[{"status":"public","publication":"Cell Reports","citation":{"mla":"Villa, Carlo Emanuele, et al. “CHD8 Haploinsufficiency Links Autism to Transient Alterations in Excitatory and Inhibitory Trajectories.” <i>Cell Reports</i>, vol. 39, no. 1, 110615, Elsevier, 2022, doi:<a href=\"https://doi.org/10.1016/j.celrep.2022.110615\">10.1016/j.celrep.2022.110615</a>.","apa":"Villa, C. E., Cheroni, C., Dotter, C., López-Tóbon, A., Oliveira, B., Sacco, R., … Novarino, G. (2022). CHD8 haploinsufficiency links autism to transient alterations in excitatory and inhibitory trajectories. <i>Cell Reports</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.celrep.2022.110615\">https://doi.org/10.1016/j.celrep.2022.110615</a>","ama":"Villa CE, Cheroni C, Dotter C, et al. CHD8 haploinsufficiency links autism to transient alterations in excitatory and inhibitory trajectories. <i>Cell Reports</i>. 2022;39(1). doi:<a href=\"https://doi.org/10.1016/j.celrep.2022.110615\">10.1016/j.celrep.2022.110615</a>","ieee":"C. E. Villa <i>et al.</i>, “CHD8 haploinsufficiency links autism to transient alterations in excitatory and inhibitory trajectories,” <i>Cell Reports</i>, vol. 39, no. 1. Elsevier, 2022.","chicago":"Villa, Carlo Emanuele, Cristina Cheroni, Christoph Dotter, Alejandro López-Tóbon, Bárbara Oliveira, Roberto Sacco, Aysan Çerağ Yahya, et al. “CHD8 Haploinsufficiency Links Autism to Transient Alterations in Excitatory and Inhibitory Trajectories.” <i>Cell Reports</i>. Elsevier, 2022. <a href=\"https://doi.org/10.1016/j.celrep.2022.110615\">https://doi.org/10.1016/j.celrep.2022.110615</a>.","short":"C.E. Villa, C. Cheroni, C. Dotter, A. López-Tóbon, B. Oliveira, R. Sacco, A.Ç. Yahya, J. Morandell, M. Gabriele, M. Tavakoli, J. Lyudchik, C.M. Sommer, M. Gabitto, J.G. Danzl, G. Testa, G. Novarino, Cell Reports 39 (2022).","ista":"Villa CE, Cheroni C, Dotter C, López-Tóbon A, Oliveira B, Sacco R, Yahya AÇ, Morandell J, Gabriele M, Tavakoli M, Lyudchik J, Sommer CM, Gabitto M, Danzl JG, Testa G, Novarino G. 2022. CHD8 haploinsufficiency links autism to transient alterations in excitatory and inhibitory trajectories. Cell Reports. 39(1), 110615."},"article_number":"110615","ddc":["570"],"ec_funded":1,"scopus_import":"1","has_accepted_license":"1","publisher":"Elsevier","file":[{"creator":"dernst","file_name":"2022_CellReports_Villa.pdf","relation":"main_file","file_id":"11164","checksum":"b4e8d68f0268dec499af333e6fd5d8e1","content_type":"application/pdf","file_size":"7808644","date_updated":"2022-04-15T09:06:25Z","access_level":"open_access","success":1,"date_created":"2022-04-15T09:06:25Z"}],"date_updated":"2026-04-28T22:30:31Z","acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"}],"year":"2022","author":[{"full_name":"Villa, Carlo Emanuele","first_name":"Carlo Emanuele","last_name":"Villa"},{"full_name":"Cheroni, Cristina","first_name":"Cristina","last_name":"Cheroni"},{"first_name":"Christoph","last_name":"Dotter","full_name":"Dotter, Christoph","orcid":"0000-0002-9033-9096","id":"4C66542E-F248-11E8-B48F-1D18A9856A87"},{"last_name":"López-Tóbon","first_name":"Alejandro","full_name":"López-Tóbon, Alejandro"},{"full_name":"Oliveira, Bárbara","first_name":"Bárbara","last_name":"Oliveira","id":"3B03AA1A-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Roberto","last_name":"Sacco","full_name":"Sacco, Roberto","id":"42C9F57E-F248-11E8-B48F-1D18A9856A87"},{"id":"365A65F8-F248-11E8-B48F-1D18A9856A87","first_name":"Aysan Çerağ","last_name":"Yahya","full_name":"Yahya, Aysan Çerağ"},{"id":"4739D480-F248-11E8-B48F-1D18A9856A87","last_name":"Morandell","first_name":"Jasmin","full_name":"Morandell, Jasmin"},{"full_name":"Gabriele, Michele","first_name":"Michele","last_name":"Gabriele"},{"last_name":"Tavakoli","first_name":"Mojtaba","full_name":"Tavakoli, Mojtaba","id":"3A0A06F4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-7667-6854"},{"last_name":"Lyudchik","first_name":"Julia","full_name":"Lyudchik, Julia","id":"46E28B80-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Christoph M","last_name":"Sommer","full_name":"Sommer, Christoph M","id":"4DF26D8C-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-1216-9105"},{"full_name":"Gabitto, Mariano","first_name":"Mariano","last_name":"Gabitto"},{"orcid":"0000-0001-8559-3973","id":"42EFD3B6-F248-11E8-B48F-1D18A9856A87","last_name":"Danzl","first_name":"Johann G","full_name":"Danzl, Johann G"},{"first_name":"Giuseppe","last_name":"Testa","full_name":"Testa, Giuseppe"},{"orcid":"0000-0002-7673-7178","id":"3E57A680-F248-11E8-B48F-1D18A9856A87","full_name":"Novarino, Gaia","last_name":"Novarino","first_name":"Gaia"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"quality_controlled":"1","article_type":"original","oa":1,"volume":39,"issue":"1","day":"05","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publication_status":"published","intvolume":"        39","pmid":1,"language":[{"iso":"eng"}],"date_published":"2022-04-05T00:00:00Z","_id":"11160","related_material":{"record":[{"status":"public","id":"18681","relation":"dissertation_contains"},{"status":"public","relation":"dissertation_contains","id":"18674"},{"id":"12364","relation":"dissertation_contains","status":"public"}]},"isi":1,"keyword":["General Biochemistry","Genetics and Molecular Biology"],"publication_identifier":{"issn":["2211-1247"]},"corr_author":"1","acknowledgement":"We thank Farnaz Freeman for technical assistance. This research was supported by the Scientific Service Units (SSU) of IST Austria through resources provided by the Bioimaging Facility (BIF) and the Life Science Facility (LSF). This work supported by the European Union’s Horizon 2020 research and innovation program (ERC) grant 715508 to G.N. (REVERSEAUTISM) and grant 825759 to G.T. (ENDpoiNTs); the Fondazione Cariplo 2017-0886 to A.L.T.; E-Rare-3 JTC 2018 IMPACT to M. Gabriele; and the Austrian Science Fund FWF I 4205-B to G.N. Graphical abstract and figures were created using BioRender.com.","abstract":[{"text":"Mutations in the chromodomain helicase DNA-binding 8 (CHD8) gene are a frequent cause of autism spectrum disorder (ASD). While its phenotypic spectrum often encompasses macrocephaly, implicating cortical abnormalities, how CHD8 haploinsufficiency affects neurodevelopmental is unclear. Here, employing human cerebral organoids, we find that CHD8 haploinsufficiency disrupted neurodevelopmental trajectories with an accelerated and delayed generation of, respectively, inhibitory and excitatory neurons that yields, at days 60 and 120, symmetrically opposite expansions in their proportions. This imbalance is consistent with an enlargement of cerebral organoids as an in vitro correlate of patients’ macrocephaly. Through an isogenic design of patient-specific mutations and mosaic organoids, we define genotype-phenotype relationships and uncover their cell-autonomous nature. Our results define cell-type-specific CHD8-dependent molecular defects related to an abnormal program of proliferation and alternative splicing. By identifying cell-type-specific effects of CHD8 mutations, our study uncovers reproducible developmental alterations that may be employed for neurodevelopmental disease modeling.","lang":"eng"}],"file_date_updated":"2022-04-15T09:06:25Z","month":"04","type":"journal_article","project":[{"name":"Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo and in vitro Models","grant_number":"715508","_id":"25444568-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"_id":"2690FEAC-B435-11E9-9278-68D0E5697425","grant_number":"I04205","name":"Identification of converging Molecular Pathways Across Chromatinopathies as Targets for Therapy","call_identifier":"FWF"}],"external_id":{"pmid":["35385734"],"isi":["000785983900003"]},"title":"CHD8 haploinsufficiency links autism to transient alterations in excitatory and inhibitory trajectories","article_processing_charge":"Yes","date_created":"2022-04-15T09:03:10Z","doi":"10.1016/j.celrep.2022.110615","oa_version":"Published Version","department":[{"_id":"JoDa"},{"_id":"GaNo"}]},{"date_updated":"2021-01-12T08:11:56Z","extern":"1","author":[{"full_name":"Torrini, Consuelo","first_name":"Consuelo","last_name":"Torrini"},{"id":"850B2E12-9CD4-11E9-837F-E719E6697425","orcid":"0000-0003-0002-1867","last_name":"Cubero","first_name":"Ryan J","full_name":"Cubero, Ryan J"},{"first_name":"Ellen","last_name":"Dirkx","full_name":"Dirkx, Ellen"},{"full_name":"Braga, Luca","first_name":"Luca","last_name":"Braga"},{"first_name":"Hashim","last_name":"Ali","full_name":"Ali, Hashim"},{"full_name":"Prosdocimo, Giulia","first_name":"Giulia","last_name":"Prosdocimo"},{"last_name":"Gutierrez","first_name":"Maria Ines","full_name":"Gutierrez, Maria Ines"},{"full_name":"Collesi, Chiara","first_name":"Chiara","last_name":"Collesi"},{"full_name":"Licastro, Danilo","last_name":"Licastro","first_name":"Danilo"},{"full_name":"Zentilin, Lorena","first_name":"Lorena","last_name":"Zentilin"},{"full_name":"Mano, Miguel","first_name":"Miguel","last_name":"Mano"},{"full_name":"Zacchigna, Serena","first_name":"Serena","last_name":"Zacchigna"},{"full_name":"Vendruscolo, Michele","last_name":"Vendruscolo","first_name":"Michele"},{"full_name":"Marsili, Matteo","first_name":"Matteo","last_name":"Marsili"},{"last_name":"Samal","first_name":"Areejit","full_name":"Samal, Areejit"},{"full_name":"Giacca, Mauro","first_name":"Mauro","last_name":"Giacca"}],"year":"2019","status":"public","publication":"Cell Reports","citation":{"short":"C. Torrini, R.J. Cubero, E. Dirkx, L. Braga, H. Ali, G. Prosdocimo, M.I. Gutierrez, C. Collesi, D. Licastro, L. Zentilin, M. Mano, S. Zacchigna, M. Vendruscolo, M. Marsili, A. Samal, M. Giacca, Cell Reports 27 (2019) 2759–2771.e5.","chicago":"Torrini, Consuelo, Ryan J Cubero, Ellen Dirkx, Luca Braga, Hashim Ali, Giulia Prosdocimo, Maria Ines Gutierrez, et al. “Common Regulatory Pathways Mediate Activity of MicroRNAs Inducing Cardiomyocyte Proliferation.” <i>Cell Reports</i>. Elsevier, 2019. <a href=\"https://doi.org/10.1016/j.celrep.2019.05.005\">https://doi.org/10.1016/j.celrep.2019.05.005</a>.","ista":"Torrini C, Cubero RJ, Dirkx E, Braga L, Ali H, Prosdocimo G, Gutierrez MI, Collesi C, Licastro D, Zentilin L, Mano M, Zacchigna S, Vendruscolo M, Marsili M, Samal A, Giacca M. 2019. Common regulatory pathways mediate activity of microRNAs inducing cardiomyocyte proliferation. Cell Reports. 27(9), 2759–2771.e5.","apa":"Torrini, C., Cubero, R. J., Dirkx, E., Braga, L., Ali, H., Prosdocimo, G., … Giacca, M. (2019). Common regulatory pathways mediate activity of microRNAs inducing cardiomyocyte proliferation. <i>Cell Reports</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.celrep.2019.05.005\">https://doi.org/10.1016/j.celrep.2019.05.005</a>","ama":"Torrini C, Cubero RJ, Dirkx E, et al. Common regulatory pathways mediate activity of microRNAs inducing cardiomyocyte proliferation. <i>Cell Reports</i>. 2019;27(9):2759-2771.e5. doi:<a href=\"https://doi.org/10.1016/j.celrep.2019.05.005\">10.1016/j.celrep.2019.05.005</a>","ieee":"C. Torrini <i>et al.</i>, “Common regulatory pathways mediate activity of microRNAs inducing cardiomyocyte proliferation,” <i>Cell Reports</i>, vol. 27, no. 9. Elsevier, p. 2759–2771.e5, 2019.","mla":"Torrini, Consuelo, et al. “Common Regulatory Pathways Mediate Activity of MicroRNAs Inducing Cardiomyocyte Proliferation.” <i>Cell Reports</i>, vol. 27, no. 9, Elsevier, 2019, p. 2759–2771.e5, doi:<a href=\"https://doi.org/10.1016/j.celrep.2019.05.005\">10.1016/j.celrep.2019.05.005</a>."},"page":"2759-2771.e5","ddc":["576"],"publisher":"Elsevier","file":[{"content_type":"application/pdf","file_size":4650750,"checksum":"c5d855d07263bfec718673385d0ea2d7","date_created":"2019-11-26T22:30:43Z","date_updated":"2020-07-14T12:47:50Z","access_level":"open_access","file_id":"7129","relation":"main_file","file_name":"torrini_cellreports_2019.pdf","creator":"rcubero"}],"has_accepted_license":"1","volume":27,"issue":"9","day":"28","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","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"},"article_type":"original","quality_controlled":"1","oa":1,"date_published":"2019-05-28T00:00:00Z","_id":"7128","keyword":["cardiomyocyte","cell cycle","Cofilin2","cytoskeleton","Hippo","microRNA","regeneration","YAP"],"intvolume":"        27","publication_status":"published","pmid":1,"language":[{"iso":"eng"}],"title":"Common regulatory pathways mediate activity of microRNAs inducing cardiomyocyte proliferation","date_created":"2019-11-26T22:30:07Z","doi":"10.1016/j.celrep.2019.05.005","oa_version":"Published Version","article_processing_charge":"Yes","publication_identifier":{"issn":["2211-1247"]},"type":"journal_article","month":"05","file_date_updated":"2020-07-14T12:47:50Z","abstract":[{"lang":"eng","text":"Loss of functional cardiomyocytes is a major determinant of heart failure after myocardial infarction. Previous high throughput screening studies have identified a few microRNAs (miRNAs) that can induce cardiomyocyte proliferation and stimulate cardiac regeneration in mice. Here, we show that all of the most effective of these miRNAs activate nuclear localization of the master transcriptional cofactor Yes-associated protein (YAP) and induce expression of YAP-responsive genes. In particular, miR-199a-3p directly targets two mRNAs coding for proteins impinging on the Hippo pathway, the upstream YAP inhibitory kinase TAOK1, and the E3 ubiquitin ligase β-TrCP, which leads to YAP degradation. Several of the pro-proliferative miRNAs (including miR-199a-3p) also inhibit filamentous actin depolymerization by targeting Cofilin2, a process that by itself activates YAP nuclear translocation. Thus, activation of YAP and modulation of the actin cytoskeleton are major components of the pro-proliferative action of miR-199a-3p and other miRNAs that induce cardiomyocyte proliferation."}],"external_id":{"pmid":["31141697"]}},{"publist_id":"7052","publication_status":"published","intvolume":"        19","language":[{"iso":"eng"}],"date_published":"2017-05-02T00:00:00Z","isi":1,"_id":"672","pubrep_id":"900","corr_author":"1","publication_identifier":{"issn":["2211-1247"]},"project":[{"name":"Cytoskeletal force generation and force transduction of migrating leukocytes","grant_number":"281556","_id":"25A603A2-B435-11E9-9278-68D0E5697425","call_identifier":"FP7"},{"call_identifier":"FWF","_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","grant_number":"Y 564-B12","name":"Cytoskeletal force generation and force transduction of migrating leukocytes"}],"external_id":{"isi":["000402124100002"]},"abstract":[{"lang":"eng","text":"Trafficking cells frequently transmigrate through epithelial and endothelial monolayers. How monolayers cooperate with the penetrating cells to support their transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic capillaries as a model system for transendothelial migration. We find that the chemokine CCL21, which is the decisive guidance cue for intravasation, mainly localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes extracellularly enriched at the sites of endothelial cell-cell junctions. When we reconstitute the transmigration process in vitro, we find that secretion of CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and selective calcium chelation in lymphatic endothelium attenuates transmigration. Altogether, our data demonstrate a chemokine-mediated feedback between DCs and lymphatic endothelium, which facilitates transendothelial migration."}],"type":"journal_article","month":"05","file_date_updated":"2020-07-14T12:47:38Z","article_processing_charge":"Yes","date_created":"2018-12-11T11:47:50Z","oa_version":"Published Version","doi":"10.1016/j.celrep.2017.04.027","title":"Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia","department":[{"_id":"MiSi"},{"_id":"Bio"},{"_id":"EM-Fac"}],"citation":{"chicago":"Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” <i>Cell Reports</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.celrep.2017.04.027\">https://doi.org/10.1016/j.celrep.2017.04.027</a>.","short":"K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling, W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909.","ista":"Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909.","mla":"Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” <i>Cell Reports</i>, vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:<a href=\"https://doi.org/10.1016/j.celrep.2017.04.027\">10.1016/j.celrep.2017.04.027</a>.","ieee":"K. Vaahtomeri <i>et al.</i>, “Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia,” <i>Cell Reports</i>, vol. 19, no. 5. Cell Press, pp. 902–909, 2017.","apa":"Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling, M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. <i>Cell Reports</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.celrep.2017.04.027\">https://doi.org/10.1016/j.celrep.2017.04.027</a>","ama":"Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. <i>Cell Reports</i>. 2017;19(5):902-909. doi:<a href=\"https://doi.org/10.1016/j.celrep.2017.04.027\">10.1016/j.celrep.2017.04.027</a>"},"page":"902 - 909","ddc":["570"],"status":"public","publication":"Cell Reports","scopus_import":"1","has_accepted_license":"1","ec_funded":1,"file":[{"file_name":"IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf","creator":"system","file_id":"5109","relation":"main_file","access_level":"open_access","date_updated":"2020-07-14T12:47:38Z","date_created":"2018-12-12T10:14:54Z","content_type":"application/pdf","checksum":"8fdddaab1f1d76a6ec9ca94dcb6b07a2","file_size":2248814}],"publisher":"Cell Press","date_updated":"2025-09-10T14:27:34Z","year":"2017","author":[{"id":"368EE576-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7829-3518","full_name":"Vaahtomeri, Kari","first_name":"Kari","last_name":"Vaahtomeri"},{"last_name":"Brown","first_name":"Markus","full_name":"Brown, Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87"},{"id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9843-3522","full_name":"Hauschild, Robert","first_name":"Robert","last_name":"Hauschild"},{"id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","last_name":"De Vries","first_name":"Ingrid","full_name":"De Vries, Ingrid"},{"full_name":"Leithner, Alexander F","first_name":"Alexander F","last_name":"Leithner","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1073-744X"},{"orcid":"0000-0001-8599-1226","id":"3C23B994-F248-11E8-B48F-1D18A9856A87","last_name":"Mehling","first_name":"Matthias","full_name":"Mehling, Matthias"},{"orcid":"0000-0001-9735-5315","id":"3F99E422-F248-11E8-B48F-1D18A9856A87","full_name":"Kaufmann, Walter","last_name":"Kaufmann","first_name":"Walter"},{"first_name":"Michael K","last_name":"Sixt","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"}],"tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","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"},"oa":1,"quality_controlled":"1","issue":"5","volume":19,"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","day":"02"},{"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","day":"16","issue":"7","volume":19,"oa":1,"quality_controlled":"1","tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","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"},"author":[{"full_name":"Lademann, Claudio","last_name":"Lademann","first_name":"Claudio"},{"id":"3F0587C8-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2856-3369","first_name":"Jörg","last_name":"Renkawitz","full_name":"Renkawitz, Jörg"},{"full_name":"Pfander, Boris","first_name":"Boris","last_name":"Pfander"},{"first_name":"Stefan","last_name":"Jentsch","full_name":"Jentsch, Stefan"}],"year":"2017","date_updated":"2025-09-10T14:23:55Z","file":[{"file_id":"5171","relation":"main_file","file_name":"IST-2017-899-v1+1_1-s2.0-S2211124717305454-main.pdf","creator":"system","date_created":"2018-12-12T10:15:48Z","access_level":"open_access","date_updated":"2020-07-14T12:47:40Z","content_type":"application/pdf","file_size":3005610,"checksum":"efc7287d9c6354983cb151880e9ad72a"}],"publisher":"Cell Press","scopus_import":"1","has_accepted_license":"1","citation":{"ama":"Lademann C, Renkawitz J, Pfander B, Jentsch S. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. <i>Cell Reports</i>. 2017;19(7):1294-1303. doi:<a href=\"https://doi.org/10.1016/j.celrep.2017.04.051\">10.1016/j.celrep.2017.04.051</a>","ieee":"C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination,” <i>Cell Reports</i>, vol. 19, no. 7. Cell Press, pp. 1294–1303, 2017.","apa":"Lademann, C., Renkawitz, J., Pfander, B., &#38; Jentsch, S. (2017). The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. <i>Cell Reports</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.celrep.2017.04.051\">https://doi.org/10.1016/j.celrep.2017.04.051</a>","mla":"Lademann, Claudio, et al. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” <i>Cell Reports</i>, vol. 19, no. 7, Cell Press, 2017, pp. 1294–303, doi:<a href=\"https://doi.org/10.1016/j.celrep.2017.04.051\">10.1016/j.celrep.2017.04.051</a>.","ista":"Lademann C, Renkawitz J, Pfander B, Jentsch S. 2017. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. 19(7), 1294–1303.","short":"C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017) 1294–1303.","chicago":"Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” <i>Cell Reports</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.celrep.2017.04.051\">https://doi.org/10.1016/j.celrep.2017.04.051</a>."},"page":"1294 - 1303","ddc":["570"],"publication":"Cell Reports","status":"public","department":[{"_id":"MiSi"}],"oa_version":"Published Version","date_created":"2018-12-11T11:47:52Z","doi":"10.1016/j.celrep.2017.04.051","article_processing_charge":"No","title":"The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination","external_id":{"isi":["000402125100002"]},"type":"journal_article","file_date_updated":"2020-07-14T12:47:40Z","month":"05","abstract":[{"lang":"eng","text":"The INO80 complex (INO80-C) is an evolutionarily conserved nucleosome remodeler that acts in transcription, replication, and genome stability. It is required for resistance against genotoxic agents and is involved in the repair of DNA double-strand breaks (DSBs) by homologous recombination (HR). However, the causes of the HR defect in INO80-C mutant cells are controversial. Here, we unite previous findings using a system to study HR with high spatial resolution in budding yeast. We find that INO80-C has at least two distinct functions during HR—DNA end resection and presynaptic filament formation. Importantly, the second function is linked to the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic filament formation is the crucial INO80-C function during HR."}],"pubrep_id":"899","publication_identifier":{"issn":["2211-1247"]},"isi":1,"_id":"677","date_published":"2017-05-16T00:00:00Z","language":[{"iso":"eng"}],"publist_id":"7046","intvolume":"        19","publication_status":"published"},{"date_updated":"2026-04-08T14:09:28Z","acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"year":"2017","author":[{"id":"3DFD581A-F248-11E8-B48F-1D18A9856A87","full_name":"Chen, Chong","first_name":"Chong","last_name":"Chen"},{"first_name":"Itaru","last_name":"Arai","full_name":"Arai, Itaru","id":"32A73F6C-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Rachel","last_name":"Satterield","full_name":"Satterield, Rachel"},{"full_name":"Young, Samuel","first_name":"Samuel","last_name":"Young"},{"full_name":"Jonas, Peter M","first_name":"Peter M","last_name":"Jonas","orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"}],"status":"public","publication":"Cell Reports","citation":{"ista":"Chen C, Arai  itaru, Satterield R, Young S, Jonas PM. 2017. Synaptotagmin 2 is the fast Ca2+ sensor at a central inhibitory synapse. Cell Reports. 18(3), 723–736.","short":"C. Chen,  itaru Arai, R. Satterield, S. Young, P.M. Jonas, Cell Reports 18 (2017) 723–736.","chicago":"Chen, Chong, itaru Arai, Rachel Satterield, Samuel Young, and Peter M Jonas. “Synaptotagmin 2 Is the Fast Ca2+ Sensor at a Central Inhibitory Synapse.” <i>Cell Reports</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.celrep.2016.12.067\">https://doi.org/10.1016/j.celrep.2016.12.067</a>.","mla":"Chen, Chong, et al. “Synaptotagmin 2 Is the Fast Ca2+ Sensor at a Central Inhibitory Synapse.” <i>Cell Reports</i>, vol. 18, no. 3, Cell Press, 2017, pp. 723–36, doi:<a href=\"https://doi.org/10.1016/j.celrep.2016.12.067\">10.1016/j.celrep.2016.12.067</a>.","ieee":"C. Chen,  itaru Arai, R. Satterield, S. Young, and P. M. Jonas, “Synaptotagmin 2 is the fast Ca2+ sensor at a central inhibitory synapse,” <i>Cell Reports</i>, vol. 18, no. 3. Cell Press, pp. 723–736, 2017.","ama":"Chen C, Arai  itaru, Satterield R, Young S, Jonas PM. Synaptotagmin 2 is the fast Ca2+ sensor at a central inhibitory synapse. <i>Cell Reports</i>. 2017;18(3):723-736. doi:<a href=\"https://doi.org/10.1016/j.celrep.2016.12.067\">10.1016/j.celrep.2016.12.067</a>","apa":"Chen, C., Arai,  itaru, Satterield, R., Young, S., &#38; Jonas, P. M. (2017). Synaptotagmin 2 is the fast Ca2+ sensor at a central inhibitory synapse. <i>Cell Reports</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.celrep.2016.12.067\">https://doi.org/10.1016/j.celrep.2016.12.067</a>"},"page":"723 - 736","ddc":["571"],"ec_funded":1,"scopus_import":"1","has_accepted_license":"1","file":[{"file_name":"IST-2017-751-v1+1_1-s2.0-S2211124716317740-main.pdf","creator":"system","file_id":"5195","relation":"main_file","content_type":"application/pdf","file_size":4427591,"date_updated":"2018-12-12T10:16:09Z","access_level":"open_access","date_created":"2018-12-12T10:16:09Z"}],"publisher":"Cell Press","volume":18,"issue":"3","day":"17","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"quality_controlled":"1","oa":1,"date_published":"2017-01-17T00:00:00Z","isi":1,"_id":"1117","related_material":{"record":[{"status":"public","id":"324","relation":"dissertation_contains"}]},"publication_status":"published","intvolume":"        18","publist_id":"6245","language":[{"iso":"eng"}],"title":"Synaptotagmin 2 is the fast Ca2+ sensor at a central inhibitory synapse","article_processing_charge":"No","doi":"10.1016/j.celrep.2016.12.067","date_created":"2018-12-11T11:50:14Z","oa_version":"Published Version","department":[{"_id":"PeJo"}],"publication_identifier":{"issn":["2211-1247"]},"pubrep_id":"751","abstract":[{"lang":"eng","text":"GABAergic synapses in brain circuits generate inhibitory output signals with submillisecond latency and temporal precision. Whether the molecular identity of the release sensor contributes to these signaling properties remains unclear. Here, we examined the Ca^2+ sensor of exocytosis at GABAergic basket cell (BC) to Purkinje cell (PC) synapses in cerebellum. Immunolabeling suggested that BC terminals selectively expressed synaptotagmin 2 (Syt2), whereas synaptotagmin 1 (Syt1) was enriched in excitatory terminals. Genetic elimination of Syt2 reduced action potential-evoked release to ∼10%, identifying Syt2 as the major Ca^2+ sensor at BC-PC synapses. Differential adenovirus-mediated rescue revealed that Syt2 triggered release with shorter latency and higher temporal precision and mediated faster vesicle pool replenishment than Syt1. Furthermore, deletion of Syt2 severely reduced and delayed disynaptic inhibition following parallel fiber stimulation. Thus, the selective use of Syt2 as release sensor at BC-PC synapses ensures fast and efficient feedforward inhibition in cerebellar microcircuits. #bioimagingfacility-author"}],"file_date_updated":"2018-12-12T10:16:09Z","type":"journal_article","month":"01","project":[{"call_identifier":"FWF","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","grant_number":"P24909-B24","name":"Mechanisms of transmitter release at GABAergic synapses"},{"call_identifier":"FP7","_id":"25C0F108-B435-11E9-9278-68D0E5697425","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","grant_number":"268548"}],"external_id":{"isi":["000396470600013"]}},{"volume":21,"issue":"8","day":"21","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","short":"CC BY (4.0)","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"quality_controlled":"1","oa":1,"date_updated":"2026-04-08T14:09:28Z","acknowledged_ssus":[{"_id":"PreCl"}],"year":"2017","author":[{"id":"3DFD581A-F248-11E8-B48F-1D18A9856A87","full_name":"Chen, Chong","last_name":"Chen","first_name":"Chong"},{"full_name":"Satterfield, Rachel","last_name":"Satterfield","first_name":"Rachel"},{"first_name":"Samuel","last_name":"Young","full_name":"Young, Samuel"},{"orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","last_name":"Jonas","first_name":"Peter M","full_name":"Jonas, Peter M"}],"publication":"Cell Reports","status":"public","ddc":["570","571"],"page":"2082 - 2089","citation":{"ieee":"C. Chen, R. Satterfield, S. Young, and P. M. Jonas, “Triple function of Synaptotagmin 7 ensures efficiency of high-frequency transmission at central GABAergic synapses,” <i>Cell Reports</i>, vol. 21, no. 8. Cell Press, pp. 2082–2089, 2017.","apa":"Chen, C., Satterfield, R., Young, S., &#38; Jonas, P. M. (2017). Triple function of Synaptotagmin 7 ensures efficiency of high-frequency transmission at central GABAergic synapses. <i>Cell Reports</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.celrep.2017.10.122\">https://doi.org/10.1016/j.celrep.2017.10.122</a>","ama":"Chen C, Satterfield R, Young S, Jonas PM. Triple function of Synaptotagmin 7 ensures efficiency of high-frequency transmission at central GABAergic synapses. <i>Cell Reports</i>. 2017;21(8):2082-2089. doi:<a href=\"https://doi.org/10.1016/j.celrep.2017.10.122\">10.1016/j.celrep.2017.10.122</a>","mla":"Chen, Chong, et al. “Triple Function of Synaptotagmin 7 Ensures Efficiency of High-Frequency Transmission at Central GABAergic Synapses.” <i>Cell Reports</i>, vol. 21, no. 8, Cell Press, 2017, pp. 2082–89, doi:<a href=\"https://doi.org/10.1016/j.celrep.2017.10.122\">10.1016/j.celrep.2017.10.122</a>.","chicago":"Chen, Chong, Rachel Satterfield, Samuel Young, and Peter M Jonas. “Triple Function of Synaptotagmin 7 Ensures Efficiency of High-Frequency Transmission at Central GABAergic Synapses.” <i>Cell Reports</i>. Cell Press, 2017. <a href=\"https://doi.org/10.1016/j.celrep.2017.10.122\">https://doi.org/10.1016/j.celrep.2017.10.122</a>.","ista":"Chen C, Satterfield R, Young S, Jonas PM. 2017. Triple function of Synaptotagmin 7 ensures efficiency of high-frequency transmission at central GABAergic synapses. Cell Reports. 21(8), 2082–2089.","short":"C. Chen, R. Satterfield, S. Young, P.M. Jonas, Cell Reports 21 (2017) 2082–2089."},"ec_funded":1,"scopus_import":"1","has_accepted_license":"1","publisher":"Cell Press","file":[{"content_type":"application/pdf","checksum":"a6afa3764909bf6edafa07982d8e1cee","file_size":2759195,"date_created":"2018-12-12T10:09:14Z","date_updated":"2020-07-14T12:47:59Z","access_level":"open_access","file_id":"4737","relation":"main_file","file_name":"IST-2017-874-v1+1_PIIS2211124717316029.pdf","creator":"system"}],"title":"Triple function of Synaptotagmin 7 ensures efficiency of high-frequency transmission at central GABAergic synapses","article_processing_charge":"No","doi":"10.1016/j.celrep.2017.10.122","date_created":"2018-12-11T11:48:18Z","oa_version":"Published Version","department":[{"_id":"PeJo"}],"publication_identifier":{"issn":["2211-1247"]},"corr_author":"1","pubrep_id":"874","abstract":[{"text":"Synaptotagmin 7 (Syt7) is thought to be a Ca2+ sensor that mediates asynchronous transmitter release and facilitation at synapses. However, Syt7 is strongly expressed in fast-spiking, parvalbumin-expressing GABAergic interneurons, and the output synapses of these neurons produce only minimal asynchronous release and show depression rather than facilitation. To resolve this apparent contradiction, we examined the effects of genetic elimination of Syt7 on synaptic transmission at the GABAergic basket cell (BC)-Purkinje cell (PC) synapse in cerebellum. Our results indicate that at the BC-PC synapse, Syt7 contributes to asynchronous release, pool replenishment, and facilitation. In combination, these three effects ensure efficient transmitter release during high-frequency activity and guarantee frequency independence of inhibition. Our results identify a distinct function of Syt7: ensuring the efficiency of high-frequency inhibitory synaptic transmission","lang":"eng"}],"month":"11","file_date_updated":"2020-07-14T12:47:59Z","type":"journal_article","project":[{"call_identifier":"FWF","name":"Mechanisms of transmitter release at GABAergic synapses","grant_number":"P24909-B24","_id":"25C26B1E-B435-11E9-9278-68D0E5697425"},{"call_identifier":"H2020","_id":"25B7EB9E-B435-11E9-9278-68D0E5697425","name":"Biophysics and circuit function of a giant cortical glutamatergic synapse","grant_number":"692692"}],"external_id":{"isi":["000416216700007"]},"date_published":"2017-11-21T00:00:00Z","isi":1,"_id":"749","related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"324"}]},"publication_status":"published","intvolume":"        21","publist_id":"6907","language":[{"iso":"eng"}]},{"title":"Cross-talk between carbon cetabolism and the DNA camage response in S. cerevisiae","oa_version":"Published Version","date_created":"2024-10-15T11:20:54Z","doi":"10.1016/j.celrep.2015.08.025","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1016/j.celrep.2015.08.025"}],"article_processing_charge":"No","type":"journal_article","month":"09","abstract":[{"text":"Yeast cells with DNA damage avoid respiration, presumably because products of oxidative metabolism can be harmful to DNA. We show that DNA damage inhibits the activity of the Snf1 (AMP-activated) protein kinase (AMPK), which activates expression of genes required for respiration. Glucose and DNA damage upregulate SUMOylation of Snf1, catalyzed by the SUMO E3 ligase Mms21, which inhibits SNF1 activity. The DNA damage checkpoint kinases Mec1/ATR and Tel1/ATM, as well as the nutrient-sensing protein kinase A (PKA), regulate Mms21 activity toward Snf1. Mec1 and Tel1 are required for two SNF1-regulated processes—glucose sensing and ADH2 gene expression—even without exogenous genotoxic stress. Our results imply that inhibition of Snf1 by SUMOylation is a mechanism by which cells lower their respiration in response to DNA damage. This raises the possibility that activation of DNA damage checkpoint mechanisms could contribute to aerobic fermentation (Warburg effect), a hallmark of cancer cells.","lang":"eng"}],"publication_identifier":{"issn":["2211-1247"]},"_id":"18365","date_published":"2015-09-22T00:00:00Z","language":[{"iso":"eng"}],"intvolume":"        12","DOAJ_listed":"1","publication_status":"published","day":"22","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","volume":12,"issue":"11","quality_controlled":"1","oa":1,"author":[{"first_name":"Kobi J.","last_name":"Simpson-Lavy","full_name":"Simpson-Lavy, Kobi J."},{"first_name":"Alexander","last_name":"Bronstein","full_name":"Bronstein, Alexander","id":"58f3726e-7cba-11ef-ad8b-e6e8cb3904e6","orcid":"0000-0001-9699-8730"},{"first_name":"Martin","last_name":"Kupiec","full_name":"Kupiec, Martin"},{"last_name":"Johnston","first_name":"Mark","full_name":"Johnston, Mark"}],"year":"2015","date_updated":"2024-12-18T12:23:56Z","extern":"1","publisher":"Elsevier","scopus_import":"1","publication":"Cell Reports","status":"public","citation":{"short":"K.J. Simpson-Lavy, A.M. Bronstein, M. Kupiec, M. Johnston, Cell Reports 12 (2015) 1865–1875.","ista":"Simpson-Lavy KJ, Bronstein AM, Kupiec M, Johnston M. 2015. Cross-talk between carbon cetabolism and the DNA camage response in S. cerevisiae. Cell Reports. 12(11), 1865–1875.","chicago":"Simpson-Lavy, Kobi J., Alex M. Bronstein, Martin Kupiec, and Mark Johnston. “Cross-Talk between Carbon Cetabolism and the DNA Camage Response in S. Cerevisiae.” <i>Cell Reports</i>. Elsevier, 2015. <a href=\"https://doi.org/10.1016/j.celrep.2015.08.025\">https://doi.org/10.1016/j.celrep.2015.08.025</a>.","ieee":"K. J. Simpson-Lavy, A. M. Bronstein, M. Kupiec, and M. Johnston, “Cross-talk between carbon cetabolism and the DNA camage response in S. cerevisiae,” <i>Cell Reports</i>, vol. 12, no. 11. Elsevier, pp. 1865–1875, 2015.","mla":"Simpson-Lavy, Kobi J., et al. “Cross-Talk between Carbon Cetabolism and the DNA Camage Response in S. Cerevisiae.” <i>Cell Reports</i>, vol. 12, no. 11, Elsevier, 2015, pp. 1865–75, doi:<a href=\"https://doi.org/10.1016/j.celrep.2015.08.025\">10.1016/j.celrep.2015.08.025</a>.","ama":"Simpson-Lavy KJ, Bronstein AM, Kupiec M, Johnston M. Cross-talk between carbon cetabolism and the DNA camage response in S. cerevisiae. <i>Cell Reports</i>. 2015;12(11):1865-1875. doi:<a href=\"https://doi.org/10.1016/j.celrep.2015.08.025\">10.1016/j.celrep.2015.08.025</a>","apa":"Simpson-Lavy, K. J., Bronstein, A. M., Kupiec, M., &#38; Johnston, M. (2015). Cross-talk between carbon cetabolism and the DNA camage response in S. cerevisiae. <i>Cell Reports</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.celrep.2015.08.025\">https://doi.org/10.1016/j.celrep.2015.08.025</a>"},"page":"1865-1875"},{"file":[{"date_created":"2020-03-23T12:23:40Z","date_updated":"2020-07-14T12:48:01Z","access_level":"open_access","content_type":"application/pdf","file_size":2755808,"checksum":"23c30de4ac98ce9879fc054121517626","file_id":"7613","relation":"main_file","file_name":"2014_CellPress_Tan.pdf","creator":"dernst"}],"publisher":"Elsevier","has_accepted_license":"1","status":"public","publication":"Cell Reports","citation":{"ista":"Tan S, Xue H-W. 2014. Casein kinase 1 regulates ethylene synthesis by phosphorylating and promoting the turnover of ACS5. Cell Reports. 9(5), 1692–1702.","short":"S. Tan, H.-W. Xue, Cell Reports 9 (2014) 1692–1702.","chicago":"Tan, Shutang, and Hong-Wei Xue. “Casein Kinase 1 Regulates Ethylene Synthesis by Phosphorylating and Promoting the Turnover of ACS5.” <i>Cell Reports</i>. Elsevier, 2014. <a href=\"https://doi.org/10.1016/j.celrep.2014.10.047\">https://doi.org/10.1016/j.celrep.2014.10.047</a>.","ieee":"S. Tan and H.-W. Xue, “Casein kinase 1 regulates ethylene synthesis by phosphorylating and promoting the turnover of ACS5,” <i>Cell Reports</i>, vol. 9, no. 5. Elsevier, pp. 1692–1702, 2014.","apa":"Tan, S., &#38; Xue, H.-W. (2014). Casein kinase 1 regulates ethylene synthesis by phosphorylating and promoting the turnover of ACS5. <i>Cell Reports</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.celrep.2014.10.047\">https://doi.org/10.1016/j.celrep.2014.10.047</a>","ama":"Tan S, Xue H-W. Casein kinase 1 regulates ethylene synthesis by phosphorylating and promoting the turnover of ACS5. <i>Cell Reports</i>. 2014;9(5):1692-1702. doi:<a href=\"https://doi.org/10.1016/j.celrep.2014.10.047\">10.1016/j.celrep.2014.10.047</a>","mla":"Tan, Shutang, and Hong-Wei Xue. “Casein Kinase 1 Regulates Ethylene Synthesis by Phosphorylating and Promoting the Turnover of ACS5.” <i>Cell Reports</i>, vol. 9, no. 5, Elsevier, 2014, pp. 1692–702, doi:<a href=\"https://doi.org/10.1016/j.celrep.2014.10.047\">10.1016/j.celrep.2014.10.047</a>."},"page":"1692-1702","ddc":["580"],"author":[{"full_name":"Tan, Shutang","first_name":"Shutang","last_name":"Tan","id":"2DE75584-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-0471-8285"},{"full_name":"Xue, Hong-Wei","last_name":"Xue","first_name":"Hong-Wei"}],"year":"2014","date_updated":"2021-01-12T08:14:24Z","extern":"1","article_type":"original","quality_controlled":"1","oa":1,"tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","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"},"day":"11","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","volume":9,"issue":"5","language":[{"iso":"eng"}],"intvolume":"         9","publication_status":"published","_id":"7598","date_published":"2014-12-11T00:00:00Z","file_date_updated":"2020-07-14T12:48:01Z","month":"12","type":"journal_article","publication_identifier":{"issn":["2211-1247"]},"title":"Casein kinase 1 regulates ethylene synthesis by phosphorylating and promoting the turnover of ACS5","doi":"10.1016/j.celrep.2014.10.047","oa_version":"Published Version","date_created":"2020-03-21T16:08:18Z","article_processing_charge":"No"}]