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.artnumber","32"],["dc.bibliographiccitation.journal","Genome Biology"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Xie, Wanhua"],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Baumgart, Simon J."],["dc.contributor.author","Kosinsky, Robyn Laura"],["dc.contributor.author","Najafova, Zeynab"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Hennion, Magali"],["dc.contributor.author","Indenbirken, Daniela"],["dc.contributor.author","Bonn, Stefan"],["dc.contributor.author","Grundhoff, Adam"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2018-11-07T10:27:18Z"],["dc.date.available","2018-11-07T10:27:18Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: Monoubiquitination of H2B (H2Bub1) is a largely enigmatic histone modification that has been linked to transcriptional elongation. Because of this association, it has been commonly assumed that H2Bub1 is an exclusively positively acting histone modification and that increased H2Bub1 occupancy correlates with increased gene expression. In contrast, depletion of the H2B ubiquitin ligases RNF20 or RNF40 alters the expression of only a subset of genes. Results: Using conditional Rnf40 knockout mouse embryo fibroblasts, we show that genes occupied by low to moderate amounts of H2Bub1 are selectively regulated in response to Rnf40 deletion, whereas genes marked by high levels of H2Bub1 are mostly unaffected by Rnf40 loss. Furthermore, we find that decreased expression of RNF40-dependent genes is highly associated with widespread narrowing of H3K4me3 peaks. H2Bub1 promotes the broadening of H3K4me3 to increase transcriptional elongation, which together lead to increased tissue- specific gene transcription. Notably, genes upregulated following Rnf40 deletion, including Foxl2, are enriched for H3K27me3, which is decreased following Rnf40 deletion due to decreased expression of the Ezh2 gene. As a consequence, increased expression of some RNF40-\"suppressed\" genes is associated with enhancer activation via FOXL2. Conclusion: Together these findings reveal the complexity and context-dependency whereby one histone modification can have divergent effects on gene transcription. Furthermore, we show that these effects are dependent upon the activity of other epigenetic regulatory proteins and histone modifications."],["dc.identifier.doi","10.1186/s13059-017-1159-5"],["dc.identifier.isi","000394828000003"],["dc.identifier.pmid","28209164"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14250"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43221"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/14993 but duplicate"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1474-760X"],["dc.rights","CC BY 4.0"],["dc.rights.access","openAccess"],["dc.rights.holder","The Author(s)."],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","RNF40 regulates gene expression in an epigenetic context-dependent manner"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["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.firstpage","127"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nucleic Acids Research"],["dc.bibliographiccitation.lastpage","141"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Najafova, Zeynab"],["dc.contributor.author","Tirado-Magallanes, Roberto"],["dc.contributor.author","Subramaniam, Malayannan"],["dc.contributor.author","Hossan, Tareq"],["dc.contributor.author","Schmidt, Geske"],["dc.contributor.author","Nagarajan, Sankari"],["dc.contributor.author","Baumgart, Simon J."],["dc.contributor.author","Mishra, Vivek Kumar"],["dc.contributor.author","Bedi, Upasana"],["dc.contributor.author","Hesse, Eric"],["dc.contributor.author","Knapp, Stefan"],["dc.contributor.author","Hawse, John R."],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2018-11-07T10:28:57Z"],["dc.date.available","2018-11-07T10:28:57Z"],["dc.date.issued","2017"],["dc.description.abstract","Proper temporal epigenetic regulation of gene expression is essential for cell fate determination and tissue development. The Bromodomain-containing Protein-4 (BRD4) was previously shown to control the transcription of defined subsets of genes in various cell systems. In this study we examined the role of BRD4 in promoting lineage-specific gene expression and show that BRD4 is essential for osteoblast differentiation. Genome-wide analyses demonstrate that BRD4 is recruited to the transcriptional start site of differentiation-induced genes. Unexpectedly, while promoter-proximal BRD4 occupancy correlated with gene expression, genes which displayed moderate expression and promoter-proximal BRD4 occupancy were most highly regulated and sensitive to BRD4 inhibition. Therefore, we examined distal BRD4 occupancy and uncovered a specific co-localization of BRD4 with the transcription factors C/EBPb, TEAD1, FOSL2 and JUND at putative osteoblast-specific enhancers. These findings reveal the intricacies of lineage specification and provide new insight into the context-dependent functions of BRD4."],["dc.identifier.doi","10.1093/nar/gkw826"],["dc.identifier.isi","000396575100016"],["dc.identifier.pmid","27651452"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14409"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43538"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1362-4962"],["dc.relation.issn","0305-1048"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","BRD4 localization to lineage-specific enhancers is associated with a distinct transcription factor repertoire"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["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"]]

[["dc.bibliographiccitation.firstpage","1831"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Applied and Environmental Microbiology"],["dc.bibliographiccitation.lastpage","1841"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Pena, R."],["dc.contributor.author","Offermann, C."],["dc.contributor.author","Simon, J."],["dc.contributor.author","Naumann, P. S."],["dc.contributor.author","Gessler, A."],["dc.contributor.author","Holst, J."],["dc.contributor.author","Dannenmann, M."],["dc.contributor.author","Mayer, H."],["dc.contributor.author","Kogel-Knabner, I."],["dc.contributor.author","Rennenberg, H."],["dc.contributor.author","Polle, A."],["dc.date.accessioned","2012-03-15T07:28:44Z"],["dc.date.accessioned","2021-10-27T13:13:28Z"],["dc.date.available","2012-03-15T07:28:44Z"],["dc.date.available","2021-10-27T13:13:28Z"],["dc.date.issued","2010"],["dc.description.abstract","The relationships between plant carbon resources, soil carbon and nitrogen content, and ectomycorrhizal fungal (EMF) diversity in a monospecific, old-growth beech (Fagus sylvatica) forest were investigated by manipulating carbon flux by girdling. We hypothesized that disruption of the carbon supply would not affect diversity and EMF species numbers if EM fungi can be supplied by plant internal carbohydrate resources or would result in selective disappearance of EMF taxa because of differences in carbon demand of different fungi. Tree carbohydrate status, root demography, EMF colonization, and EMF taxon abundance were measured repeatedly during 1 year after girdling. Girdling did not affect root colonization but decreased EMF species richness of an estimated 79 to 90 taxa to about 40 taxa. Cenococcum geophilum, Lactarius blennius, and Tomentella lapida were dominant, colonizing about 70% of the root tips, and remained unaffected by girdling. Mainly cryptic EMF species disappeared. Therefore, the Shannon-Wiener index (H ) decreased but evenness was unaffected. H was positively correlated with glucose, fructose, and starch concentrations of fine roots and also with the ratio of dissolved organic carbon to dissolved organic nitrogen (DOC/DON), suggesting that both H and DOC/DON were governed by changes in belowground carbon allocation. Our results suggest that beech maintains numerous rare EMF species by recent photosynthate. These EM fungi may constitute biological insurance for adaptation to changing environmental conditions. The preservation of taxa previously not known to colonize beech may, thus, form an important reservoir for future forest development"],["dc.identifier.doi","10.1128/AEM.01703-09"],["dc.identifier.fs","572334"],["dc.identifier.gro","3147778"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7440"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/91781"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0099-2240"],["dc.relation.orgunit","Fakultät für Forstwissenschaften und Waldökologie"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject","carbon flux; Cenococcum geophilum; diversity; ectomycorrhiza; insurance 60 hypothesis 61"],["dc.title","Girdling Affects Ectomycorrhizal Fungal (EMF) Diversity and Reveals Functional Differences in EMF Community Composition in a Beech Forest"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]