Urlaub, Henning

[["dc.bibliographiccitation.journal","Haematologica"],["dc.bibliographiccitation.volume","100"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Beck, J."],["dc.contributor.author","Pan, K.-T."],["dc.contributor.author","Döbele, Carmen"],["dc.contributor.author","Wachter, Astrid"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Beißbarth, Tim"],["dc.contributor.author","Schuetz, Eckehardt"],["dc.contributor.author","Tomska, Katarzyna"],["dc.contributor.author","Sellner, L."],["dc.contributor.author","Zenz, Thorsten"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Urlaub, Henning"],["dc.date.accessioned","2018-11-07T09:56:10Z"],["dc.date.available","2018-11-07T09:56:10Z"],["dc.date.issued","2015"],["dc.format.extent","178"],["dc.identifier.isi","000361204901386"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36907"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ferrata Storti Foundation"],["dc.publisher.place","Pavia"],["dc.relation.eventlocation","Vienna, AUSTRIA"],["dc.relation.issn","0390-6078"],["dc.title","THE B CELL RECEPTOR SIGNALING OUTPUT IN BURKITT'S LYMPHOMA IS GENOTYPE-SPECIFIC AND IMPACTS SENSITIVITY TOWARDS BCR SIGNALING INHIBITORS"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Henric-Petri, Hannah"],["dc.contributor.author","Lenz, Christof"],["dc.contributor.author","Emmert, Alexander"],["dc.contributor.author","Bremmer, Felix"],["dc.contributor.author","Strecker, Jasmin"],["dc.contributor.author","Holland, Rainer"],["dc.contributor.author","Hinterthaner, Marc"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Wagner, Sebastian"],["dc.contributor.author","Kueffer, Stefan"],["dc.contributor.author","Sebastian, Martin"],["dc.contributor.author","Bergmann, Lothar"],["dc.contributor.author","Danner, Bernd"],["dc.contributor.author","Schoendube, Friedrich Albert"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T09:33:49Z"],["dc.date.available","2018-11-07T09:33:49Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1158/1538-7445.AM2014-2487"],["dc.identifier.isi","000349906903219"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32050"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","105th Annual Meeting of the American-Association-for-Cancer-Research (AACR)"],["dc.relation.eventlocation","San Diego, CA"],["dc.relation.issn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","Comprehensive quantitative proteomic profiling of lung cancers reveals novel biomarkers and potential drug targets"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5354"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","The journal of immunology"],["dc.bibliographiccitation.lastpage","5358"],["dc.bibliographiccitation.volume","191"],["dc.contributor.author","Engelke, Michael"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Dittmann, Kai"],["dc.contributor.author","Hsiao, He-Hsuan"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Wienands, Jürgen"],["dc.date.accessioned","2017-09-07T11:47:02Z"],["dc.date.available","2017-09-07T11:47:02Z"],["dc.date.issued","2013"],["dc.description.abstract","Ag-mediated B cell stimulation relies on phospholipase C gamma 2 (PLC gamma 2) for Ca2+ mobilization. Enzymatic activity of PLC gamma 2 is triggered upon Src homology 2 domain-mediated binding to the tyrosine-phosphorylated adaptor SLP65. However, SLP65 phosphorylation outlasts the elevation of cytosolic Ca2+ concentration suggesting additional levels of PLC gamma 2 regulation. We show in this article that the functionality of the PLC gamma 2/SLP65 complex is controlled by the weakly characterized C2 domain of PLC gamma 2. Usually C2 domains bind membrane lipids, but that of PLC gamma 2 docks in a Ca2+-regulated manner to a distinct phosphotyrosine of SLP65. Hence, early Ca2+ fluxing provides feed-forward signal amplification by promoting anchoring of the PLC gamma 2 C2 domain to phospho-SLP65. As the cellular Ca2+ resources become exhausted, the concomitant decline of Ca2+ dampens the C2-phosphotyrosine interaction so that PLC gamma 2 activation terminates despite sustained SLP65 phosphorylation."],["dc.identifier.doi","10.4049/jimmunol.1301326"],["dc.identifier.gro","3142245"],["dc.identifier.isi","000327180600005"],["dc.identifier.pmid","24166973"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6143"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Deutsche Forschungsgemeinschaft [SFB 860, B5]"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Amer Assoc Immunologists"],["dc.relation.eissn","1550-6606"],["dc.relation.issn","0022-1767"],["dc.title","Cutting Edge: Feed-Forward Activation of Phospholipase C gamma 2 via C2 Domain-Mediated Binding to SLP65"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","69"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","78"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Goellner, Stefanie"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Agrawal-Singh, Shuchi"],["dc.contributor.author","Schenk, Tino"],["dc.contributor.author","Klein, Hans-Ulrich"],["dc.contributor.author","Rohde, Christian"],["dc.contributor.author","Pabst, Caroline"],["dc.contributor.author","Sauer, Tim"],["dc.contributor.author","Lerdrup, Mads"],["dc.contributor.author","Tavor, Sigal"],["dc.contributor.author","Stoelzel, Friedrich"],["dc.contributor.author","Herold, Sylvia"],["dc.contributor.author","Ehninger, Gerhard"],["dc.contributor.author","Koehler, Gabriele"],["dc.contributor.author","Pan, Kuan-Ting"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Dugas, Martin"],["dc.contributor.author","Spiekermann, Karsten"],["dc.contributor.author","Vick, Binje"],["dc.contributor.author","Jeremias, Irmela"],["dc.contributor.author","Berdel, Wolfgang E."],["dc.contributor.author","Hansen, Klaus"],["dc.contributor.author","Zelent, Arthur"],["dc.contributor.author","Wickenhauser, Claudia"],["dc.contributor.author","Mueller, Lutz P."],["dc.contributor.author","Thiede, Christian"],["dc.contributor.author","Mueller-Tidow, Carsten"],["dc.date.accessioned","2018-11-07T10:29:28Z"],["dc.date.available","2018-11-07T10:29:28Z"],["dc.date.issued","2017"],["dc.description.abstract","In acute myeloid leukemia (AML), therapy resistance frequently occurs, leading to high mortality among patients. However, the mechanisms that render leukemic cells drug resistant remain largely undefined. Here, we identified loss of the histone methyltransferase EZH2 and subsequent reduction of histone H3K27 trimethylation as a novel pathway of acquired resistance to tyrosine kinase inhibitors (TKIs) and cytotoxic drugs in AML. Low EZH2 protein levels correlated with poor prognosis in AML patients. Suppression of EZH2 protein expression induced chemoresistance of AML cell lines and primary cells in vitro and in vivo. Low EZH2 levels resulted in derepression of HOX genes, and knockdown of HOXB7 and HOXA9 in the resistant cells was sufficient to improve sensitivity to TKIs and cytotoxic drugs. The endogenous loss of EZH2 expression in resistant cells and primary blasts from a subset of relapsed AML patients resulted from enhanced CDK1-dependent phosphorylation of EZH2 at Thr487. This interaction was stabilized by heat shock protein 90 (HSP9O) and followed by proteasomal degradation of EZH2 in drug-resistant cells. Accordingly, inhibitors of HSP9O, CDK1 and the proteasome prevented EZH2 degradation, decreased HOX gene expression and restored drug sensitivity. Finally, patients with reduced EZH2 levels at progression to standard therapy responded to the combination of bortezomib and cytarabine, concomitant with the re-establishment of EZH2 expression and blast clearance. These data suggest restoration of EZH2 protein as a viable approach to overcome treatment resistance in this AML patient population."],["dc.identifier.doi","10.1038/nm.4247"],["dc.identifier.isi","000391646800015"],["dc.identifier.pmid","27941792"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43651"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1546-170X"],["dc.relation.issn","1078-8956"],["dc.title","Loss of the histone methyltransferase EZH2 induces resistance to multiple drugs in acute myeloid leukemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.volume","126"],["dc.contributor.author","Doebele, Carmen"],["dc.contributor.author","Kovar, Johannes"],["dc.contributor.author","Yepes, Diego"],["dc.contributor.author","Muench, Silvia"],["dc.contributor.author","Schnuetgen, Frank"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Koehler, Anne"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T09:47:45Z"],["dc.date.available","2018-11-07T09:47:45Z"],["dc.date.issued","2015"],["dc.identifier.isi","000368020101291"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35167"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.publisher.place","Washington"],["dc.relation.conference","57th Annual Meeting of the American-Society-of-Hematology"],["dc.relation.eventlocation","Orlando, FL"],["dc.relation.issn","1528-0020"],["dc.relation.issn","0006-4971"],["dc.title","Phosphoproteomic Profiling of the Signaling Output of FLT3-ITD and Its AC220-Resistant Mutants Reveals Profound Signaling Differences and Differential Responsiveness to Inhibition of Downstream Kinases"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Oncology Research and Treatment"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Walter, Roland"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Pan, K.-T"],["dc.contributor.author","Doebele, Carmen"],["dc.contributor.author","Yepes, Diego"],["dc.contributor.author","Sellner, L."],["dc.contributor.author","Tomska, Katarzyna"],["dc.contributor.author","Bohnenberger, H."],["dc.contributor.author","Zenz, Thorsten"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2018-11-07T10:07:37Z"],["dc.date.available","2018-11-07T10:07:37Z"],["dc.date.issued","2016"],["dc.format.extent","219"],["dc.identifier.isi","000385691300540"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39316"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Karger"],["dc.publisher.place","Basel"],["dc.relation.issn","2296-5262"],["dc.relation.issn","2296-5270"],["dc.title","Elucidation of tonic and activated B cell receptor signaling in Burkitt's lymphoma reveals insights into non-oncogene addiction"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3889"],["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.lastpage","3899"],["dc.bibliographiccitation.volume","121"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Oellerich, Mark F."],["dc.contributor.author","Engelke, Michael"],["dc.contributor.author","Muench, Silvia"],["dc.contributor.author","Mohr, Sebastian"],["dc.contributor.author","Nimz, Marika"],["dc.contributor.author","Hsiao, He-Hsuan"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Zhang, J."],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Berg, Tobias"],["dc.contributor.author","Rieger, Michael A."],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Bug, Gesine"],["dc.contributor.author","Brandts, Christian"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Serve, Hubert"],["dc.date.accessioned","2018-11-07T09:24:43Z"],["dc.date.available","2018-11-07T09:24:43Z"],["dc.date.issued","2013"],["dc.description.abstract","Spleen tyrosine kinase (Syk) induces cell survival and proliferation in a high proportion of acute myeloid leukemia (AML) blasts, but the underlying molecular events of Syk signaling have not been investigated. Proteomic techniques have allowed us to identify the multiprotein complex that is nucleated by constitutively active Syk in AML cells. This complex differs from the B-lymphoid Syk interactome with respect to several proteins, especially the integrin receptor Mac-1, the Fc-gamma receptor I (Fc gamma RI), and the transcription factors STAT3 and STAT5. We show in several AML cell line models that tonic signals derived from the Fc-gamma chain lead to Syk-dependent activation of STAT3 and STAT5, which in turn induces cell survival and proliferation. Moreover, stimulation of Mac-1 or Fc gamma RI intensifies the constitutive Syk-mediated STAT3/5 activation in AML cells, a scenario likely to take place in the bone marrow niche. In accordance with these findings, we observed that beta(2) integrins, including Mac-1, trigger proliferation of AML cells in an AML cell/stroma coculture model. Taken together, we identified an oncogenic integrin/Syk/STAT3/5 signaling axis that might serve as a therapeutic target of AML in the future."],["dc.identifier.doi","10.1182/blood-2012-09-457887"],["dc.identifier.isi","000321870900019"],["dc.identifier.pmid","23509157"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29892"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.relation.issn","0006-4971"],["dc.title","beta(2) integrin-derived signals induce cell survival and proliferation of AML blasts by activating a Syk/STAT signaling axis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Mohr, Sebastian"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Dubey, Anjali"],["dc.contributor.author","Muench, Silvia"],["dc.contributor.author","Wicht, Johannes"],["dc.contributor.author","Oellerich, Mark F."],["dc.contributor.author","Perske, Christina"],["dc.contributor.author","Bug, Gesine"],["dc.contributor.author","Stroebel, Philipp"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Serve, Hubert"],["dc.date.accessioned","2018-11-07T09:33:50Z"],["dc.date.available","2018-11-07T09:33:50Z"],["dc.date.issued","2014"],["dc.identifier.doi","10.1158/1538-7445.AM2014-4203"],["dc.identifier.isi","000349910202180"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32054"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","105th Annual Meeting of the American-Association-for-Cancer-Research (AACR)"],["dc.relation.eventlocation","San Diego, CA"],["dc.relation.issn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","A transducer module consisting of Toll-like receptor 9 and Bruton's tyrosine kinase triggers acute myeloid leukemia blast proliferation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","26318"],["dc.bibliographiccitation.issue","42"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences"],["dc.bibliographiccitation.lastpage","26327"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Fish, Kamonwan"],["dc.contributor.author","Comoglio, Federico"],["dc.contributor.author","Shaffer, Arthur L."],["dc.contributor.author","Ji, Yanlong"],["dc.contributor.author","Pan, Kuan-Ting"],["dc.contributor.author","Scheich, Sebastian"],["dc.contributor.author","Oellerich, Angelika"],["dc.contributor.author","Doebele, Carmen"],["dc.contributor.author","Ikeda, Masato"],["dc.contributor.author","Schaller, Samantha J."],["dc.contributor.author","Nguyen, Hang"],["dc.contributor.author","Muppidi, Jagan"],["dc.contributor.author","Wright, George W."],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Serve, Hubert"],["dc.contributor.author","Staudt, Louis M."],["dc.contributor.author","Longnecker, Richard"],["dc.contributor.author","Oellerich, Thomas"],["dc.date.accessioned","2021-04-14T08:31:41Z"],["dc.date.available","2021-04-14T08:31:41Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1073/pnas.2007946117"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83683"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1091-6490"],["dc.relation.issn","0027-8424"],["dc.title","Rewiring of B cell receptor signaling by Epstein–Barr virus LMP2A"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Blood"],["dc.bibliographiccitation.volume","124"],["dc.contributor.author","Oellerich, Thomas"],["dc.contributor.author","Mohr, Sebastian"],["dc.contributor.author","Beck, Julia"],["dc.contributor.author","Bohnenberger, Hanibal"],["dc.contributor.author","Doebele, Carmen"],["dc.contributor.author","Corso, Jasmin"],["dc.contributor.author","Bug, Gesine"],["dc.contributor.author","Schuetz, Ekkehard"],["dc.contributor.author","Urlaub, Henning"],["dc.contributor.author","Serve, Hubert"],["dc.date.accessioned","2018-11-07T09:31:26Z"],["dc.date.available","2018-11-07T09:31:26Z"],["dc.date.issued","2014"],["dc.identifier.isi","000349233803024"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31533"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Hematology"],["dc.publisher.place","Washington"],["dc.relation.conference","56th Annual Meeting of the American-Society-of-Hematology"],["dc.relation.eventlocation","San Francisco, CA"],["dc.relation.issn","1528-0020"],["dc.relation.issn","0006-4971"],["dc.title","Syk and Btk Transduce Survival and Proliferation-Inducing Signals By Activating Distinct Signaling Pathways and Transcriptional Programs in AML Cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]