Kari, Vijaya Lakshmi

[["dc.bibliographiccitation.artnumber","P4479"],["dc.bibliographiccitation.firstpage","937"],["dc.bibliographiccitation.issue","suppl_1"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Iyer, L. M."],["dc.contributor.author","Noack, C."],["dc.contributor.author","Nagarajan, S."],["dc.contributor.author","Woelfer, M."],["dc.contributor.author","Schoger, E."],["dc.contributor.author","Pang, S. T."],["dc.contributor.author","Kari, V."],["dc.contributor.author","Zafeiriou, M. P."],["dc.contributor.author","Toischer, K."],["dc.contributor.author","Hasenfuss, G."],["dc.contributor.author","Johnsen, S. A."],["dc.contributor.author","Zelarayan, L. C."],["dc.date.accessioned","2019-02-19T13:47:43Z"],["dc.date.available","2019-02-19T13:47:43Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1093/eurheartj/ehx504.P4479"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57586"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/177"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C07: Kardiomyozyten Wnt/β-catenin Komplex Aktivität im pathologischen Herz-Remodeling - als gewebespezifischer therapeutischer Ansatz"],["dc.relation.issn","0195-668X"],["dc.relation.workinggroup","RG Hasenfuß (Transition zur Herzinsuffizienz)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.relation.workinggroup","RG Zelarayán-Behrend (Developmental Pharmacology)"],["dc.title","B-catenin/TCF7L2 signaling orchestrates initiation of pathological hypertrophic cardiac remodeling by inducing chromatin modifications"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","8959"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Nucleic Acids Research"],["dc.bibliographiccitation.lastpage","8976"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Wüst, Hannah M"],["dc.contributor.author","Wegener, Amélie"],["dc.contributor.author","Fröb, Franziska"],["dc.contributor.author","Hartwig, Anna C"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Schimmel, Margit"],["dc.contributor.author","Tamm, Ernst R"],["dc.contributor.author","Johnsen, Steven A"],["dc.contributor.author","Wegner, Michael"],["dc.contributor.author","Sock, Elisabeth"],["dc.date.accessioned","2021-04-14T08:22:59Z"],["dc.date.available","2021-04-14T08:22:59Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1093/nar/gkaa606"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80763"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1362-4962"],["dc.relation.issn","0305-1048"],["dc.title","Egr2-guided histone H2B monoubiquitination is required for peripheral nervous system myelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3495"],["dc.bibliographiccitation.issue","20"],["dc.bibliographiccitation.journal","Cell Cycle"],["dc.bibliographiccitation.lastpage","3504"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Shchebet, Andrei"],["dc.contributor.author","Neumann, Heinz"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2018-11-07T08:50:42Z"],["dc.date.available","2018-11-07T08:50:42Z"],["dc.date.issued","2011"],["dc.description.abstract","Many anticancer therapies function largely by inducing DNA double-strand breaks (DSBs) or altering the ability of cancer cells to repair them. Proper and timely DNA repair requires dynamic changes in chromatin assembly and disassembly characterized by histone H3 lysine 56 acetylation (H3K56ac) and phosphorylation of the variant histone H2AX (gamma H2AX). Similarly, histone H2B monoubiquitination (H2Bub1) functions in DNA repair, but its role in controlling dynamic changes in chromatin structure following DSBs and the histone chaperone complexes involved remain unknown. Therefore, we investigated the role of the H2B ubiquitin ligase RNF40 in the DSB response. We show that RNF40 depletion results in sustained H2AX phosphorylation and a decrease in rapid cell cycle checkpoint activation. Furthermore, RNF40 knockdown resulted in decreased H3K56ac and decreased recruitment of the facilitates chromatin transcription (FACT) complex to chromatin following DSB. Knockdown of the FACT component suppressor of Ty homolog-16 (SUPT16H) phenocopied the effects of RNF40 knockdown on both gamma H2AX and H3K56ac following DSB induction. Consistently, both RNF40 and SUPT16H were required for proper DNA end resection and timely DNA repair, suggesting that H2Bub1 and FACT cooperate to increase chromatin dynamics, which facilitates proper checkpoint activation and timely DNA repair. These results provide important mechanistic insights into the tumor suppressor function of H2Bub1 and provide a rational basis for pursuing H2Bub1-based therapies in conjunction with traditional chemo-and radiotherapy."],["dc.identifier.doi","10.4161/cc.10.20.17769"],["dc.identifier.isi","000296570700027"],["dc.identifier.pmid","22031019"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21752"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Landes Bioscience"],["dc.relation.issn","1538-4101"],["dc.title","The H2B ubiquitin ligase RNF40 cooperates with SUPT16H to induce dynamic changes in chromatin structure during DNA double-strand break repair"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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.firstpage","6334"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Nucleic Acids Research"],["dc.bibliographiccitation.lastpage","6349"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Mishra, Vivek Kumar"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Kosinsky, Robyn Laura"],["dc.contributor.author","Sen, Madhobi"],["dc.contributor.author","Baumgartner, Roland"],["dc.contributor.author","Wulff, Tanja"],["dc.contributor.author","Siveke, Jens T."],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Najafova, Zeynab"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Kohlhof, Hella"],["dc.contributor.author","Hessmann, Elisabeth"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2018-11-07T10:22:37Z"],["dc.date.available","2018-11-07T10:22:37Z"],["dc.date.issued","2017"],["dc.description.abstract","Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with a particularly dismal prognosis. Histone deacetylases (HDAC) are epigenetic modulators whose activity is frequently deregulated in various cancers including PDAC. In particular, class-I HDACs (HDAC 1, 2, 3 and 8) have been shown to play an important role in PDAC. In this study, we investigated the effects of the class Ispecific HDAC inhibitor (HDACi) 4SC-202 in multiple PDAC cell lines in promoting tumor cell differentiation. We show that 4SC-202 negatively affects TGF beta signaling and inhibits TGF beta-induced epithelial-tomesenchymal transition (EMT). Moreover, 4SC-202 markedly induced p21 (CDKN1A) expression and significantly attenuated cell proliferation. Mechanistically, genome-wide studies revealed that 4SC-202-induced genes were enriched for Bromodomain-containing Protein-4 (BRD4) and MYC occupancy. BRD4, a well-characterized acetyllysine reader, has been shown to play a major role in regulating transcription of selected subsets of genes. Importantly, BRD4 and MYC are essential for the expression of a subgroup of genes induced by class-I HDACi. Taken together, our study uncovers a previously unknown role of BRD4 and MYC in eliciting the HDACi-mediated induction of a subset of genes and provides molecular insight into the mechanisms of HDACi action in PDAC."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.1093/nar/gkx212"],["dc.identifier.isi","000403693000023"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14605"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42309"],["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","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Histone deacetylase class-I inhibition promotes epithelial gene expression in pancreatic cancer cells in a BRD4-and MYC-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.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"]]

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[["dc.bibliographiccitation.firstpage","497"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Gut"],["dc.bibliographiccitation.lastpage","507"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Hessmann, E."],["dc.contributor.author","Patzak, M S"],["dc.contributor.author","Klein, L"],["dc.contributor.author","Chen, N"],["dc.contributor.author","Kari, V"],["dc.contributor.author","Ramu, I"],["dc.contributor.author","Bapiro, T E"],["dc.contributor.author","Frese, K K"],["dc.contributor.author","Gopinathan, A"],["dc.contributor.author","Richards, F M"],["dc.contributor.author","Jodrell, D I"],["dc.contributor.author","Verbeke, C"],["dc.contributor.author","Li, X"],["dc.contributor.author","Heuchel, R"],["dc.contributor.author","Löhr, J M"],["dc.contributor.author","Johnsen, S A"],["dc.contributor.author","Gress, T M"],["dc.contributor.author","Ellenrieder, V"],["dc.contributor.author","Neesse, A"],["dc.date.accessioned","2020-12-10T18:37:14Z"],["dc.date.available","2020-12-10T18:37:14Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1136/gutjnl-2016-311954"],["dc.identifier.eissn","1468-3288"],["dc.identifier.issn","0017-5749"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/76887"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Fibroblast drug scavenging increases intratumoural gemcitabine accumulation in murine pancreas cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","UNSP e63745"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Karpiuk, Oleksandra"],["dc.contributor.author","Tieg, Bettina"],["dc.contributor.author","Kriegs, Malte"],["dc.contributor.author","Dikomey, Ekkehard"],["dc.contributor.author","Krebber, Heike"],["dc.contributor.author","Begus-Nahrmann, Yvonne"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2018-11-07T09:24:36Z"],["dc.date.available","2018-11-07T09:24:36Z"],["dc.date.issued","2013"],["dc.description.abstract","Unlike other metazoan mRNAs, replication-dependent histone gene transcripts are not polyadenylated but instead have a conserved stem-loop structure at their 39 end. Our previous work has shown that under certain conditions replication-dependent histone genes can produce alternative transcripts that are polyadenylated at the 39 end and, in some cases, spliced. A number of microarray studies examining the expression of polyadenylated mRNAs identified changes in the levels of histone transcripts e. g. during differentiation and tumorigenesis. However, it remains unknown which histone genes produce polyadenylated transcripts and which conditions regulate this process. In the present study we examined the expression and polyadenylation of the human histone H2B gene complement in various cell lines. We demonstrate that H2B genes display a distinct expression pattern that is varies between different cell lines. Further we show that the fraction of polyadenylated HIST1H2BD and HIST1H2AC transcripts is increased during differentiation of human mesenchymal stem cells (hMSCs) and human fetal osteoblast (hFOB 1.19). Furthermore, we observed an increased fraction of polyadenylated transcripts produced from the histone genes in cells following ionizing radiation. Finally, we show that polyadenylated transcripts are transported to the cytoplasm and found on polyribosomes. Thus, we propose that the production of polyadenylated histone mRNAs from replication-dependent histone genes is a regulated process induced under specific cellular circumstances."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2013"],["dc.identifier.doi","10.1371/journal.pone.0063745"],["dc.identifier.isi","000320362700053"],["dc.identifier.pmid","23717473"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9111"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29865"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","A Subset of Histone H2B Genes Produces Polyadenylated mRNAs under a Variety of Cellular Conditions"],["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","131"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cell Reports"],["dc.bibliographiccitation.lastpage","139"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Schmidt, Johanna M."],["dc.contributor.author","Panzilius, Elena"],["dc.contributor.author","Bartsch, Harald S."],["dc.contributor.author","Irmler, Martin"],["dc.contributor.author","Beckers, Johannes"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Linnemann, Jelena R."],["dc.contributor.author","Dragoi, Diana"],["dc.contributor.author","Hirschi, Benjamin"],["dc.contributor.author","Kloos, Uwe J."],["dc.contributor.author","Sass, Steffen"],["dc.contributor.author","Theis, Fabian J."],["dc.contributor.author","Kahlert, Steffen"],["dc.contributor.author","Johnsen, Steven A."],["dc.contributor.author","Sotlar, Karl"],["dc.contributor.author","Scheel, Christina H."],["dc.date.accessioned","2018-11-07T10:02:12Z"],["dc.date.available","2018-11-07T10:02:12Z"],["dc.date.issued","2015"],["dc.description.abstract","Master regulators of the epithelial-mesenchymal transition such as Twist1 and Snail1 have been implicated in invasiveness and the generation of cancer stem cells, but their persistent activity inhibits stem-cell-like properties and the outgrowth of disseminated cancer cells into macroscopic metastases. Here, we show that Twist1 activation primes a subset of mammary epithelial cells for stem-cell-like properties, which only emerge and stably persist following Twist1 deactivation. Consequently, when cells undergo a mesenchymal-epithelial transition (MET), they do not return to their original epithelial cell state, evidenced by acquisition of invasive growth behavior and a distinct gene expression profile. These data provide an explanation for how transient Twist1 activation may promote all steps of the metastatic cascade; i.e., invasion, dissemination, and metastatic outgrowth at distant sites."],["dc.description.sponsorship","German Cancer Aid Foundation [110225, 111600]"],["dc.identifier.doi","10.1016/j.celrep.2014.12.032"],["dc.identifier.isi","000348036600002"],["dc.identifier.pmid","25578726"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38183"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","2211-1247"],["dc.title","Stem-Cell-like Properties and Epithelial Plasticity Arise as Stable Traits after Transient Twist1 Activation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]