[{"oa_version":"None","citation":{"ista":"Weber M. 2012. NextGen speaks 13 . Science. 336(6077), 32–34.","short":"M. Weber, Science 336 (2012) 32–34.","mla":"Weber, Michele. “NextGen Speaks 13 .” <i>Science</i>, vol. 336, no. 6077, American Association for the Advancement of Science, 2012, pp. 32–34, doi:<a href=\"https://doi.org/10.1126/science.336.6077.32\">10.1126/science.336.6077.32</a>.","chicago":"Weber, Michele. “NextGen Speaks 13 .” <i>Science</i>. American Association for the Advancement of Science, 2012. <a href=\"https://doi.org/10.1126/science.336.6077.32\">https://doi.org/10.1126/science.336.6077.32</a>.","ieee":"M. Weber, “NextGen speaks 13 ,” <i>Science</i>, vol. 336, no. 6077. American Association for the Advancement of Science, pp. 32–34, 2012.","apa":"Weber, M. (2012). NextGen speaks 13 . <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.336.6077.32\">https://doi.org/10.1126/science.336.6077.32</a>","ama":"Weber M. NextGen speaks 13 . <i>Science</i>. 2012;336(6077):32-34. doi:<a href=\"https://doi.org/10.1126/science.336.6077.32\">10.1126/science.336.6077.32</a>"},"month":"04","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","publication_status":"published","type":"journal_article","author":[{"full_name":"Weber, Michele","first_name":"Michele","last_name":"Weber","id":"3A3FC708-F248-11E8-B48F-1D18A9856A87"}],"language":[{"iso":"eng"}],"issue":"6077","popular_science":"1","publist_id":"3516","status":"public","date_created":"2018-12-11T12:01:47Z","date_updated":"2025-05-20T07:14:51Z","_id":"3167","oa":1,"department":[{"_id":"MiSi"}],"article_type":"letter_note","date_published":"2012-04-06T00:00:00Z","intvolume":"       336","title":"NextGen speaks 13 ","volume":336,"day":"06","OA_type":"free access","fulldoi":"https://doi.org/10.1126/science.336.6077.32","year":"2012","doi":"10.1126/science.336.6077.32","publisher":"American Association for the Advancement of Science","publication":"Science","page":"32-34","external_id":{"pmid":["22491839"]},"pmid":1,"main_file_link":[{"url":"https://doi.org/10.1126/science.336.6077.32","open_access":"1"}]},{"_id":"506","corr_author":"1","department":[{"_id":"MiSi"}],"oa":1,"article_type":"original","date_published":"2012-04-30T00:00:00Z","license":"https://creativecommons.org/licenses/by-nc-sa/3.0/","intvolume":"       197","title":"Cell migration: Fibroblasts find a new way to get ahead","scopus_import":"1","volume":197,"day":"30","fulldoi":"https://doi.org/10.1083/jcb.201204039","year":"2012","das_tickbox":"1","doi":"10.1083/jcb.201204039","publisher":"Rockefeller University Press","external_id":{"isi":["000303467800004"]},"page":"347 - 349","publication":"Journal of Cell Biology","tmp":{"image":"/images/cc_by_nc_sa.png","short":"CC BY-NC-SA (3.0)","name":"Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported (CC BY-NC-SA 3.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/3.0/legalcode"},"oa_version":"Published Version","citation":{"ama":"Sixt MK. Cell migration: Fibroblasts find a new way to get ahead. <i>Journal of Cell Biology</i>. 2012;197(3):347-349. doi:<a href=\"https://doi.org/10.1083/jcb.201204039\">10.1083/jcb.201204039</a>","apa":"Sixt, M. K. (2012). Cell migration: Fibroblasts find a new way to get ahead. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1083/jcb.201204039\">https://doi.org/10.1083/jcb.201204039</a>","ieee":"M. K. Sixt, “Cell migration: Fibroblasts find a new way to get ahead,” <i>Journal of Cell Biology</i>, vol. 197, no. 3. Rockefeller University Press, pp. 347–349, 2012.","chicago":"Sixt, Michael K. “Cell Migration: Fibroblasts Find a New Way to Get Ahead.” <i>Journal of Cell Biology</i>. Rockefeller University Press, 2012. <a href=\"https://doi.org/10.1083/jcb.201204039\">https://doi.org/10.1083/jcb.201204039</a>.","mla":"Sixt, Michael K. “Cell Migration: Fibroblasts Find a New Way to Get Ahead.” <i>Journal of Cell Biology</i>, vol. 197, no. 3, Rockefeller University Press, 2012, pp. 347–49, doi:<a href=\"https://doi.org/10.1083/jcb.201204039\">10.1083/jcb.201204039</a>.","short":"M.K. Sixt, Journal of Cell Biology 197 (2012) 347–349.","ista":"Sixt MK. 2012. Cell migration: Fibroblasts find a new way to get ahead. Journal of Cell Biology. 197(3), 347–349."},"month":"04","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","file_date_updated":"2020-07-14T12:46:36Z","quality_controlled":"1","publication_status":"published","type":"journal_article","author":[{"full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"}],"ddc":["570"],"language":[{"iso":"eng"}],"isi":1,"issue":"3","status":"public","publist_id":"7314","has_accepted_license":"1","date_updated":"2026-07-28T09:22:21Z","date_created":"2018-12-11T11:46:51Z","file":[{"content_type":"application/pdf","checksum":"45c02be33ebd99fc3077d60b9c90bdfa","file_name":"2012_CellBiology_Sixt.pdf","creator":"kschuh","relation":"main_file","date_created":"2019-02-12T09:03:09Z","date_updated":"2020-07-14T12:46:36Z","access_level":"open_access","file_size":986566,"file_id":"5957"}]},{"date_updated":"2025-09-30T09:24:17Z","date_created":"2018-12-11T11:46:46Z","publist_id":"7329","status":"public","language":[{"iso":"eng"}],"isi":1,"issue":"198","publication_status":"published","author":[{"full_name":"Eichner, Alexander","first_name":"Alexander","last_name":"Eichner","id":"4DFA52AE-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Michael K","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","orcid":"0000-0002-6620-9179"}],"type":"journal_article","quality_controlled":"1","article_processing_charge":"No","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","citation":{"chicago":"Eichner, Alexander, and Michael K Sixt. “Setting the Clock for Recirculating Lymphocytes.” <i>Science Signaling</i>. American Association for the Advancement of Science, 2011. <a href=\"https://doi.org/10.1126/scisignal.2002617\">https://doi.org/10.1126/scisignal.2002617</a>.","apa":"Eichner, A., &#38; Sixt, M. K. (2011). Setting the clock for recirculating lymphocytes. <i>Science Signaling</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/scisignal.2002617\">https://doi.org/10.1126/scisignal.2002617</a>","ieee":"A. Eichner and M. K. Sixt, “Setting the clock for recirculating lymphocytes,” <i>Science Signaling</i>, vol. 4, no. 198. American Association for the Advancement of Science, 2011.","ama":"Eichner A, Sixt MK. Setting the clock for recirculating lymphocytes. <i>Science Signaling</i>. 2011;4(198). doi:<a href=\"https://doi.org/10.1126/scisignal.2002617\">10.1126/scisignal.2002617</a>","ista":"Eichner A, Sixt MK. 2011. Setting the clock for recirculating lymphocytes. Science Signaling. 4(198), pe43.","short":"A. Eichner, M.K. Sixt, Science Signaling 4 (2011).","mla":"Eichner, Alexander, and Michael K. Sixt. “Setting the Clock for Recirculating Lymphocytes.” <i>Science Signaling</i>, vol. 4, no. 198, pe43, American Association for the Advancement of Science, 2011, doi:<a href=\"https://doi.org/10.1126/scisignal.2002617\">10.1126/scisignal.2002617</a>."},"oa_version":"None","month":"11","external_id":{"isi":["000296800500002"]},"publication":"Science Signaling","publisher":"American Association for the Advancement of Science","fulldoi":"https://doi.org/10.1126/scisignal.2002617","day":"08","doi":"10.1126/scisignal.2002617","year":"2011","volume":4,"abstract":[{"lang":"eng","text":"In their search for antigens, lymphocytes continuously shuttle among blood vessels, lymph vessels, and lymphatic tissues. Chemokines mediate entry of lymphocytes into lymphatic tissues, and sphingosine 1-phosphate (S1P) promotes localization of lymphocytes to the vasculature. Both signals are sensed through G protein-coupled receptors (GPCRs). Most GPCRs undergo ligand-dependent homologous receptor desensitization, a process that decreases their signaling output after previous exposure to high ligand concentration. Such desensitization can explain why lymphocytes do not take an intermediate position between two signals but rather oscillate between them. The desensitization of S1P receptor 1 (S1PR1) is mediated by GPCR kinase 2 (GRK2). Deletion of GRK2 in lymphocytes compromises desensitization by high vascular S1P concentrations, thereby reducing responsiveness to the chemokine signal and trapping the cells in the vascular compartment. The desensitization kinetics of S1PR1 allows lymphocytes to dynamically shuttle between vasculature and lymphatic tissue, although the positional information in both compartments is static."}],"title":"Setting the clock for recirculating lymphocytes","scopus_import":"1","intvolume":"         4","article_number":"pe43","date_published":"2011-11-08T00:00:00Z","corr_author":"1","department":[{"_id":"MiSi"}],"_id":"491"},{"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199389/","open_access":"1"}],"pmid":1,"publisher":"Wiley-Blackwell","external_id":{"pmid":["21857646"],"isi":["000296715800018"]},"publication":"EMBO Journal","page":"4309 - 4322","year":"2011","doi":"10.1038/emboj.2011.301","day":"19","fulldoi":"https://doi.org/10.1038/emboj.2011.301","abstract":[{"text":"Cancer stem cells or cancer initiating cells are believed to contribute to cancer recurrence after therapy. MicroRNAs (miRNAs) are short RNA molecules with fundamental roles in gene regulation. The role of miRNAs in cancer stem cells is only poorly understood. Here, we report miRNA expression profiles of glioblastoma stem cell-containing CD133 + cell populations. We find that miR-9, miR-9 * (referred to as miR-9/9 *), miR-17 and miR-106b are highly abundant in CD133 + cells. Furthermore, inhibition of miR-9/9 * or miR-17 leads to reduced neurosphere formation and stimulates cell differentiation. Calmodulin-binding transcription activator 1 (CAMTA1) is a putative transcription factor, which induces the expression of the anti-proliferative cardiac hormone natriuretic peptide A (NPPA). We identify CAMTA1 as an miR-9/9 * and miR-17 target. CAMTA1 expression leads to reduced neurosphere formation and tumour growth in nude mice, suggesting that CAMTA1 can function as tumour suppressor. Consistently, CAMTA1 and NPPA expression correlate with patient survival. Our findings could provide a basis for novel strategies of glioblastoma therapy.","lang":"eng"}],"volume":30,"intvolume":"        30","title":"CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells","scopus_import":"1","article_type":"original","date_published":"2011-10-19T00:00:00Z","department":[{"_id":"MiSi"}],"oa":1,"_id":"518","date_updated":"2025-09-30T09:23:51Z","date_created":"2018-12-11T11:46:55Z","status":"public","publist_id":"7301","isi":1,"issue":"20","language":[{"iso":"eng"}],"type":"journal_article","author":[{"last_name":"Schraivogel","full_name":"Schraivogel, Daniel","first_name":"Daniel"},{"last_name":"Weinmann","full_name":"Weinmann, Lasse","first_name":"Lasse"},{"full_name":"Beier, Dagmar","first_name":"Dagmar","last_name":"Beier"},{"full_name":"Tabatabai, Ghazaleh","first_name":"Ghazaleh","last_name":"Tabatabai"},{"first_name":"Alexander","full_name":"Eichner, Alexander","id":"4DFA52AE-F248-11E8-B48F-1D18A9856A87","last_name":"Eichner"},{"last_name":"Zhu","first_name":"Jia","full_name":"Zhu, Jia"},{"last_name":"Anton","full_name":"Anton, Martina","first_name":"Martina"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","orcid":"0000-0002-6620-9179","first_name":"Michael K","full_name":"Sixt, Michael K"},{"first_name":"Michael","full_name":"Weller, Michael","last_name":"Weller"},{"first_name":"Christoph","full_name":"Beier, Christoph","last_name":"Beier"},{"first_name":"Gunter","full_name":"Meister, Gunter","last_name":"Meister"}],"publication_status":"published","quality_controlled":"1","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","article_processing_charge":"No","month":"10","citation":{"ama":"Schraivogel D, Weinmann L, Beier D, et al. CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells. <i>EMBO Journal</i>. 2011;30(20):4309-4322. doi:<a href=\"https://doi.org/10.1038/emboj.2011.301\">10.1038/emboj.2011.301</a>","apa":"Schraivogel, D., Weinmann, L., Beier, D., Tabatabai, G., Eichner, A., Zhu, J., … Meister, G. (2011). CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells. <i>EMBO Journal</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1038/emboj.2011.301\">https://doi.org/10.1038/emboj.2011.301</a>","ieee":"D. Schraivogel <i>et al.</i>, “CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells,” <i>EMBO Journal</i>, vol. 30, no. 20. Wiley-Blackwell, pp. 4309–4322, 2011.","chicago":"Schraivogel, Daniel, Lasse Weinmann, Dagmar Beier, Ghazaleh Tabatabai, Alexander Eichner, Jia Zhu, Martina Anton, et al. “CAMTA1 Is a Novel Tumour Suppressor Regulated by MiR-9/9 * in Glioblastoma Stem Cells.” <i>EMBO Journal</i>. Wiley-Blackwell, 2011. <a href=\"https://doi.org/10.1038/emboj.2011.301\">https://doi.org/10.1038/emboj.2011.301</a>.","mla":"Schraivogel, Daniel, et al. “CAMTA1 Is a Novel Tumour Suppressor Regulated by MiR-9/9 * in Glioblastoma Stem Cells.” <i>EMBO Journal</i>, vol. 30, no. 20, Wiley-Blackwell, 2011, pp. 4309–22, doi:<a href=\"https://doi.org/10.1038/emboj.2011.301\">10.1038/emboj.2011.301</a>.","ista":"Schraivogel D, Weinmann L, Beier D, Tabatabai G, Eichner A, Zhu J, Anton M, Sixt MK, Weller M, Beier C, Meister G. 2011. CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells. EMBO Journal. 30(20), 4309–4322.","short":"D. Schraivogel, L. Weinmann, D. Beier, G. Tabatabai, A. Eichner, J. Zhu, M. Anton, M.K. Sixt, M. Weller, C. Beier, G. Meister, EMBO Journal 30 (2011) 4309–4322."},"oa_version":"Submitted Version"},{"date_created":"2018-12-11T12:02:24Z","pubrep_id":"11","date_updated":"2026-04-09T14:36:24Z","file":[{"file_id":"6177","file_size":4487708,"access_level":"closed","creator":"dernst","file_name":"2011_Thesis_Kathrin_Schumann.pdf","date_created":"2019-03-26T08:12:21Z","date_updated":"2020-07-14T12:46:06Z","relation":"main_file","content_type":"application/pdf","checksum":"e69eee6252660f0b694a2ea8923ddc72"},{"checksum":"71727d63f424b5b446f68f4b87ecadc0","content_type":"application/pdf","relation":"main_file","date_created":"2021-02-22T11:24:30Z","date_updated":"2021-02-22T11:24:30Z","success":1,"file_name":"2011_Thesis_Schumann_noS.pdf","creator":"dernst","access_level":"open_access","file_size":4313127,"file_id":"9175"}],"language":[{"iso":"eng"}],"ddc":["570","579"],"OA_place":"publisher","degree_awarded":"PhD","has_accepted_license":"1","status":"public","publist_id":"3371","file_date_updated":"2021-02-22T11:24:30Z","publication_status":"published","supervisor":[{"first_name":"Michael K","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","orcid":"0000-0002-6620-9179"}],"alternative_title":["ISTA Thesis"],"author":[{"last_name":"Schumann","id":"F44D762E-4F9D-11E9-B64C-9EB26CEFFB5F","full_name":"Schumann, Kathrin","first_name":"Kathrin"}],"type":"dissertation","oa_version":"Published Version","citation":{"apa":"Schumann, K. (2011). <i>The role of chemotactic gradients in dendritic cell migration</i>. Institute of Science and Technology Austria.","ieee":"K. Schumann, “The role of chemotactic gradients in dendritic cell migration,” Institute of Science and Technology Austria, 2011.","ama":"Schumann K. The role of chemotactic gradients in dendritic cell migration. 2011.","chicago":"Schumann, Kathrin. “The Role of Chemotactic Gradients in Dendritic Cell Migration.” Institute of Science and Technology Austria, 2011.","mla":"Schumann, Kathrin. <i>The Role of Chemotactic Gradients in Dendritic Cell Migration</i>. Institute of Science and Technology Austria, 2011.","short":"K. Schumann, The Role of Chemotactic Gradients in Dendritic Cell Migration, Institute of Science and Technology Austria, 2011.","ista":"Schumann K. 2011. The role of chemotactic gradients in dendritic cell migration. Institute of Science and Technology Austria."},"month":"03","article_processing_charge":"No","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","page":"141","publisher":"Institute of Science and Technology Austria","abstract":[{"lang":"eng","text":"Chemokines organize immune cell trafficking by inducing either directed (tactic) or random (kinetic) migration and by activating integrins in order to support surface adhesion (haptic). Beyond that the same chemokines can establish clearly defined functional areas in secondary lymphoid organs. Until now it is unclear how chemokines can fulfill such diverse functions. One decisive prerequisite to explain these capacities is to know how chemokines are presented in tissue. In theory chemokines could occur either soluble or immobilized, and could be distributed either homogenously or as a concentration gradient. To dissect if and how the presenting mode of chemokines influences immune cells, I tested the response of dendritic cells (DCs) to differentially displayed chemokines. DCs are antigen presenting cells that reside in the periphery and migrate into draining lymph nodes (LNs) once exposed to inflammatory stimuli to activate naïve T cells. DCs are guided to and within the LN by the chemokine receptor CCR7, which has two ligands, the chemokines CCL19 and CCL21. Both CCR7 ligands are expressed by fibroblastic reticular cells in the LN, but differ in their ability to bind to heparan sulfate residues. CCL21 has a highly charged C-terminal extension, which mediates binding to anionic surfaces, whereas CCL19 is lacking such residues and likely distributes as a soluble molecule. This study shows that surface-bound CCL21 causes random, haptokinetic DC motility, which is confined to the chemokine coated area by insideout activation of β2 integrins that mediate cell binding to the surface. CCL19 on the other hand forms concentration gradients which trigger directional, chemotactic movement, but no surface adhesion. In addition DCs can actively manipulate this system by recruiting and activating serine proteases on their surfaces, which create - by proteolytically removing the adhesive C-terminus - a solubilized variant of CCL21 that functionally resembles CCL19. By generating a CCL21 concentration gradient DCs establish a positive feedback loop to recruit further DCs from the periphery to the CCL21 coated region. In addition DCs can sense chemotactic gradients as well as immobilized haptokinetic fields at the same time and integrate these signals. The result is chemotactically biased haptokinesis - directional migration confined to a chemokine coated track or area - which could explain the dynamic but spatially tightly controlled swarming leukocyte locomotion patterns that have been observed in lymphatic organs by intravital microscopists. The finding that DCs can approach soluble cues in a non-adhesive manner while they attach to surfaces coated with immobilized cues raises the question how these cells transmit intracellular forces to the environment, especially in the non-adherent migration mode. In order to migrate, cells have to generate and transmit force to the extracellular substrate. Force transmission is the prerequisite to procure an expansion of the leading edge and a forward motion of the whole cell body. In the current conceptions actin polymerization at the leading edge is coupled to extracellular ligands via the integrin family of transmembrane receptors, which allows the transmission of intracellular force. Against the paradigm of force transmission during migration, leukocytes, like DCs, are able to migrate in threedimensional environments without using integrin transmembrane receptors (Lämmermann et al., 2008). This reflects the biological function of leukocytes, as they can invade almost all tissues, whereby their migration has to be independent from the extracellular environment. How the cells can achieve this is unclear. For this study I examined DC migration in a defined threedimensional environment and highlighted actin-dynamics with the probe Lifeact-GFP. The result was that chemotactic DCs can switch between integrin-dependent and integrin- independent locomotion and can thereby adapt to the adhesive properties of their environment. If the cells are able to couple their actin cytoskeleton to the substrate, actin polymerization is entirely converted into protrusion. Without coupling the actin cortex undergoes slippage and retrograde actin flow can be observed. But retrograde actin flow can be completely compensated by higher actin polymerization rate keeping the migration velocity and the shape of the cells unaltered. Mesenchymal cells like fibroblast cannot balance the loss of adhesive interaction, cannot protrude into open space and, therefore, strictly depend on integrinmediated force coupling. This leukocyte specific phenomenon of “adaptive force transmission” endows these cells with the unique ability to transit and invade almost every type of tissue. "}],"day":"01","acknowledgement":"I would like to express my sincere gratitude to the following people who made with their continuous support and encouragement this thesis possible: First, I want to thank Prof. Dr. Michael Sixt for his excellent supervision and mentoring, especially for the nice, relaxed working atmosphere, a lot of brilliant ideas and the freedom to work in my own way.\r\n\r\nProf. Dr. Reinhard Fässler for his constant support of the Sixt lab and for providing excellent working conditions. \r\n\r\nProf. Dr. Sanjiv Luther and Prof. Dr. Tobias Bollenbach for agreeing to be member of my thesis committee and to evaluate my work.\r\n\r\nDr. Walther Göhring, Carmen Schmitz, the Recombinant Protein Production core facility and the animal care takers for providing the “infrastructure” for this thesis. \r\n\r\nProf. Dr. Daniel Legler, Markus Bruckner and Dr. Julien Polleux for very fruitful collaborations and discussions.\r\n\r\nMy labmates for their help, a lot of discussions and to make the Sixt lab to a convenient place to work : Karin Hirsch, Tim Lämmeramnn, Holger Pflicke, Jörg Renkawitz, Michele Weber and Alexander Eichner All members of the Department of Molecular Medicine for their help. Especially I want to thank Sarah Schmidt, Karin Hirsch and Raphael Ruppert for their friendship, nice chats and their uncensored point of view. ","year":"2011","date_published":"2011-03-01T00:00:00Z","title":"The role of chemotactic gradients in dendritic cell migration","_id":"3275","corr_author":"1","publication_identifier":{"issn":["2663-337X"]},"department":[{"_id":"MiSi"}],"oa":1},{"publication_status":"published","author":[{"orcid":"0000-0003-4088-8633","last_name":"Ruprecht","id":"4D71A03A-F248-11E8-B48F-1D18A9856A87","full_name":"Ruprecht, Verena","first_name":"Verena"},{"first_name":"Markus","full_name":"Axmann, Markus","last_name":"Axmann"},{"orcid":"0000-0002-2670-2217","id":"355AA5A0-F248-11E8-B48F-1D18A9856A87","last_name":"Wieser","first_name":"Stefan","full_name":"Wieser, Stefan"},{"first_name":"Gerhard","full_name":"Schuetz, Gerhard","last_name":"Schuetz"}],"type":"journal_article","quality_controlled":"1","article_processing_charge":"No","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","oa_version":"None","citation":{"chicago":"Ruprecht, Verena, Markus Axmann, Stefan Wieser, and Gerhard Schuetz. “What Can We Learn from Single Molecule Trajectories?” <i>Current Protein &#38; Peptide Science</i>. Bentham Science Publishers, 2011. <a href=\"https://doi.org/10.2174/138920311798841753\">https://doi.org/10.2174/138920311798841753</a>.","ieee":"V. Ruprecht, M. Axmann, S. Wieser, and G. Schuetz, “What can we learn from single molecule trajectories?,” <i>Current Protein &#38; Peptide Science</i>, vol. 12, no. 8. Bentham Science Publishers, pp. 714–724, 2011.","apa":"Ruprecht, V., Axmann, M., Wieser, S., &#38; Schuetz, G. (2011). What can we learn from single molecule trajectories? <i>Current Protein &#38; Peptide Science</i>. Bentham Science Publishers. <a href=\"https://doi.org/10.2174/138920311798841753\">https://doi.org/10.2174/138920311798841753</a>","ama":"Ruprecht V, Axmann M, Wieser S, Schuetz G. What can we learn from single molecule trajectories? <i>Current Protein &#38; Peptide Science</i>. 2011;12(8):714-724. doi:<a href=\"https://doi.org/10.2174/138920311798841753\">10.2174/138920311798841753</a>","short":"V. Ruprecht, M. Axmann, S. Wieser, G. Schuetz, Current Protein &#38; Peptide Science 12 (2011) 714–724.","ista":"Ruprecht V, Axmann M, Wieser S, Schuetz G. 2011. What can we learn from single molecule trajectories? Current Protein &#38; Peptide Science. 12(8), 714–724.","mla":"Ruprecht, Verena, et al. “What Can We Learn from Single Molecule Trajectories?” <i>Current Protein &#38; Peptide Science</i>, vol. 12, no. 8, Bentham Science Publishers, 2011, pp. 714–24, doi:<a href=\"https://doi.org/10.2174/138920311798841753\">10.2174/138920311798841753</a>."},"month":"12","date_created":"2018-12-11T12:02:28Z","date_updated":"2025-09-30T09:21:31Z","status":"public","publist_id":"3358","language":[{"iso":"eng"}],"isi":1,"issue":"8","title":"What can we learn from single molecule trajectories?","scopus_import":"1","intvolume":"        12","date_published":"2011-12-01T00:00:00Z","department":[{"_id":"CaHe"},{"_id":"MiSi"}],"_id":"3287","external_id":{"isi":["000299672600005"]},"page":"714 - 724","publication":"Current Protein & Peptide Science","publisher":"Bentham Science Publishers","fulldoi":"https://doi.org/10.2174/138920311798841753","day":"01","year":"2011","doi":"10.2174/138920311798841753","volume":12,"abstract":[{"text":"Diffusing membrane constituents are constantly exposed to a variety of forces that influence their stochastic path. Single molecule experiments allow for resolving trajectories at extremely high spatial and temporal accuracy, thereby offering insights into en route interactions of the tracer. In this review we discuss approaches to derive information about the underlying processes, based on single molecule tracking experiments. In particular, we focus on a new versatile way to analyze single molecule diffusion in the absence of a full analytical treatment. The method is based on comprehensive comparison of an experimental data set against the hypothetical outcome of multiple experiments performed on the computer. Since Monte Carlo simulations can be easily and rapidly performed even on state-of-the-art PCs, our method provides a simple way for testing various - even complicated - diffusion models. We describe the new method in detail, and show the applicability on two specific examples: firstly, kinetic rate constants can be derived for the transient interaction of mobile membrane proteins; secondly, residence time and corral size can be extracted for confined diffusion.","lang":"eng"}]},{"month":"03","oa_version":"Published Version","tmp":{"name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","image":"/images/cc_by_nc_sa.png","short":"CC BY-NC-SA (4.0)"},"citation":{"chicago":"Sixt, Michael K, and Carole Parent. “Cells on the Move in Philadelphia.” <i>Molecular Biology and Evolution</i>. Oxford University Press, 2011. <a href=\"https://doi.org/10.1091/mbc.E10-12-0958\">https://doi.org/10.1091/mbc.E10-12-0958</a>.","ama":"Sixt MK, Parent C. Cells on the move in Philadelphia. <i>Molecular Biology and Evolution</i>. 2011;22(6):724. doi:<a href=\"https://doi.org/10.1091/mbc.E10-12-0958\">10.1091/mbc.E10-12-0958</a>","apa":"Sixt, M. K., &#38; Parent, C. (2011). Cells on the move in Philadelphia. <i>Molecular Biology and Evolution</i>. Oxford University Press. <a href=\"https://doi.org/10.1091/mbc.E10-12-0958\">https://doi.org/10.1091/mbc.E10-12-0958</a>","ieee":"M. K. Sixt and C. Parent, “Cells on the move in Philadelphia,” <i>Molecular Biology and Evolution</i>, vol. 22, no. 6. Oxford University Press, p. 724, 2011.","ista":"Sixt MK, Parent C. 2011. Cells on the move in Philadelphia. Molecular Biology and Evolution. 22(6), 724.","short":"M.K. Sixt, C. Parent, Molecular Biology and Evolution 22 (2011) 724.","mla":"Sixt, Michael K., and Carole Parent. “Cells on the Move in Philadelphia.” <i>Molecular Biology and Evolution</i>, vol. 22, no. 6, Oxford University Press, 2011, p. 724, doi:<a href=\"https://doi.org/10.1091/mbc.E10-12-0958\">10.1091/mbc.E10-12-0958</a>."},"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","article_processing_charge":"No","quality_controlled":"1","file_date_updated":"2020-07-14T12:46:11Z","type":"journal_article","author":[{"full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"},{"first_name":"Carole","full_name":"Parent, Carole","last_name":"Parent"}],"publication_status":"published","issue":"6","isi":1,"language":[{"iso":"eng"}],"ddc":["570"],"status":"public","publist_id":"3238","has_accepted_license":"1","date_updated":"2025-09-30T08:58:51Z","date_created":"2018-12-11T12:02:57Z","pubrep_id":"373","file":[{"file_size":105421,"access_level":"open_access","file_id":"5283","checksum":"3467986ab7a64e7694ffd1013b5d9da9","content_type":"application/pdf","date_updated":"2020-07-14T12:46:11Z","date_created":"2018-12-12T10:17:29Z","relation":"main_file","file_name":"IST-2015-373-v1+1_Mol._Biol._Cell-2011-Sixt-724.pdf","creator":"system"}],"_id":"3371","department":[{"_id":"MiSi"}],"oa":1,"article_type":"original","date_published":"2011-03-15T00:00:00Z","intvolume":"        22","scopus_import":"1","title":"Cells on the move in Philadelphia","license":"https://creativecommons.org/licenses/by-nc-sa/4.0/","abstract":[{"lang":"eng","text":"The Minisymposium “Cell Migration and Motility” was attended by approximately 500 visitors and covered a broad range of questions in the field using diverse model systems. Topics comprised actin dynamics, cell polarity, force transduction, signal transduction, bar- rier transmigration, and chemotactic guidance."}],"volume":22,"doi":"10.1091/mbc.E10-12-0958","year":"2011","day":"15","fulldoi":"https://doi.org/10.1091/mbc.E10-12-0958","publisher":"Oxford University Press","external_id":{"isi":["000288368200010"]},"publication":"Molecular Biology and Evolution","page":"724"},{"department":[{"_id":"MiSi"}],"corr_author":"1","_id":"3385","scopus_import":"1","title":"Interstitial locomotion of leukocytes","intvolume":"       138","date_published":"2011-07-01T00:00:00Z","article_type":"review","year":"2011","doi":"10.1016/j.imlet.2011.02.013","fulldoi":"https://doi.org/10.1016/j.imlet.2011.02.013","day":"01","volume":138,"publication":"Immunology Letters","external_id":{"isi":["000292714800011"]},"page":"32 - 34","publisher":"Elsevier","article_processing_charge":"No","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","month":"07","citation":{"chicago":"Sixt, Michael K. “Interstitial Locomotion of Leukocytes.” <i>Immunology Letters</i>. Elsevier, 2011. <a href=\"https://doi.org/10.1016/j.imlet.2011.02.013\">https://doi.org/10.1016/j.imlet.2011.02.013</a>.","ama":"Sixt MK. Interstitial locomotion of leukocytes. <i>Immunology Letters</i>. 2011;138(1):32-34. doi:<a href=\"https://doi.org/10.1016/j.imlet.2011.02.013\">10.1016/j.imlet.2011.02.013</a>","ieee":"M. K. Sixt, “Interstitial locomotion of leukocytes,” <i>Immunology Letters</i>, vol. 138, no. 1. Elsevier, pp. 32–34, 2011.","apa":"Sixt, M. K. (2011). Interstitial locomotion of leukocytes. <i>Immunology Letters</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.imlet.2011.02.013\">https://doi.org/10.1016/j.imlet.2011.02.013</a>","ista":"Sixt MK. 2011. Interstitial locomotion of leukocytes. Immunology Letters. 138(1), 32–34.","short":"M.K. Sixt, Immunology Letters 138 (2011) 32–34.","mla":"Sixt, Michael K. “Interstitial Locomotion of Leukocytes.” <i>Immunology Letters</i>, vol. 138, no. 1, Elsevier, 2011, pp. 32–34, doi:<a href=\"https://doi.org/10.1016/j.imlet.2011.02.013\">10.1016/j.imlet.2011.02.013</a>."},"oa_version":"None","author":[{"full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"}],"type":"journal_article","publication_status":"published","quality_controlled":"1","status":"public","publist_id":"3222","issue":"1","isi":1,"language":[{"iso":"eng"}],"date_created":"2018-12-11T12:03:02Z","date_updated":"2025-09-30T08:47:13Z"},{"isi":1,"issue":"5","language":[{"iso":"eng"}],"publist_id":"3215","status":"public","date_created":"2018-12-11T12:03:04Z","date_updated":"2025-09-30T08:43:55Z","month":"09","oa_version":"None","citation":{"mla":"Soriano, Silvia, et al. “In Vivo Analysis of Uropod Function during Physiological T Cell Trafficking.” <i>Journal of Immunology</i>, vol. 187, no. 5, American Association of Immunologists, 2011, pp. 2356–64, doi:<a href=\"https://doi.org/10.4049/jimmunol.1100935\">10.4049/jimmunol.1100935</a>.","short":"S. Soriano, M. Hons, K. Schumann, V. Kumar, T. Dennier, R. Lyck, M.K. Sixt, J. Stein, Journal of Immunology 187 (2011) 2356–2364.","ista":"Soriano S, Hons M, Schumann K, Kumar V, Dennier T, Lyck R, Sixt MK, Stein J. 2011. In vivo analysis of uropod function during physiological T cell trafficking. Journal of Immunology. 187(5), 2356–2364.","apa":"Soriano, S., Hons, M., Schumann, K., Kumar, V., Dennier, T., Lyck, R., … Stein, J. (2011). In vivo analysis of uropod function during physiological T cell trafficking. <i>Journal of Immunology</i>. American Association of Immunologists. <a href=\"https://doi.org/10.4049/jimmunol.1100935\">https://doi.org/10.4049/jimmunol.1100935</a>","ieee":"S. Soriano <i>et al.</i>, “In vivo analysis of uropod function during physiological T cell trafficking,” <i>Journal of Immunology</i>, vol. 187, no. 5. American Association of Immunologists, pp. 2356–2364, 2011.","ama":"Soriano S, Hons M, Schumann K, et al. In vivo analysis of uropod function during physiological T cell trafficking. <i>Journal of Immunology</i>. 2011;187(5):2356-2364. doi:<a href=\"https://doi.org/10.4049/jimmunol.1100935\">10.4049/jimmunol.1100935</a>","chicago":"Soriano, Silvia, Miroslav Hons, Kathrin Schumann, Varsha Kumar, Timo Dennier, Ruth Lyck, Michael K Sixt, and Jens Stein. “In Vivo Analysis of Uropod Function during Physiological T Cell Trafficking.” <i>Journal of Immunology</i>. American Association of Immunologists, 2011. <a href=\"https://doi.org/10.4049/jimmunol.1100935\">https://doi.org/10.4049/jimmunol.1100935</a>."},"user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","article_processing_charge":"No","quality_controlled":"1","type":"journal_article","author":[{"last_name":"Soriano","full_name":"Soriano, Silvia","first_name":"Silvia"},{"full_name":"Hons, Miroslav","first_name":"Miroslav","last_name":"Hons","orcid":"0000-0002-6625-3348"},{"full_name":"Schumann, Kathrin","first_name":"Kathrin","last_name":"Schumann"},{"full_name":"Kumar, Varsha","first_name":"Varsha","last_name":"Kumar"},{"last_name":"Dennier","first_name":"Timo","full_name":"Dennier, Timo"},{"last_name":"Lyck","first_name":"Ruth","full_name":"Lyck, Ruth"},{"full_name":"Sixt, Michael K","first_name":"Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179"},{"last_name":"Stein","full_name":"Stein, Jens","first_name":"Jens"}],"publication_status":"published","abstract":[{"text":"Migrating lymphocytes acquire a polarized phenotype with a leading and a trailing edge, or uropod. Although in vitro experiments in cell lines or activated primary cell cultures have established that Rho-p160 coiled-coil kinase (ROCK)-myosin II-mediated uropod contractility is required for integrin de-adhesion on two-dimensional surfaces and nuclear propulsion through narrow pores in three-dimensional matrices, less is known about the role of these two events during the recirculation of primary, nonactivated lymphocytes. Using pharmacological antagonists of ROCK and myosin II, we report that inhibition of uropod contractility blocked integrin-independent mouse T cell migration through narrow, but not large, pores in vitro. T cell crawling on chemokine-coated endothelial cells under shear was severely impaired by ROCK inhibition, whereas transendothelial migration was only reduced through endothelial cells with high, but not low, barrier properties. Using three-dimensional thick-tissue imaging and dynamic two-photon microscopy of T cell motility in lymphoid tissue, we demonstrated a significant role for uropod contractility in intraluminal crawling and transendothelial migration through lymph node, but not bone marrow, endothelial cells. Finally, we demonstrated that ICAM-1, but not anatomical constraints or integrin-independent interactions, reduced parenchymal motility of inhibitor-treated T cells within the dense lymphoid microenvironment, thus assigning context-dependent roles for uropod contraction during lymphocyte recirculation.","lang":"eng"}],"volume":187,"year":"2011","doi":"10.4049/jimmunol.1100935","day":"01","fulldoi":"https://doi.org/10.4049/jimmunol.1100935","publisher":"American Association of Immunologists","page":"2356 - 2364","external_id":{"isi":["000294059500040"]},"publication":"Journal of Immunology","_id":"3392","department":[{"_id":"MiSi"}],"publication_identifier":{"eissn":["1550-6606"],"issn":["0022-1767"]},"article_type":"original","date_published":"2011-09-01T00:00:00Z","intvolume":"       187","title":"In vivo analysis of uropod function during physiological T cell trafficking","scopus_import":"1"},{"intvolume":"       769","title":"In vitro analysis of chemotactic leukocyte migration in 3D environments","scopus_import":"1","article_type":"original","date_published":"2011-05-17T00:00:00Z","corr_author":"1","oa":1,"department":[{"_id":"MiSi"}],"_id":"3505","main_file_link":[{"url":"https://pure.mpg.de/pubman/item/item_3219628_1/component/file_3219630/Sixt%20et%20al..pdf","open_access":"1"}],"publisher":"Springer","page":"149 - 165","publication":"Cell Migration","day":"17","fulldoi":"https://doi.org/10.1007/978-1-61779-207-6_11","year":"2011","doi":"10.1007/978-1-61779-207-6_11","volume":769,"abstract":[{"lang":"eng","text":"Cell migration on two-dimensional (2D) substrates follows entirely different rules than cell migration in three-dimensional (3D) environments. This is especially relevant for leukocytes that are able to migrate in the absence of adhesion receptors within the confined geometry of artificial 3D extracellular matrix scaffolds and within the interstitial space in vivo. Here, we describe in detail a simple and economical protocol to visualize dendritic cell migration in 3D collagen scaffolds along chemotactic gradients. This method can be adapted to other cell types and may serve as a physiologically relevant paradigm for the directed locomotion of most amoeboid cells."}],"publication_status":"published","alternative_title":["Methods in Molecular Biology"],"type":"journal_article","author":[{"last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","first_name":"Michael K"},{"full_name":"Lämmermann, Tim","first_name":"Tim","last_name":"Lämmermann"}],"quality_controlled":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","citation":{"apa":"Sixt, M. K., &#38; Lämmermann, T. (2011). In vitro analysis of chemotactic leukocyte migration in 3D environments. <i>Cell Migration</i>. Springer. <a href=\"https://doi.org/10.1007/978-1-61779-207-6_11\">https://doi.org/10.1007/978-1-61779-207-6_11</a>","ieee":"M. K. Sixt and T. Lämmermann, “In vitro analysis of chemotactic leukocyte migration in 3D environments,” <i>Cell Migration</i>, vol. 769. Springer, pp. 149–165, 2011.","ama":"Sixt MK, Lämmermann T. In vitro analysis of chemotactic leukocyte migration in 3D environments. <i>Cell Migration</i>. 2011;769:149-165. doi:<a href=\"https://doi.org/10.1007/978-1-61779-207-6_11\">10.1007/978-1-61779-207-6_11</a>","chicago":"Sixt, Michael K, and Tim Lämmermann. “In Vitro Analysis of Chemotactic Leukocyte Migration in 3D Environments.” <i>Cell Migration</i>. Springer, 2011. <a href=\"https://doi.org/10.1007/978-1-61779-207-6_11\">https://doi.org/10.1007/978-1-61779-207-6_11</a>.","mla":"Sixt, Michael K., and Tim Lämmermann. “In Vitro Analysis of Chemotactic Leukocyte Migration in 3D Environments.” <i>Cell Migration</i>, vol. 769, Springer, 2011, pp. 149–65, doi:<a href=\"https://doi.org/10.1007/978-1-61779-207-6_11\">10.1007/978-1-61779-207-6_11</a>.","short":"M.K. Sixt, T. Lämmermann, Cell Migration 769 (2011) 149–165.","ista":"Sixt MK, Lämmermann T. 2011. In vitro analysis of chemotactic leukocyte migration in 3D environments. Cell Migration. 769, 149–165."},"oa_version":"Published Version","month":"05","date_created":"2018-12-11T12:03:41Z","date_updated":"2026-06-18T18:46:10Z","status":"public","publist_id":"2882","ddc":["570"],"language":[{"iso":"eng"}]}]