Baumgart, Simon J.

[["dc.bibliographiccitation.firstpage","1609"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","EMBO Reports"],["dc.bibliographiccitation.lastpage","1623"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Mansour, Wael Yassin"],["dc.contributor.author","Raul, Sanjay Kumar"],["dc.contributor.author","Baumgart, Simon J."],["dc.contributor.author","Mund, Andreas"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Sirma, Hueseyin"],["dc.contributor.author","Simon, Ronald"],["dc.contributor.author","Will, Hans"],["dc.contributor.author","Dobbelstein, Matthias"],["dc.contributor.author","Dikomey, Ekkehard"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2018-11-07T10:06:25Z"],["dc.date.available","2018-11-07T10:06:25Z"],["dc.date.issued","2016"],["dc.description.abstract","The CHD1 gene, encoding the chromo-domain helicase DNA-binding protein-1, is one of the most frequently deleted genes in prostate cancer. Here, we examined the role of CHD1 in DNA double-strand break (DSB) repair in prostate cancer cells. We show that CHD1 is required for the recruitment of CtIP to chromatin and subsequent end resection during DNA DSB repair. Our data support a role for CHD1 in opening the chromatin around the DSB to facilitate the recruitment of homologous recombination (HR) proteins. Consequently, depletion of CHD1 specifically affects HR-mediated DNA repair but not non-homologous end joining. Together, we provide evidence for a previously unknown role of CHD1 in DNA DSB repair via HR and show that CHD1 depletion sensitizes cells to PARP inhibitors, which has potential therapeutic relevance. Our findings suggest that CHD1 deletion, like BRCA1/2 mutation in ovarian cancer, may serve as a marker for prostate cancer patient stratification and the utilization of targeted therapies such as PARP inhibitors, which specifically target tumors with HR defects."],["dc.identifier.doi","10.15252/embr.201642352"],["dc.identifier.isi","000387148700012"],["dc.identifier.pmid","27596623"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39090"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1469-3178"],["dc.relation.issn","1469-221X"],["dc.title","Loss of CHD1 causes DNA repair defects and enhances prostate cancer therapeutic responsiveness"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Mishra, Vivek Kumar"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Subramaniam, Malayannan"],["dc.contributor.author","Baumgart, Simon J."],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Spelsberg, Thomas C."],["dc.contributor.author","Hawse, John R."],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2018-11-07T10:19:22Z"],["dc.date.available","2018-11-07T10:19:22Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1158/1538-7445.CHROMEPI15-A03"],["dc.identifier.isi","000368930800003"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41642"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Assoc Cancer Research"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","American-Association-for-Cancer-Research (AACR) Special Conference on Chromatin and Epigenetics in Cancer"],["dc.relation.eventlocation","Atlanta, GA"],["dc.relation.issn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","Kruppel-like Transcription Factor-10 (KLF10) suppresses the TGF beta-induced epithelial-to-mesenchymal transition"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","7722"],["dc.bibliographiccitation.issue","13"],["dc.bibliographiccitation.journal","Nucleic Acids Research"],["dc.bibliographiccitation.lastpage","7735"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Baumgart, Simon J."],["dc.contributor.author","Najafova, Zeynab"],["dc.contributor.author","Hossan, Tareq"],["dc.contributor.author","Xie, Wanhua"],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Ditzel, Nicholas"],["dc.contributor.author","Kassem, Moustapha"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2020-12-10T18:19:34Z"],["dc.date.available","2020-12-10T18:19:34Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1093/nar/gkx377"],["dc.identifier.eissn","1362-4962"],["dc.identifier.issn","0305-1048"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/75295"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","CHD1 regulates cell fate determination by activation of differentiation-induced genes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1369"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Stem Cells"],["dc.bibliographiccitation.lastpage","1376"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Hossan, Tareq"],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Baumgart, Simon J."],["dc.contributor.author","Xie, Wanhua"],["dc.contributor.author","Magallanes, Roberto Tirado"],["dc.contributor.author","Hernandez, Celine"],["dc.contributor.author","Chiaroni, Pierre-Marie"],["dc.contributor.author","Indenbirken, Daniela"],["dc.contributor.author","Spitzner, Melanie"],["dc.contributor.author","Thomas-Chollier, Morgane"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Thieffry, Denis"],["dc.contributor.author","Grundhoff, Adam"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2018-11-07T10:15:04Z"],["dc.date.available","2018-11-07T10:15:04Z"],["dc.date.issued","2016"],["dc.description.abstract","Cellular differentiation is accompanied by dramatic changes in chromatin structure which direct the activation of lineage-specific transcriptional programs. Structure-specific recognition protein-1 (SSRP1) is a histone chaperone which is important for chromatin-associated processes such as transcription, DNA replication and repair. Since the function of SSRP1 during cell differentiation remains unclear, we investigated its potential role in controlling lineage determination. Depletion of SSRP1 in human mesenchymal stem cells elicited lineage-specific effects by increasing expression of adipocyte-specific genes and decreasing the expression of osteoblast-specific genes. Consistent with a role in controlling lineage specification, transcriptome-wide RNA-sequencing following SSRP1 depletion and the induction of osteoblast differentiation revealed a specific decrease in the expression of genes involved in biological processes related to osteoblast differentiation. Importantly, we observed a specific downregulation of target genes of the canonical Wnt signaling pathway, which was accompanied by decreased nuclear localization of active beta-catenin. Together our data uncover a previously unknown role for SSRP1 in promoting the activation of the Wnt signaling pathway activity during cellular differentiation."],["dc.identifier.doi","10.1002/stem.2287"],["dc.identifier.isi","000375896900021"],["dc.identifier.pmid","27146025"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40740"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1549-4918"],["dc.relation.issn","1066-5099"],["dc.title","Histone Chaperone SSRP1 is Essential for Wnt Signaling Pathway Activity During Osteoblast Differentiation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2387"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Cancer Research"],["dc.bibliographiccitation.lastpage","2400"],["dc.bibliographiccitation.volume","77"],["dc.contributor.author","Mishra, Vivek Kumar"],["dc.contributor.author","Subramaniam, Malayannan"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Pitel, Kevin S."],["dc.contributor.author","Baumgart, Simon J."],["dc.contributor.author","Naylor, Ryan M."],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Ellenrieder, Volker"],["dc.contributor.author","Hawse, John R."],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2020-12-10T18:37:44Z"],["dc.date.available","2020-12-10T18:37:44Z"],["dc.date.issued","2017"],["dc.description.abstract","TGFb-SMAD signaling exerts a contextual effect that suppresses malignant growth early in epithelial tumorigenesis but promotes metastasis at later stages. Longstanding challenges in resolving this functional dichotomy may uncover new strategies to treat advanced carcinomas. The Kruppel-like transcription factor, KLF10, is a pivotal effector of TGF beta/SMAD signaling that mediates antiproliferative effects of TGF beta. In this study, we show how KLF10 opposes the prometastatic effects of TGFb by limiting its ability to induce epithelial-to-mesenchymal transition (EMT). KLF10 depletion accentuated induction of EMT as assessed by multiple metrics. KLF10 occupied GC-rich sequences in the promoter region of the EMT-promoting transcription factor SLUG/SNAI2, repressing its transcription by recruiting HDAC1 and licensing the removal of activating histone acetylation marks. In clinical specimens of lung adenocarcinoma, low KLF10 expression associated with decreased patient survival, consistent with a pivotal role for KLF10 in distinguishing the antiproliferative versus prometastatic functions of TGFb. Our results establish that KLF10 functions to suppress TGFb-induced EMT, establishing a molecular basis for the dichotomy of TGFb function during tumor progression. (C) 2017 AACR."],["dc.identifier.doi","10.1158/0008-5472.CAN-16-2589"],["dc.identifier.eissn","1538-7445"],["dc.identifier.isi","000400270100021"],["dc.identifier.issn","0008-5472"],["dc.identifier.pmid","28249899"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77078"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Amer Assoc Cancer Research"],["dc.relation.issn","1538-7445"],["dc.relation.issn","0008-5472"],["dc.title","Krüppel-like Transcription Factor KLF10 Suppresses TGFβ-Induced Epithelial-to-Mesenchymal Transition via a Negative Feedback Mechanism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Cancer Gene Therapy"],["dc.contributor.author","Oh-Hohenhorst, Su Jung"],["dc.contributor.author","Tilki, Derya"],["dc.contributor.author","Ahlers, Ann-Kristin"],["dc.contributor.author","Suling, Anna"],["dc.contributor.author","Hahn, Oliver"],["dc.contributor.author","Tennstedt, Pierre"],["dc.contributor.author","Matuszcak, Christiane"],["dc.contributor.author","Maar, Hanna"],["dc.contributor.author","Labitzky, Vera"],["dc.contributor.author","Hanika, Sandra"],["dc.contributor.author","Starzonek, Sarah"],["dc.contributor.author","Baumgart, Simon"],["dc.contributor.author","Johnsen, Steven A."],["dc.contributor.author","Kluth, Martina"],["dc.contributor.author","Sirma, Hüseyin"],["dc.contributor.author","Simon, Ronald"],["dc.contributor.author","Sauter, Guido"],["dc.contributor.author","Huland, Hartwig"],["dc.contributor.author","Schumacher, Udo"],["dc.contributor.author","Lange, Tobias"],["dc.date.accessioned","2021-04-14T08:30:19Z"],["dc.date.available","2021-04-14T08:30:19Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1038/s41417-020-00288-z"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83187"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1476-5500"],["dc.relation.issn","0929-1903"],["dc.title","CHD1 loss negatively influences metastasis-free survival in R0-resected prostate cancer patients and promotes spontaneous metastasis in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]