[{"volume":18,"related_material":{"record":[{"relation":"dissertation_contains","id":"323","status":"public"}]},"ec_funded":1,"license":"https://creativecommons.org/licenses/by-nc-sa/4.0/","file":[{"date_created":"2020-05-14T16:33:46Z","file_name":"2018_NatureCell_Leithner.pdf","creator":"dernst","date_updated":"2020-07-14T12:44:43Z","file_size":4433280,"checksum":"e1411cb7c99a2d9089c178a6abef25e7","file_id":"7844","access_level":"open_access","relation":"main_file","content_type":"application/pdf"}],"language":[{"iso":"eng"}],"publication_status":"published","month":"10","intvolume":" 18","scopus_import":1,"oa_version":"Submitted Version","abstract":[{"text":"Most migrating cells extrude their front by the force of actin polymerization. Polymerization requires an initial nucleation step, which is mediated by factors establishing either parallel filaments in the case of filopodia or branched filaments that form the branched lamellipodial network. Branches are considered essential for regular cell motility and are initiated by the Arp2/3 complex, which in turn is activated by nucleation-promoting factors of the WASP and WAVE families. Here we employed rapid amoeboid crawling leukocytes and found that deletion of the WAVE complex eliminated actin branching and thus lamellipodia formation. The cells were left with parallel filaments at the leading edge, which translated, depending on the differentiation status of the cell, into a unipolar pointed cell shape or cells with multiple filopodia. Remarkably, unipolar cells migrated with increased speed and enormous directional persistence, while they were unable to turn towards chemotactic gradients. Cells with multiple filopodia retained chemotactic activity but their migration was progressively impaired with increasing geometrical complexity of the extracellular environment. These findings establish that diversified leading edge protrusions serve as explorative structures while they slow down actual locomotion.","lang":"eng"}],"acknowledged_ssus":[{"_id":"SSU"}],"department":[{"_id":"MiSi"},{"_id":"NanoFab"},{"_id":"Bio"}],"file_date_updated":"2020-07-14T12:44:43Z","ddc":["570"],"date_updated":"2024-03-27T23:30:16Z","status":"public","type":"journal_article","article_type":"original","tmp":{"name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","image":"/images/cc_by_nc_sa.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","short":"CC BY-NC-SA (4.0)"},"_id":"1321","date_published":"2016-10-24T00:00:00Z","doi":"10.1038/ncb3426","date_created":"2018-12-11T11:51:21Z","page":"1253 - 1259","day":"24","publication":"Nature Cell Biology","has_accepted_license":"1","year":"2016","publisher":"Nature Publishing Group","quality_controlled":"1","oa":1,"acknowledgement":"This work was supported by the German Research Foundation (DFG) Priority Program SP 1464 to T.E.B.S. and M.S., and European Research Council (ERC GA 281556) and Human Frontiers Program grants to M.S.\r\nService Units of IST Austria for excellent technical support.","title":"Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes","publist_id":"5949","author":[{"first_name":"Alexander F","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","full_name":"Leithner, Alexander F","orcid":"0000-0002-1073-744X","last_name":"Leithner"},{"last_name":"Eichner","full_name":"Eichner, Alexander","first_name":"Alexander","id":"4DFA52AE-F248-11E8-B48F-1D18A9856A87"},{"id":"AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D","first_name":"Jan","last_name":"Müller","full_name":"Müller, Jan"},{"id":"35B76592-F248-11E8-B48F-1D18A9856A87","first_name":"Anne","orcid":"0000-0003-0666-8928","full_name":"Reversat, Anne","last_name":"Reversat"},{"id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","first_name":"Markus","last_name":"Brown","full_name":"Brown, Markus"},{"id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","first_name":"Jan","last_name":"Schwarz","full_name":"Schwarz, Jan"},{"full_name":"Merrin, Jack","orcid":"0000-0001-5145-4609","last_name":"Merrin","id":"4515C308-F248-11E8-B48F-1D18A9856A87","first_name":"Jack"},{"first_name":"David","last_name":"De Gorter","full_name":"De Gorter, David"},{"first_name":"Florian","id":"48AD8942-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4790-8078","full_name":"Schur, Florian","last_name":"Schur"},{"full_name":"Bayerl, Jonathan","last_name":"Bayerl","first_name":"Jonathan"},{"first_name":"Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","last_name":"De Vries","full_name":"De Vries, Ingrid"},{"first_name":"Stefan","id":"355AA5A0-F248-11E8-B48F-1D18A9856A87","full_name":"Wieser, Stefan","orcid":"0000-0002-2670-2217","last_name":"Wieser"},{"id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","first_name":"Robert","last_name":"Hauschild","full_name":"Hauschild, Robert","orcid":"0000-0001-9843-3522"},{"last_name":"Lai","full_name":"Lai, Frank","first_name":"Frank"},{"full_name":"Moser, Markus","last_name":"Moser","first_name":"Markus"},{"first_name":"Dontscho","last_name":"Kerjaschki","full_name":"Kerjaschki, Dontscho"},{"first_name":"Klemens","full_name":"Rottner, Klemens","last_name":"Rottner"},{"last_name":"Small","full_name":"Small, Victor","first_name":"Victor"},{"first_name":"Theresia","last_name":"Stradal","full_name":"Stradal, Theresia"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt"}],"article_processing_charge":"No","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","citation":{"ista":"Leithner AF, Eichner A, Müller J, Reversat A, Brown M, Schwarz J, Merrin J, De Gorter D, Schur FK, Bayerl J, de Vries I, Wieser S, Hauschild R, Lai F, Moser M, Kerjaschki D, Rottner K, Small V, Stradal T, Sixt MK. 2016. Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. 18, 1253–1259.","chicago":"Leithner, Alexander F, Alexander Eichner, Jan Müller, Anne Reversat, Markus Brown, Jan Schwarz, Jack Merrin, et al. “Diversified Actin Protrusions Promote Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/ncb3426.","ama":"Leithner AF, Eichner A, Müller J, et al. Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. 2016;18:1253-1259. doi:10.1038/ncb3426","apa":"Leithner, A. F., Eichner, A., Müller, J., Reversat, A., Brown, M., Schwarz, J., … Sixt, M. K. (2016). Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb3426","ieee":"A. F. Leithner et al., “Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes,” Nature Cell Biology, vol. 18. Nature Publishing Group, pp. 1253–1259, 2016.","short":"A.F. Leithner, A. Eichner, J. Müller, A. Reversat, M. Brown, J. Schwarz, J. Merrin, D. De Gorter, F.K. Schur, J. Bayerl, I. de Vries, S. Wieser, R. Hauschild, F. Lai, M. Moser, D. Kerjaschki, K. Rottner, V. Small, T. Stradal, M.K. Sixt, Nature Cell Biology 18 (2016) 1253–1259.","mla":"Leithner, Alexander F., et al. “Diversified Actin Protrusions Promote Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature Cell Biology, vol. 18, Nature Publishing Group, 2016, pp. 1253–59, doi:10.1038/ncb3426."},"project":[{"call_identifier":"FP7","_id":"25A603A2-B435-11E9-9278-68D0E5697425","grant_number":"281556","name":"Cytoskeletal force generation and force transduction of migrating leukocytes (EU)"}]},{"month":"02","intvolume":" 588","quality_controlled":"1","publisher":"Elsevier","scopus_import":1,"oa_version":"None","abstract":[{"text":"MicroRNAs (miRNAs) are small RNAs that play important regulatory roles in many cellular pathways. MiRNAs associate with members of the Argonaute protein family and bind to partially complementary sequences on mRNAs and induce translational repression or mRNA decay. Using deep sequencing and Northern blotting, we characterized miRNA expression in wild type and miR-155-deficient dendritic cells (DCs) and macrophages. Analysis of different stimuli (LPS, LDL, eLDL, oxLDL) reveals a direct influence of miR-155 on the expression levels of other miRNAs. For example, miR-455 is negatively regulated in miR-155-deficient cells possibly due to inhibition of the transcription factor C/EBPbeta by miR-155. Based on our comprehensive data sets, we propose a model of hierarchical miRNA expression dominated by miR-155 in DCs and macrophages.","lang":"eng"}],"doi":"10.1016/j.febslet.2014.01.009","issue":"4","date_published":"2014-02-14T00:00:00Z","volume":588,"date_created":"2018-12-11T11:56:31Z","page":"632 - 640","day":"14","publication":"FEBS Letters","language":[{"iso":"eng"}],"publication_identifier":{"issn":["00145793"]},"year":"2014","publication_status":"published","status":"public","type":"journal_article","_id":"2242","department":[{"_id":"MiSi"}],"title":"A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation","publist_id":"4714","author":[{"first_name":"Anne","full_name":"Dueck, Anne","last_name":"Dueck"},{"last_name":"Eichner","full_name":"Eichner, Alexander","id":"4DFA52AE-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt"},{"first_name":"Gunter","last_name":"Meister","full_name":"Meister, Gunter"}],"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","citation":{"ista":"Dueck A, Eichner A, Sixt MK, Meister G. 2014. A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation. FEBS Letters. 588(4), 632–640.","chicago":"Dueck, Anne, Alexander Eichner, Michael K Sixt, and Gunter Meister. “A MiR-155-Dependent MicroRNA Hierarchy in Dendritic Cell Maturation and Macrophage Activation.” FEBS Letters. Elsevier, 2014. https://doi.org/10.1016/j.febslet.2014.01.009.","short":"A. Dueck, A. Eichner, M.K. Sixt, G. Meister, FEBS Letters 588 (2014) 632–640.","ieee":"A. Dueck, A. Eichner, M. K. Sixt, and G. Meister, “A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation,” FEBS Letters, vol. 588, no. 4. Elsevier, pp. 632–640, 2014.","ama":"Dueck A, Eichner A, Sixt MK, Meister G. A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation. FEBS Letters. 2014;588(4):632-640. doi:10.1016/j.febslet.2014.01.009","apa":"Dueck, A., Eichner, A., Sixt, M. K., & Meister, G. (2014). A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation. FEBS Letters. Elsevier. https://doi.org/10.1016/j.febslet.2014.01.009","mla":"Dueck, Anne, et al. “A MiR-155-Dependent MicroRNA Hierarchy in Dendritic Cell Maturation and Macrophage Activation.” FEBS Letters, vol. 588, no. 4, Elsevier, 2014, pp. 632–40, doi:10.1016/j.febslet.2014.01.009."},"date_updated":"2021-01-12T06:56:14Z"},{"abstract":[{"text":"MicroRNAs (miRNAs) are small noncoding RNAs that function in literally all cellular processes. miRNAs interact with Argonaute (Ago) proteins and guide them to specific target sites located in the 3′-untranslated region (3′-UTR) of target mRNAs leading to translational repression and deadenylation-induced mRNA degradation. Most miRNAs are processed from hairpin-structured precursors by the consecutive action of the RNase III enzymes Drosha and Dicer. However, processing of miR-451 is Dicer independent and cleavage is mediated by the endonuclease Ago2. Here we have characterized miR-451 sequence and structure requirements for processing as well as sorting of miRNAs into different Ago proteins. Pre-miR-451 appears to be optimized for Ago2 cleavage and changes result in reduced processing. In addition, we show that the mature miR-451 only associates with Ago2 suggesting that mature miRNAs are not exchanged between different members of the Ago protein family. Based on cloning and deep sequencing of endogenous miRNAs associated with Ago1-3, we do not find evidence for miRNA sorting in human cells. However, Ago identity appears to influence the length of some miRNAs, while others remain unaffected.","lang":"eng"}],"oa_version":"Published Version","scopus_import":1,"intvolume":" 40","month":"10","publication_status":"published","language":[{"iso":"eng"}],"file":[{"date_created":"2018-12-12T10:13:12Z","file_name":"IST-2015-383-v1+1_Nucl._Acids_Res.-2012-Dueck-9850-62.pdf","date_updated":"2020-07-14T12:45:55Z","file_size":8126936,"creator":"system","file_id":"4993","checksum":"1bb8d1ff894014b481657a21083c941c","content_type":"application/pdf","access_level":"open_access","relation":"main_file"}],"license":"https://creativecommons.org/licenses/by-nc/4.0/","volume":40,"issue":"19","_id":"2946","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by-nc/4.0/legalcode","image":"/images/cc_by_nc.png","name":"Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)","short":"CC BY-NC (4.0)"},"type":"journal_article","pubrep_id":"383","status":"public","date_updated":"2021-01-12T07:39:57Z","ddc":["570"],"department":[{"_id":"MiSi"}],"file_date_updated":"2020-07-14T12:45:55Z","acknowledgement":"Deutsche Forschungsgemeinschaft (DFG) (SFB 960 and FOR855); European Research Council (ERC grant ‘sRNAs’); European Union (FP7 project ‘ONCOMIRs’); German Bundesministerium für Bildung und Forschung (BMBF, NGFN+, FKZ PIM-01GS0804-5); Bavarian Genome Research Network (BayGene to G.M.); The Netherlands Organization for Scientific Research (NWO, VIDI grant to E.B.). Funding for open access charge: DFG via the open access publishing program. \r\n\r\nWe thank Sigrun Ammon and Corinna Friederich for technical assistance and Sebastian Petri and Daniel Schraivogel for helpful discussions.","oa":1,"quality_controlled":"1","publisher":"Oxford University Press","year":"2012","has_accepted_license":"1","publication":"Nucleic Acids Research","day":"01","page":"9850 - 9862","date_created":"2018-12-11T12:00:29Z","date_published":"2012-10-01T00:00:00Z","doi":"10.1093/nar/gks705","citation":{"ama":"Dueck A, Ziegler C, Eichner A, Berezikov E, Meister G. MicroRNAs associated with the different human Argonaute proteins. Nucleic Acids Research. 2012;40(19):9850-9862. doi:10.1093/nar/gks705","apa":"Dueck, A., Ziegler, C., Eichner, A., Berezikov, E., & Meister, G. (2012). MicroRNAs associated with the different human Argonaute proteins. Nucleic Acids Research. Oxford University Press. https://doi.org/10.1093/nar/gks705","short":"A. Dueck, C. Ziegler, A. Eichner, E. Berezikov, G. Meister, Nucleic Acids Research 40 (2012) 9850–9862.","ieee":"A. Dueck, C. Ziegler, A. Eichner, E. Berezikov, and G. Meister, “MicroRNAs associated with the different human Argonaute proteins,” Nucleic Acids Research, vol. 40, no. 19. Oxford University Press, pp. 9850–9862, 2012.","mla":"Dueck, Anne, et al. “MicroRNAs Associated with the Different Human Argonaute Proteins.” Nucleic Acids Research, vol. 40, no. 19, Oxford University Press, 2012, pp. 9850–62, doi:10.1093/nar/gks705.","ista":"Dueck A, Ziegler C, Eichner A, Berezikov E, Meister G. 2012. MicroRNAs associated with the different human Argonaute proteins. Nucleic Acids Research. 40(19), 9850–9862.","chicago":"Dueck, Anne, Christian Ziegler, Alexander Eichner, Eugène Berezikov, and Gunter Meister. “MicroRNAs Associated with the Different Human Argonaute Proteins.” Nucleic Acids Research. Oxford University Press, 2012. https://doi.org/10.1093/nar/gks705."},"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","publist_id":"3786","author":[{"full_name":"Dueck, Anne","last_name":"Dueck","first_name":"Anne"},{"last_name":"Ziegler","full_name":"Ziegler, Christian","first_name":"Christian"},{"full_name":"Eichner, Alexander","last_name":"Eichner","first_name":"Alexander","id":"4DFA52AE-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Eugène","full_name":"Berezikov, Eugène","last_name":"Berezikov"},{"last_name":"Meister","full_name":"Meister, Gunter","first_name":"Gunter"}],"title":"MicroRNAs associated with the different human Argonaute proteins"},{"date_created":"2018-12-11T11:46:46Z","doi":"10.1126/scisignal.2002617","issue":"198","date_published":"2011-11-08T00:00:00Z","volume":4,"publication":"Science Signaling","language":[{"iso":"eng"}],"day":"08","publication_status":"published","year":"2011","intvolume":" 4","month":"11","publisher":"American Association for the Advancement of Science","quality_controlled":"1","scopus_import":1,"oa_version":"None","abstract":[{"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.","lang":"eng"}],"title":"Setting the clock for recirculating lymphocytes","department":[{"_id":"MiSi"}],"publist_id":"7329","author":[{"id":"4DFA52AE-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander","last_name":"Eichner","full_name":"Eichner, Alexander"},{"last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","citation":{"chicago":"Eichner, Alexander, and Michael K Sixt. “Setting the Clock for Recirculating Lymphocytes.” Science Signaling. American Association for the Advancement of Science, 2011. https://doi.org/10.1126/scisignal.2002617.","ista":"Eichner A, Sixt MK. 2011. Setting the clock for recirculating lymphocytes. Science Signaling. 4(198), pe43.","mla":"Eichner, Alexander, and Michael K. Sixt. “Setting the Clock for Recirculating Lymphocytes.” Science Signaling, vol. 4, no. 198, pe43, American Association for the Advancement of Science, 2011, doi:10.1126/scisignal.2002617.","ieee":"A. Eichner and M. K. Sixt, “Setting the clock for recirculating lymphocytes,” Science Signaling, vol. 4, no. 198. American Association for the Advancement of Science, 2011.","short":"A. Eichner, M.K. Sixt, Science Signaling 4 (2011).","apa":"Eichner, A., & Sixt, M. K. (2011). Setting the clock for recirculating lymphocytes. Science Signaling. American Association for the Advancement of Science. https://doi.org/10.1126/scisignal.2002617","ama":"Eichner A, Sixt MK. Setting the clock for recirculating lymphocytes. Science Signaling. 2011;4(198). doi:10.1126/scisignal.2002617"},"date_updated":"2021-01-12T08:01:02Z","status":"public","type":"journal_article","article_number":"pe43","_id":"491"},{"publist_id":"7301","author":[{"first_name":"Daniel","last_name":"Schraivogel","full_name":"Schraivogel, Daniel"},{"full_name":"Weinmann, Lasse","last_name":"Weinmann","first_name":"Lasse"},{"first_name":"Dagmar","last_name":"Beier","full_name":"Beier, Dagmar"},{"full_name":"Tabatabai, Ghazaleh","last_name":"Tabatabai","first_name":"Ghazaleh"},{"last_name":"Eichner","full_name":"Eichner, Alexander","id":"4DFA52AE-F248-11E8-B48F-1D18A9856A87","first_name":"Alexander"},{"full_name":"Zhu, Jia","last_name":"Zhu","first_name":"Jia"},{"last_name":"Anton","full_name":"Anton, Martina","first_name":"Martina"},{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179"},{"first_name":"Michael","last_name":"Weller","full_name":"Weller, Michael"},{"first_name":"Christoph","last_name":"Beier","full_name":"Beier, Christoph"},{"last_name":"Meister","full_name":"Meister, Gunter","first_name":"Gunter"}],"article_processing_charge":"No","external_id":{"pmid":["21857646"]},"title":"CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells","citation":{"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.” EMBO Journal. Wiley-Blackwell, 2011. https://doi.org/10.1038/emboj.2011.301.","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.","mla":"Schraivogel, Daniel, et al. “CAMTA1 Is a Novel Tumour Suppressor Regulated by MiR-9/9 * in Glioblastoma Stem Cells.” EMBO Journal, vol. 30, no. 20, Wiley-Blackwell, 2011, pp. 4309–22, doi:10.1038/emboj.2011.301.","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. EMBO Journal. Wiley-Blackwell. https://doi.org/10.1038/emboj.2011.301","ama":"Schraivogel D, Weinmann L, Beier D, et al. CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells. EMBO Journal. 2011;30(20):4309-4322. doi:10.1038/emboj.2011.301","ieee":"D. Schraivogel et al., “CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells,” EMBO Journal, vol. 30, no. 20. Wiley-Blackwell, pp. 4309–4322, 2011.","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."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publisher":"Wiley-Blackwell","quality_controlled":"1","oa":1,"page":"4309 - 4322","date_published":"2011-10-19T00:00:00Z","doi":"10.1038/emboj.2011.301","date_created":"2018-12-11T11:46:55Z","year":"2011","day":"19","publication":"EMBO Journal","article_type":"original","type":"journal_article","status":"public","_id":"518","department":[{"_id":"MiSi"}],"date_updated":"2021-01-12T08:01:19Z","scopus_import":1,"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199389/"}],"month":"10","intvolume":" 30","abstract":[{"lang":"eng","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."}],"oa_version":"Submitted Version","pmid":1,"issue":"20","volume":30,"publication_status":"published","language":[{"iso":"eng"}]}]