Kessel, Michael

[["dc.bibliographiccitation.artnumber","16"],["dc.bibliographiccitation.journal","BMC Biochemistry"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Pitulescu, Mara E."],["dc.contributor.author","Teichmann, Martin"],["dc.contributor.author","Luo, Lingfei"],["dc.contributor.author","Kessel, Michael"],["dc.date.accessioned","2019-07-09T11:52:37Z"],["dc.date.available","2019-07-09T11:52:37Z"],["dc.date.issued","2009"],["dc.description.abstract","Background The re-replication inhibitor Geminin binds to several transcription factors including homeodomain proteins, and to members of the polycomb and the SWI/SNF complexes. Results Here we describe the TATA-binding protein-like factor-interacting protein (TIPT) isoform 2, as a strong binding partner of Geminin. TIPT2 is widely expressed in mouse embryonic and adult tissues, residing both in cyto- and nucleoplasma, and enriched in the nucleolus. Like Geminin, also TIPT2 interacts with several polycomb factors, with the general transcription factor TBP (TATA box binding protein), and with the related protein TBPL1 (TRF2). TIPT2 synergizes with geminin and TBP in the activation of TATA box-containing promoters, and with TBPL1 and geminin in the activation of the TATA-less NF1 promoter. Geminin and TIPT2 were detected in the chromatin near TBP/TBPL1 binding sites. Conclusion Together, our study introduces a novel transcriptional regulator and its function in cooperation with chromatin associated factors and the basal transcription machinery."],["dc.identifier.doi","10.1186/1471-2091-10-16"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60240"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.subject.ddc","610"],["dc.subject.ddc","573"],["dc.subject.ddc","573.8"],["dc.subject.ddc","612"],["dc.subject.ddc","612.8"],["dc.title","TIPT2 and geminin interact with basal transcription factors to synergize in transcriptional regulation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1842"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.lastpage","1854"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Narayanan, Ramanathan"],["dc.contributor.author","Pirouz, Mehdi"],["dc.contributor.author","Kerimoglu, Cemil"],["dc.contributor.author","Pham, Linh"],["dc.contributor.author","Wagener, Robin J."],["dc.contributor.author","Kiszka, Kamila A."],["dc.contributor.author","Rosenbusch, Joachim"],["dc.contributor.author","Seong, Rho H."],["dc.contributor.author","Kessel, Michael"],["dc.contributor.author","Fischer, Andre"],["dc.contributor.author","Stoykova, Anastassia"],["dc.contributor.author","Staiger, Jochen F."],["dc.contributor.author","Tuoc, Tran"],["dc.date.accessioned","2017-09-07T11:54:50Z"],["dc.date.available","2017-09-07T11:54:50Z"],["dc.date.issued","2015"],["dc.description.abstract","BAF (Brg/Brm-associated factors) complexes play important roles in development and are linked to chromatin plasticity at selected genomic loci. Nevertheless, a full understanding of their role in development and chromatin remodeling has been hindered by the absence of mutants completely lacking BAF complexes. Here, we report that the loss of BAF155/BAF170 in double-conditional knockout (dcKO) mice eliminates all known BAF subunits, resulting in an overall reduction in active chromatin marks (H3K9Ac), a global increase in repressive marks (H3K27me2/3), and downregulation of gene expression. We demonstrate that BAF complexes interact with H3K27 demethylases (JMJD3 and UTX) and potentiate their activity. Importantly, BAF complexes are indispensable for forebrain development, including proliferation, differentiation, and cell survival of neural progenitor cells. Our findings reveal a molecular mechanism mediated by BAF complexes that controls the global transcriptional program and chromatin state in development."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.1016/j.celrep.2015.10.046"],["dc.identifier.gro","3141775"],["dc.identifier.isi","000366047000012"],["dc.identifier.pmid","26655900"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12641"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/935"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Cell Press"],["dc.relation.issn","2211-1247"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Loss of BAF (mSWI/SNF) Complexes Causes Global Transcriptional and Chromatin State Changes in Forebrain Development"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e001770"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of the American Heart Association"],["dc.bibliographiccitation.lastpage","21"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Gogiraju, Rajinikanth"],["dc.contributor.author","Xu, Xingbo"],["dc.contributor.author","Bochenek, Magdalena L."],["dc.contributor.author","Steinbrecher, Julia H."],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Wenzel, Philip"],["dc.contributor.author","Kessel, Michael"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Dobbelstein, Matthias"],["dc.contributor.author","Schäfer, Katrin"],["dc.date.accessioned","2018-05-07T11:17:45Z"],["dc.date.available","2018-05-07T11:17:45Z"],["dc.date.issued","2015"],["dc.description.abstract","Cardiac dysfunction developing in response to chronic pressure overload is associated with apoptotic cell death and myocardial vessel rarefaction. We examined whether deletion of tumor suppressor p53 in endothelial cells may prevent the transition from cardiac hypertrophy to heart failure."],["dc.identifier.doi","10.1161/JAHA.115.001770"],["dc.identifier.gro","3142397"],["dc.identifier.pmid","25713289"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12727"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/14615"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/81"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation","SFB 1002 | C06: Mechanismen und Regulation der koronaren Gefäßneubildung"],["dc.relation.eissn","2047-9980"],["dc.relation.issn","2047-9980"],["dc.relation.issn","2047-9980"],["dc.relation.workinggroup","RG Lehnart (Cellular Biophysics and Translational Cardiology Section)"],["dc.relation.workinggroup","RG Schäfer (Translationale Vaskuläre Biologie)"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Endothelial p53 deletion improves angiogenesis and prevents cardiac fibrosis and heart failure induced by pressure overload in mice"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]