivirus and AAV: Recent advances and remaining challenges","day":"10","year":"2019","doi":"10.1016/j.neulet.2019.134310","publisher":"Elsevier","_id":"6521","citation":{"short":"M.E. Maes, G. Colombo, R. Schulz, S. Siegert, Neuroscience Letters 707 (2019).","apa":"Maes, M. E., Colombo, G., Schulz, R., &#38; Siegert, S. (2019). Targeting microglia with lentivirus and AAV: Recent advances and remaining challenges. <i>Neuroscience Letters</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neulet.2019.134310\">https://doi.org/10.1016/j.neulet.2019.134310</a>","ista":"Maes ME, Colombo G, Schulz R, Siegert S. 2019. Targeting microglia with lentivirus and AAV: Recent advances and remaining challenges. Neuroscience Letters. 707, 134310.","mla":"Maes, Margaret E., et al. “Targeting Microglia with Lentivirus and AAV: Recent Advances and Remaining Challenges.” <i>Neuroscience Letters</i>, vol. 707, 134310, Elsevier, 2019, doi:<a href=\"https://doi.org/10.1016/j.neulet.2019.134310\">10.1016/j.neulet.2019.134310</a>.","ama":"Maes ME, Colombo G, Schulz R, Siegert S. Targeting microglia with lentivirus and AAV: Recent advances and remaining challenges. <i>Neuroscience Letters</i>. 2019;707. doi:<a href=\"https://doi.org/10.1016/j.neulet.2019.134310\">10.1016/j.neulet.2019.134310</a>","chicago":"Maes, Margaret E, Gloria Colombo, Rouven Schulz, and Sandra Siegert. “Targeting Microglia with Lentivirus and AAV: Recent Advances and Remaining Challenges.” <i>Neuroscience Letters</i>. Elsevier, 2019. <a href=\"https://doi.org/10.1016/j.neulet.2019.134310\">https://doi.org/10.1016/j.neulet.2019.134310</a>.","ieee":"M. E. Maes, G. Colombo, R. Schulz, and S. Siegert, “Targeting microglia with lentivirus and AAV: Recent advances and remaining challenges,” <i>Neuroscience Letters</i>, vol. 707. Elsevier, 2019."},"file":[{"date_updated":"2020-07-14T12:47:33Z","relation":"main_file","date_created":"2019-06-08T11:44:20Z","file_id":"6551","checksum":"553c9dbd39727fbed55ee991c51ca4d1","file_name":"2019_Neuroscience_Maes.pdf","content_type":"application/pdf","access_level":"open_access","file_size":1779287,"creator":"dernst"}],"publication_status":"published","project":[{"_id":"2564DBCA-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"665385","name":"International IST Doctoral Program"},{"grant_number":"715571","_id":"25D4A630-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"Microglia action towards neuronal circuit formation and function in health and disease"},{"name":"Modulating microglia through G protein-coupled receptor (GPCR) signaling","_id":"267F75D8-B435-11E9-9278-68D0E5697425"}],"type":"journal_article","author":[{"full_name":"Maes, Margaret E","orcid":"0000-0001-9642-1085","first_name":"Margaret E","last_name":"Maes","id":"3838F452-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Colombo","id":"3483CF6C-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9434-8902","full_name":"Colombo, Gloria","first_name":"Gloria"},{"first_name":"Rouven","full_name":"Schulz, Rouven","orcid":"0000-0001-5297-733X","id":"4C5E7B96-F248-11E8-B48F-1D18A9856A87","last_name":"Schulz"},{"id":"36ACD32E-F248-11E8-B48F-1D18A9856A87","last_name":"Siegert","first_name":"Sandra","orcid":"0000-0001-8635-0877","full_name":"Siegert, Sandra"}],"date_created":"2019-06-05T13:16:24Z","article_number":"134310","file_date_updated":"2020-07-14T12:47:33Z","pmid":1,"language":[{"iso":"eng"}],"oa":1,"external_id":{"pmid":["31158432"],"isi":["000486094600037"]},"ec_funded":1,"article_processing_charge":"No","abstract":[{"lang":"eng","text":"Microglia have emerged as a critical component of neurodegenerative diseases. Genetic manipulation of microglia can elucidate their functional impact in disease. In neuroscience, recombinant viruses such as lentiviruses and adeno-associated viruses (AAVs) have been successfully used to target various cell types in the brain, although effective transduction of microglia is rare. In this review, we provide a short background of lentiviruses and AAVs, and strategies for designing recombinant viral vectors. Then, we will summarize recent literature on successful microglial transductions in vitro and in vivo, and discuss the current challenges. Finally, we provide guidelines for reporting the efficiency and specificity of viral targeting in microglia, which will enable the microglial research community to assess and improve methodologies for future studies."}],"intvolume":"       707","department":[{"_id":"SaSi"}],"date_published":"2019-08-10T00:00:00Z","publication":"Neuroscience Letters","status":"public","ddc":["570"],"has_accepted_license":"1","scopus_import":"1"},{"date_published":"2019-11-12T00:00:00Z","department":[{"_id":"SaSi"}],"intvolume":"         9","abstract":[{"lang":"eng","text":"BAX, a member of the BCL2 gene family, controls the committed step of the intrinsic apoptotic program. Mitochondrial fragmentation is a commonly observed feature of apoptosis, which occurs through the process of mitochondrial fission. BAX has consistently been associated with mitochondrial fission, yet how BAX participates in the process of mitochondrial fragmentation during apoptosis remains to be tested. Time-lapse imaging of BAX recruitment and mitochondrial fragmentation demonstrates that rapid mitochondrial fragmentation during apoptosis occurs after the complete recruitment of BAX to the mitochondrial outer membrane (MOM). The requirement of a fully functioning BAX protein for the fission process was demonstrated further in BAX/BAK-deficient HCT116 cells expressing a P168A mutant of BAX. The mutant performed fusion to restore the mitochondrial network. but was not demonstrably recruited to the MOM after apoptosis induction. Under these conditions, mitochondrial fragmentation was blocked. Additionally, we show that loss of the fission protein, dynamin-like protein 1 (DRP1), does not temporally affect the initiation time or rate of BAX recruitment, but does reduce the final level of BAX recruited to the MOM during the late phase of BAX recruitment. These correlative observations suggest a model where late-stage BAX oligomers play a functional part of the mitochondrial fragmentation machinery in apoptotic cells."}],"article_processing_charge":"No","external_id":{"pmid":["31719602"],"isi":["000495857600019"]},"language":[{"iso":"eng"}],"oa":1,"pmid":1,"has_accepted_license":"1","scopus_import":"1","ddc":["570"],"publication":"Scientific Reports","status":"public","publication_status":"published","file":[{"date_updated":"2020-07-14T12:47:49Z","file_id":"7096","checksum":"9ab397ed9c1c454b34bffb8cc863d734","date_created":"2019-11-25T07:49:52Z","relation":"main_file","file_name":"2019_ScientificReports_Maes.pdf","content_type":"application/pdf","file_size":6467393,"access_level":"open_access","creator":"dernst"}],"citation":{"ista":"Maes ME, Grosser JA, Fehrman RL, Schlamp CL, Nickells RW. 2019. Completion of BAX recruitment correlates with mitochondrial fission during apoptosis. Scientific Reports. 9, 16565.","ieee":"M. E. Maes, J. A. Grosser, R. L. Fehrman, C. L. Schlamp, and R. W. Nickells, “Completion of BAX recruitment correlates with mitochondrial fission during apoptosis,” <i>Scientific Reports</i>, vol. 9. Springer Nature, 2019.","ama":"Maes ME, Grosser JA, Fehrman RL, Schlamp CL, Nickells RW. Completion of BAX recruitment correlates with mitochondrial fission during apoptosis. <i>Scientific Reports</i>. 2019;9. doi:<a href=\"https://doi.org/10.1038/s41598-019-53049-w\">10.1038/s41598-019-53049-w</a>","mla":"Maes, Margaret E., et al. “Completion of BAX Recruitment Correlates with Mitochondrial Fission during Apoptosis.” <i>Scientific Reports</i>, vol. 9, 16565, Springer Nature, 2019, doi:<a href=\"https://doi.org/10.1038/s41598-019-53049-w\">10.1038/s41598-019-53049-w</a>.","chicago":"Maes, Margaret E, J. A. Grosser, R. L. Fehrman, C. L. Schlamp, and R. W. Nickells. “Completion of BAX Recruitment Correlates with Mitochondrial Fission during Apoptosis.” <i>Scientific Reports</i>. Springer Nature, 2019. <a href=\"https://doi.org/10.1038/s41598-019-53049-w\">https://doi.org/10.1038/s41598-019-53049-w</a>.","short":"M.E. Maes, J.A. Grosser, R.L. Fehrman, C.L. Schlamp, R.W. Nickells, Scientific Reports 9 (2019).","apa":"Maes, M. E., Grosser, J. A., Fehrman, R. L., Schlamp, C. L., &#38; Nickells, R. W. (2019). Completion of BAX recruitment correlates with mitochondrial fission during apoptosis. <i>Scientific Reports</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41598-019-53049-w\">https://doi.org/10.1038/s41598-019-53049-w</a>"},"file_date_updated":"2020-07-14T12:47:49Z","article_number":"16565","date_created":"2019-11-25T07:45:17Z","author":[{"id":"3838F452-F248-11E8-B48F-1D18A9856A87","last_name":"Maes","first_name":"Margaret E","full_name":"Maes, Margaret E","orcid":"0000-0001-9642-1085"},{"last_name":"Grosser","full_name":"Grosser, J. A.","first_name":"J. A."},{"full_name":"Fehrman, R. L.","first_name":"R. L.","last_name":"Fehrman"},{"full_name":"Schlamp, C. L.","first_name":"C. L.","last_name":"Schlamp"},{"last_name":"Nickells","full_name":"Nickells, R. W.","first_name":"R. W."}],"type":"journal_article","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","month":"11","article_type":"original","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"_id":"7095","publisher":"Springer Nature","doi":"10.1038/s41598-019-53049-w","year":"2019","day":"12","title":"Completion of BAX recruitment correlates with mitochondrial fission during apoptosis","oa_version":"Published Version","isi":1,"publication_identifier":{"eissn":["2045-2322"]},"quality_controlled":"1","fulldoi":"https://doi.org/10.1038/s41598-019-53049-w","volume":9,"date_updated":"2023-08-30T07:26:54Z"},{"acknowledgement":"This work was supported by Deutsche Forschungsgemeinschaft (DFG) grant KU2569/1-1 (to M.K.); DFG project EXC307Centre for Integrative Neuroscience (CIN), including grant Pool Project 2011-12 (jointly to M.K. and I.E.); and the Charitable Hertie Foundation (to I.E.). CIN is an Excellence Cluster funded by the DFG within the framework of the Excellence Initiative for 2008–2018. M.K. is supported by the Tistou & Charlotte Kerstan Foundation.","_id":"32","publisher":"Elsevier","doi":"10.1016/j.celrep.2018.09.066","title":"In Vivo regulation of Oligodendrocyte processor cell proliferation and differentiation by the AMPA-receptor Subunit GluA2","year":"2018","day":"23","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","month":"10","tmp":{"short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)"},"fulldoi":"https://doi.org/10.1016/j.celrep.2018.09.066","quality_controlled":"1","date_updated":"2023-09-11T14:13:32Z","volume":25,"oa_version":"Published Version","isi":1,"scopus_import":"1","has_accepted_license":"1","ddc":["570"],"status":"public","publication":"Cell Reports","publist_id":"8023","article_processing_charge":"No","oa":1,"language":[{"iso":"eng"}],"external_id":{"isi":["000448219500005"]},"department":[{"_id":"SaSi"}],"date_published":"2018-10-23T00:00:00Z","abstract":[{"text":"The functional role of AMPA receptor (AMPAR)-mediated synaptic signaling between neurons and oligodendrocyte precursor cells (OPCs) remains enigmatic. We modified the properties of AMPARs at axon-OPC synapses in the mouse corpus callosum in vivo during the peak of myelination by targeting the GluA2 subunit. Expression of the unedited (Ca2+ permeable) or the pore-dead GluA2 subunit of AMPARs triggered proliferation of OPCs and reduced their differentiation into oligodendrocytes. Expression of the cytoplasmic C-terminal (GluA2(813-862)) of the GluA2 subunit (C-tail), a modification designed to affect the interaction between GluA2 and AMPAR-binding proteins and to perturb trafficking of GluA2-containing AMPARs, decreased the differentiation of OPCs without affecting their proliferation. These findings suggest that ionotropic and non-ionotropic properties of AMPARs in OPCs, as well as specific aspects of AMPAR-mediated signaling at axon-OPC synapses in the mouse corpus callosum, are important for balancing the response of OPCs to proliferation and differentiation cues. In the brain, oligodendrocyte precursor cells (OPCs) receive glutamatergic AMPA-receptor-mediated synaptic input from neurons. Chen et al. show that modifying AMPA-receptor properties at axon-OPC synapses alters proliferation and differentiation of OPCs. This expands the traditional view of synaptic transmission by suggesting neurons also use synapses to modulate behavior of glia.","lang":"eng"}],"intvolume":"        25","file_date_updated":"2020-07-14T12:46:03Z","issue":"4","author":[{"full_name":"Chen, Ting","first_name":"Ting","last_name":"Chen"},{"last_name":"Kula","full_name":"Kula, Bartosz","first_name":"Bartosz"},{"first_name":"Balint","orcid":"0000-0002-4002-4686","full_name":"Nagy, Balint","id":"30F830CE-02D1-11E9-9BAA-DAF4881429F2","last_name":"Nagy"},{"last_name":"Barzan","first_name":"Ruxandra","full_name":"Barzan, Ruxandra"},{"last_name":"Gall","full_name":"Gall, Andrea","first_name":"Andrea"},{"last_name":"Ehrlich","first_name":"Ingrid","full_name":"Ehrlich, Ingrid"},{"full_name":"Kukley, Maria","first_name":"Maria","last_name":"Kukley"}],"type":"journal_article","date_created":"2018-12-11T11:44:16Z","page":"852 - 861.e7","publication_status":"published","file":[{"file_id":"5703","checksum":"d9f74277fd57176e04732707d575cf08","relation":"main_file","date_created":"2018-12-17T12:42:57Z","date_updated":"2020-07-14T12:46:03Z","creator":"dernst","file_size":4461997,"access_level":"open_access","file_name":"2018_CellReports_Chen.pdf","content_type":"application/pdf"}],"citation":{"short":"T. Chen, B. Kula, B. Nagy, R. Barzan, A. Gall, I. Ehrlich, M. Kukley, Cell Reports 25 (2018) 852–861.e7.","apa":"Chen, T., Kula, B., Nagy, B., Barzan, R., Gall, A., Ehrlich, I., &#38; Kukley, M. (2018). In Vivo regulation of Oligodendrocyte processor cell proliferation and differentiation by the AMPA-receptor Subunit GluA2. <i>Cell Reports</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.celrep.2018.09.066\">https://doi.org/10.1016/j.celrep.2018.09.066</a>","ista":"Chen T, Kula B, Nagy B, Barzan R, Gall A, Ehrlich I, Kukley M. 2018. In Vivo regulation of Oligodendrocyte processor cell proliferation and differentiation by the AMPA-receptor Subunit GluA2. Cell Reports. 25(4), 852–861.e7.","ama":"Chen T, Kula B, Nagy B, et al. In Vivo regulation of Oligodendrocyte processor cell proliferation and differentiation by the AMPA-receptor Subunit GluA2. <i>Cell Reports</i>. 2018;25(4):852-861.e7. doi:<a href=\"https://doi.org/10.1016/j.celrep.2018.09.066\">10.1016/j.celrep.2018.09.066</a>","mla":"Chen, Ting, et al. “In Vivo Regulation of Oligodendrocyte Processor Cell Proliferation and Differentiation by the AMPA-Receptor Subunit GluA2.” <i>Cell Reports</i>, vol. 25, no. 4, Elsevier, 2018, p. 852–861.e7, doi:<a href=\"https://doi.org/10.1016/j.celrep.2018.09.066\">10.1016/j.celrep.2018.09.066</a>.","ieee":"T. Chen <i>et al.</i>, “In Vivo regulation of Oligodendrocyte processor cell proliferation and differentiation by the AMPA-receptor Subunit GluA2,” <i>Cell Reports</i>, vol. 25, no. 4. Elsevier, p. 852–861.e7, 2018.","chicago":"Chen, Ting, Bartosz Kula, Balint Nagy, Ruxandra Barzan, Andrea Gall, Ingrid Ehrlich, and Maria Kukley. “In Vivo Regulation of Oligodendrocyte Processor Cell Proliferation and Differentiation by the AMPA-Receptor Subunit GluA2.” <i>Cell Reports</i>. Elsevier, 2018. <a href=\"https://doi.org/10.1016/j.celrep.2018.09.066\">https://doi.org/10.1016/j.celrep.2018.09.066</a>."}},{"day":"22","year":"2017","corr_author":"1","title":"Different patterns of neuronal activity trigger distinct responses of oligodendrocyte precursor cells in the corpus callosum","doi":"10.1371/journal.pbio.2001993","_id":"708","publisher":"Public Library of Science","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","month":"08","volume":15,"date_updated":"2025-09-10T11:05:19Z","publication_identifier":{"issn":["1544-9173"]},"quality_controlled":"1","fulldoi":"https://doi.org/10.1371/journal.pbio.2001993","isi":1,"oa_version":"Published Version","publist_id":"6983","publication":"PLoS Biology","status":"public","ddc":["576","610"],"scopus_import":"1","has_accepted_license":"1","abstract":[{"text":"In the developing and adult brain, oligodendrocyte precursor cells (OPCs) are influenced by neuronal activity: they are involved in synaptic signaling with neurons, and their proliferation and differentiation into myelinating glia can be altered by transient changes in neuronal firing. An important question that has been unanswered is whether OPCs can discriminate different patterns of neuronal activity and respond to them in a distinct way. Here, we demonstrate in brain slices that the pattern of neuronal activity determines the functional changes triggered at synapses between axons and OPCs. Furthermore, we show that stimulation of the corpus callosum at different frequencies in vivo affects proliferation and differentiation of OPCs in a dissimilar way. Our findings suggest that neurons do not influence OPCs in “all-or-none” fashion but use their firing pattern to tune the response and behavior of these nonneuronal cells.","lang":"eng"}],"intvolume":"        15","date_published":"2017-08-22T00:00:00Z","department":[{"_id":"SaSi"}],"language":[{"iso":"eng"}],"oa":1,"external_id":{"isi":["000408756200005"]},"article_processing_charge":"No","article_number":"e2001993","date_created":"2018-12-11T11:48:03Z","type":"journal_article","author":[{"id":"30F830CE-02D1-11E9-9BAA-DAF4881429F2","last_name":"Nagy","first_name":"Balint","orcid":"0000-0002-4002-4686","full_name":"Nagy, Balint"},{"first_name":"Anahit","full_name":"Hovhannisyan, Anahit","last_name":"Hovhannisyan"},{"last_name":"Barzan","full_name":"Barzan, Ruxandra","first_name":"Ruxandra"},{"last_name":"Chen","first_name":"Ting","full_name":"Chen, Ting"},{"last_name":"Kukley","first_name":"Maria","full_name":"Kukley, Maria"}],"issue":"8","file_date_updated":"2020-07-14T12:47:49Z","citation":{"ista":"Nagy B, Hovhannisyan A, Barzan R, Chen T, Kukley M. 2017. Different patterns of neuronal activity trigger distinct responses of oligodendrocyte precursor cells in the corpus callosum. PLoS Biology. 15(8), e2001993.","ama":"Nagy B, Hovhannisyan A, Barzan R, Chen T, Kukley M. Different patterns of neuronal activity trigger distinct responses of oligodendrocyte precursor cells in the corpus callosum. <i>PLoS Biology</i>. 2017;15(8). doi:<a href=\"https://doi.org/10.1371/journal.pbio.2001993\">10.1371/journal.pbio.2001993</a>","chicago":"Nagy, Balint, Anahit Hovhannisyan, Ruxandra Barzan, Ting Chen, and Maria Kukley. “Different Patterns of Neuronal Activity Trigger Distinct Responses of Oligodendrocyte Precursor Cells in the Corpus Callosum.” <i>PLoS Biology</i>. Public Library of Science, 2017. <a href=\"https://doi.org/10.1371/journal.pbio.2001993\">https://doi.org/10.1371/journal.pbio.2001993</a>.","mla":"Nagy, Balint, et al. “Different Patterns of Neuronal Activity Trigger Distinct Responses of Oligodendrocyte Precursor Cells in the Corpus Callosum.” <i>PLoS Biology</i>, vol. 15, no. 8, e2001993, Public Library of Science, 2017, doi:<a href=\"https://doi.org/10.1371/journal.pbio.2001993\">10.1371/journal.pbio.2001993</a>.","ieee":"B. Nagy, A. Hovhannisyan, R. Barzan, T. Chen, and M. Kukley, “Different patterns of neuronal activity trigger distinct responses of oligodendrocyte precursor cells in the corpus callosum,” <i>PLoS Biology</i>, vol. 15, no. 8. Public Library of Science, 2017.","short":"B. Nagy, A. Hovhannisyan, R. Barzan, T. Chen, M. Kukley, PLoS Biology 15 (2017).","apa":"Nagy, B., Hovhannisyan, A., Barzan, R., Chen, T., &#38; Kukley, M. (2017). Different patterns of neuronal activity trigger distinct responses of oligodendrocyte precursor cells in the corpus callosum. <i>PLoS Biology</i>. Public Library of Science. <a href=\"https://doi.org/10.1371/journal.pbio.2001993\">https://doi.org/10.1371/journal.pbio.2001993</a>"},"pubrep_id":"889","file":[{"access_level":"open_access","file_size":18155365,"creator":"system","file_name":"IST-2017-889-v1+1_journal.pbio.2001993.pdf","content_type":"application/pdf","date_updated":"2020-07-14T12:47:49Z","relation":"main_file","date_created":"2018-12-12T10:15:35Z","file_id":"5156","checksum":"0c974f430682dc832ea7b27ab5a93124"}],"publication_status":"published"},{"file_date_updated":"2020-07-14T12:47:04Z","date_created":"2018-12-11T11:47:10Z","page":"6091 - 6104","issue":"14","author":[{"last_name":"Nickells","first_name":"Robert","full_name":"Nickells, Robert"},{"full_name":"Schmitt, Heather","first_name":"Heather","last_name":"Schmitt"},{"full_name":"Maes, Margaret E","orcid":"0000-0001-9642-1085","first_name":"Margaret E","last_name":"Maes","id":"3838F452-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Cassandra","full_name":"Schlamp, Cassandra","last_name":"Schlamp"}],"type":"journal_article","publication_status":"published","pubrep_id":"920","file":[{"date_updated":"2020-07-14T12:47:04Z","relation":"main_file","date_created":"2018-12-12T10:17:53Z","file_id":"5311","checksum":"d7a7b6f1fa9211a04e5e65634a0265d9","content_type":"application/pdf","file_name":"IST-2018-920-v1+1_i1552-5783-58-14-6091.pdf","access_level":"open_access","file_size":2955559,"creator":"system"}],"citation":{"ieee":"R. Nickells, H. Schmitt, M. E. Maes, and C. Schlamp, “AAV2 mediated transduction of the mouse retina after optic nerve injury,” <i>Investigative Ophthalmology and Visual Science</i>, vol. 58, no. 14. Association for Research in Vision &#38; Ophthalmology, pp. 6091–6104, 2017.","ama":"Nickells R, Schmitt H, Maes ME, Schlamp C. AAV2 mediated transduction of the mouse retina after optic nerve injury. <i>Investigative Ophthalmology and Visual Science</i>. 2017;58(14):6091-6104. doi:<a href=\"https://doi.org/10.1167/iovs.17-22634\">10.1167/iovs.17-22634</a>","mla":"Nickells, Robert, et al. “AAV2 Mediated Transduction of the Mouse Retina after Optic Nerve Injury.” <i>Investigative Ophthalmology and Visual Science</i>, vol. 58, no. 14, Association for Research in Vision &#38; Ophthalmology, 2017, pp. 6091–104, doi:<a href=\"https://doi.org/10.1167/iovs.17-22634\">10.1167/iovs.17-22634</a>.","chicago":"Nickells, Robert, Heather Schmitt, Margaret E Maes, and Cassandra Schlamp. “AAV2 Mediated Transduction of the Mouse Retina after Optic Nerve Injury.” <i>Investigative Ophthalmology and Visual Science</i>. Association for Research in Vision &#38; Ophthalmology, 2017. <a href=\"https://doi.org/10.1167/iovs.17-22634\">https://doi.org/10.1167/iovs.17-22634</a>.","ista":"Nickells R, Schmitt H, Maes ME, Schlamp C. 2017. AAV2 mediated transduction of the mouse retina after optic nerve injury. Investigative Ophthalmology and Visual Science. 58(14), 6091–6104.","apa":"Nickells, R., Schmitt, H., Maes, M. E., &#38; Schlamp, C. (2017). AAV2 mediated transduction of the mouse retina after optic nerve injury. <i>Investigative Ophthalmology and Visual Science</i>. Association for Research in Vision &#38; Ophthalmology. <a href=\"https://doi.org/10.1167/iovs.17-22634\">https://doi.org/10.1167/iovs.17-22634</a>","short":"R. Nickells, H. Schmitt, M.E. Maes, C. Schlamp, Investigative Ophthalmology and Visual Science 58 (2017) 6091–6104."},"scopus_import":"1","has_accepted_license":"1","ddc":["576"],"publication":"Investigative Ophthalmology and Visual Science","status":"public","publist_id":"7254","department":[{"_id":"SaSi"}],"date_published":"2017-12-14T00:00:00Z","abstract":[{"text":"PURPOSE. Gene therapy of retinal ganglion cells (RGCs) has promise as a powerful therapeutic for the rescue and regeneration of these cells after optic nerve damage. However, early after damage, RGCs undergo atrophic changes, including gene silencing. It is not known if these changes will deleteriously affect transduction and transgene expression, or if the therapeutic protein can influence reactivation of the endogenous genome. METHODS. Double-transgenic mice carrying a Rosa26-(LoxP)-tdTomato reporter, and a mutant allele for the proapoptotic Bax gene were reared. The Bax mutant blocks apoptosis, but RGCs still exhibit nuclear atrophy and gene silencing. At times ranging from 1 hour to 4 weeks after optic nerve crush (ONC), eyes received an intravitreal injection of AAV2 virus carrying the Cre recombinase. Successful transduction was monitored by expression of the tdTomato reporter. Immunostaining was used to localize tdTomato expression in select cell types. RESULTS. Successful transduction of RGCs was achieved at all time points after ONC using AAV2 expressing Cre from the phosphoglycerate kinase (Pgk) promoter, but not the CMV promoter. ONC promoted an increase in the transduction of cell types in the inner nuclear layer, including Müller cells and rod bipolar neurons. There was minimal evidence of transduction of amacrine cells and astrocytes in the inner retina or optic nerve. CONCLUSIONS. Damaged RGCs can be transduced and at least some endogenous genes can be subsequently activated. Optic nerve damage may change retinal architecture to allow greater penetration of an AAV2 virus to transduce several additional cell types in the inner nuclear layer.","lang":"eng"}],"intvolume":"        58","article_processing_charge":"No","language":[{"iso":"eng"}],"external_id":{"isi":["000426781300012"]},"oa":1,"quality_controlled":"1","publication_identifier":{"issn":["0146-0404"]},"fulldoi":"https://doi.org/10.1167/iovs.17-22634","volume":58,"date_updated":"2026-08-12T11:16:45Z","oa_version":"Published Version","isi":1,"publisher":"Association for Research in Vision & Ophthalmology","_id":"557","doi":"10.1167/iovs.17-22634","year":"2017","day":"14","title":"AAV2 mediated transduction of the mouse retina after optic nerve injury","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","month":"12","tmp":{"short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)"}},{"publication":"JAMA Psychiatry","publist_id":"6074","status":"public","scopus_import":"1","has_accepted_license":"1","ddc":["576","610"],"pmid":1,"department":[{"_id":"SaSi"}],"date_published":"2016-04-01T00:00:00Z","abstract":[{"text":"This article provides an introduction to the role of microRNAs in the nervous system and outlines their potential involvement in the pathophysiology of schizophrenia, which is hypothesized to arise owing to environmental factors and genetic predisposition.","lang":"eng"}],"intvolume":"        73","article_processing_charge":"No","oa":1,"external_id":{"isi":["000373444700017"],"pmid":["26963490"]},"language":[{"iso":"eng"}],"date_created":"2018-12-11T11:50:58Z","page":"409 - 410","issue":"4","author":[{"full_name":"Tsai, Lihuei","first_name":"Lihuei","last_name":"Tsai"},{"last_name":"Siegert","id":"36ACD32E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8635-0877","full_name":"Siegert, Sandra","first_name":"Sandra"}],"type":"journal_article","file_date_updated":"2020-07-14T12:44:41Z","pubrep_id":"981","file":[{"date_updated":"2020-07-14T12:44:41Z","date_created":"2018-12-12T10:17:24Z","relation":"main_file","checksum":"649aee381f30f7ef7e9efa912d41c2e3","file_id":"5278","access_level":"open_access","file_size":601679,"creator":"system","content_type":"application/pdf","file_name":"IST-2018-981-v1+1_YNP150011_annotatedproof_FINAL.pdf"}],"citation":{"chicago":"Tsai, Lihuei, and Sandra Siegert. “How MicroRNAs Are Involved in Splitting the Mind.” <i>JAMA Psychiatry</i>. American Medical Association, 2016. <a href=\"https://doi.org/10.1001/jamapsychiatry.2015.3144\">https://doi.org/10.1001/jamapsychiatry.2015.3144</a>.","ama":"Tsai L, Siegert S. How MicroRNAs Are involved in splitting the mind. <i>JAMA Psychiatry</i>. 2016;73(4):409-410. doi:<a href=\"https://doi.org/10.1001/jamapsychiatry.2015.3144\">10.1001/jamapsychiatry.2015.3144</a>","ieee":"L. Tsai and S. Siegert, “How MicroRNAs Are involved in splitting the mind,” <i>JAMA Psychiatry</i>, vol. 73, no. 4. American Medical Association, pp. 409–410, 2016.","mla":"Tsai, Lihuei, and Sandra Siegert. “How MicroRNAs Are Involved in Splitting the Mind.” <i>JAMA Psychiatry</i>, vol. 73, no. 4, American Medical Association, 2016, pp. 409–10, doi:<a href=\"https://doi.org/10.1001/jamapsychiatry.2015.3144\">10.1001/jamapsychiatry.2015.3144</a>.","ista":"Tsai L, Siegert S. 2016. How MicroRNAs Are involved in splitting the mind. JAMA Psychiatry. 73(4), 409–410.","short":"L. Tsai, S. Siegert, JAMA Psychiatry 73 (2016) 409–410.","apa":"Tsai, L., &#38; Siegert, S. (2016). How MicroRNAs Are involved in splitting the mind. <i>JAMA Psychiatry</i>. American Medical Association. <a href=\"https://doi.org/10.1001/jamapsychiatry.2015.3144\">https://doi.org/10.1001/jamapsychiatry.2015.3144</a>"},"publication_status":"published","year":"2016","day":"01","title":"How MicroRNAs Are involved in splitting the mind","_id":"1253","publisher":"American Medical Association","doi":"10.1001/jamapsychiatry.2015.3144","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","month":"04","volume":73,"date_updated":"2025-09-22T09:08:34Z","quality_controlled":"1","publication_identifier":{"issn":["2168-622X"]},"fulldoi":"https://doi.org/10.1001/jamapsychiatry.2015.3144","isi":1,"oa_version":"Submitted Version"}]