--- _id: '1321' abstract: - lang: eng 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. acknowledged_ssus: - _id: SSU 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." article_processing_charge: No article_type: original author: - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Alexander full_name: Eichner, Alexander id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87 last_name: Eichner - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: David full_name: De Gorter, David last_name: De Gorter - first_name: Florian full_name: Schur, Florian id: 48AD8942-F248-11E8-B48F-1D18A9856A87 last_name: Schur orcid: 0000-0003-4790-8078 - first_name: Jonathan full_name: Bayerl, Jonathan last_name: Bayerl - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Stefan full_name: Wieser, Stefan id: 355AA5A0-F248-11E8-B48F-1D18A9856A87 last_name: Wieser orcid: 0000-0002-2670-2217 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Frank full_name: Lai, Frank last_name: Lai - first_name: Markus full_name: Moser, Markus last_name: Moser - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner - first_name: Victor full_name: Small, Victor last_name: Small - first_name: Theresia full_name: Stradal, Theresia last_name: Stradal - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: 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 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. 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. 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. 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. 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. date_created: 2018-12-11T11:51:21Z date_published: 2016-10-24T00:00:00Z date_updated: 2024-03-27T23:30:16Z day: '24' ddc: - '570' department: - _id: MiSi - _id: NanoFab - _id: Bio doi: 10.1038/ncb3426 ec_funded: 1 file: - access_level: open_access checksum: e1411cb7c99a2d9089c178a6abef25e7 content_type: application/pdf creator: dernst date_created: 2020-05-14T16:33:46Z date_updated: 2020-07-14T12:44:43Z file_id: '7844' file_name: 2018_NatureCell_Leithner.pdf file_size: 4433280 relation: main_file file_date_updated: 2020-07-14T12:44:43Z has_accepted_license: '1' intvolume: ' 18' language: - iso: eng license: https://creativecommons.org/licenses/by-nc-sa/4.0/ month: '10' oa: 1 oa_version: Submitted Version page: 1253 - 1259 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Nature Cell Biology publication_status: published publisher: Nature Publishing Group publist_id: '5949' quality_controlled: '1' related_material: record: - id: '323' relation: dissertation_contains status: public scopus_import: 1 status: public title: Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 18 year: '2016' ... --- _id: '2242' abstract: - lang: eng 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. author: - first_name: Anne full_name: Dueck, Anne last_name: Dueck - first_name: Alexander full_name: Eichner, Alexander id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87 last_name: Eichner - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Gunter full_name: Meister, Gunter last_name: Meister citation: 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 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. 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. 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. 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. short: A. Dueck, A. Eichner, M.K. Sixt, G. Meister, FEBS Letters 588 (2014) 632–640. date_created: 2018-12-11T11:56:31Z date_published: 2014-02-14T00:00:00Z date_updated: 2021-01-12T06:56:14Z day: '14' department: - _id: MiSi doi: 10.1016/j.febslet.2014.01.009 intvolume: ' 588' issue: '4' language: - iso: eng month: '02' oa_version: None page: 632 - 640 publication: FEBS Letters publication_identifier: issn: - '00145793' publication_status: published publisher: Elsevier publist_id: '4714' quality_controlled: '1' scopus_import: 1 status: public title: A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 588 year: '2014' ... --- _id: '2946' abstract: - lang: eng 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. 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." author: - first_name: Anne full_name: Dueck, Anne last_name: Dueck - first_name: Christian full_name: Ziegler, Christian last_name: Ziegler - first_name: Alexander full_name: Eichner, Alexander id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87 last_name: Eichner - first_name: Eugène full_name: Berezikov, Eugène last_name: Berezikov - first_name: Gunter full_name: Meister, Gunter last_name: Meister 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 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. 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. 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. 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. short: A. Dueck, C. Ziegler, A. Eichner, E. Berezikov, G. Meister, Nucleic Acids Research 40 (2012) 9850–9862. date_created: 2018-12-11T12:00:29Z date_published: 2012-10-01T00:00:00Z date_updated: 2021-01-12T07:39:57Z day: '01' ddc: - '570' department: - _id: MiSi doi: 10.1093/nar/gks705 file: - access_level: open_access checksum: 1bb8d1ff894014b481657a21083c941c content_type: application/pdf creator: system date_created: 2018-12-12T10:13:12Z date_updated: 2020-07-14T12:45:55Z file_id: '4993' file_name: IST-2015-383-v1+1_Nucl._Acids_Res.-2012-Dueck-9850-62.pdf file_size: 8126936 relation: main_file file_date_updated: 2020-07-14T12:45:55Z has_accepted_license: '1' intvolume: ' 40' issue: '19' language: - iso: eng license: https://creativecommons.org/licenses/by-nc/4.0/ month: '10' oa: 1 oa_version: Published Version page: 9850 - 9862 publication: Nucleic Acids Research publication_status: published publisher: Oxford University Press publist_id: '3786' pubrep_id: '383' quality_controlled: '1' scopus_import: 1 status: public title: MicroRNAs associated with the different human Argonaute proteins tmp: image: /images/cc_by_nc.png legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) short: CC BY-NC (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 40 year: '2012' ... --- _id: '491' 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. article_number: pe43 author: - first_name: Alexander full_name: Eichner, Alexander id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87 last_name: Eichner - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Eichner A, Sixt MK. Setting the clock for recirculating lymphocytes. Science Signaling. 2011;4(198). doi:10.1126/scisignal.2002617 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 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. 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. 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. short: A. Eichner, M.K. Sixt, Science Signaling 4 (2011). date_created: 2018-12-11T11:46:46Z date_published: 2011-11-08T00:00:00Z date_updated: 2021-01-12T08:01:02Z day: '08' department: - _id: MiSi doi: 10.1126/scisignal.2002617 intvolume: ' 4' issue: '198' language: - iso: eng month: '11' oa_version: None publication: Science Signaling publication_status: published publisher: American Association for the Advancement of Science publist_id: '7329' quality_controlled: '1' scopus_import: 1 status: public title: Setting the clock for recirculating lymphocytes type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 4 year: '2011' ... --- _id: '518' 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. article_processing_charge: No article_type: original author: - first_name: Daniel full_name: Schraivogel, Daniel last_name: Schraivogel - first_name: Lasse full_name: Weinmann, Lasse last_name: Weinmann - first_name: Dagmar full_name: Beier, Dagmar last_name: Beier - first_name: Ghazaleh full_name: Tabatabai, Ghazaleh last_name: Tabatabai - first_name: Alexander full_name: Eichner, Alexander id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87 last_name: Eichner - first_name: Jia full_name: Zhu, Jia last_name: Zhu - first_name: Martina full_name: Anton, Martina last_name: Anton - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - 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 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. EMBO Journal. 2011;30(20):4309-4322. 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 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. 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. 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. 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. date_created: 2018-12-11T11:46:55Z date_published: 2011-10-19T00:00:00Z date_updated: 2021-01-12T08:01:19Z day: '19' department: - _id: MiSi doi: 10.1038/emboj.2011.301 external_id: pmid: - '21857646' intvolume: ' 30' issue: '20' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199389/ month: '10' oa: 1 oa_version: Submitted Version page: 4309 - 4322 pmid: 1 publication: EMBO Journal publication_status: published publisher: Wiley-Blackwell publist_id: '7301' quality_controlled: '1' scopus_import: 1 status: public title: CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 30 year: '2011' ...