Kari, Vijaya Lakshmi

[["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.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"]]