S
Svetlana Kotliarova
Researcher at National Institutes of Health
Publications - 27
Citations - 4456
Svetlana Kotliarova is an academic researcher from National Institutes of Health. The author has contributed to research in topics: DNA methylation & Glioma. The author has an hindex of 22, co-authored 27 publications receiving 4184 citations. Previous affiliations of Svetlana Kotliarova include RIKEN Brain Science Institute & University of Tokyo.
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Journal ArticleDOI
Tumor stem cells derived from glioblastomas cultured in bFGF and EGF more closely mirror the phenotype and genotype of primary tumors than do serum-cultured cell lines.
Jeongwu Lee,Svetlana Kotliarova,Yuri Kotliarov,Aiguo Li,Qin Su,Nicholas M. Donin,Sandra Pastorino,Benjamin Purow,Neil Christopher,Wei Zhang,John K. Park,Howard A. Fine +11 more
TL;DR: Significant phenotypic and genotypic differences are demonstrated between primary human tumor-derived TSCs and their matched glioma cell lines, suggesting that TSC's may be a more reliable model than many commonly utilized cancer cell lines for understanding the biology of primary human tumors.
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Epigenetic-mediated dysfunction of the bone morphogenetic protein pathway inhibits differentiation of glioblastoma-initiating cells.
Jeongwu Lee,Myung Jin Son,Kevin D. Woolard,Nicholas M. Donin,Aiguo Li,Chui H. Cheng,Svetlana Kotliarova,Yuri Kotliarov,Jennifer Walling,Susie Ahn,Misuk Kim,Mariam Totonchy,Thomas Cusack,Chibawanye I. Ene,Hilary Ma,Qin Su,Jean C. Zenklusen,Wei Zhang,Dragan Maric,Howard A. Fine +19 more
TL;DR: It is demonstrated that both bone morphogenetic protein (BMP)-mediated and ciliary neurotrophic factor (CNTF)-mediated Jak/STAT-dependent astroglial differentiation is impaired due to EZH2-dependent epigenetic silencing of BMP receptor 1B (BMPR1B) in a subset of glioblastoma TICs.
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Co-chaperone CHIP Associates with Expanded Polyglutamine Protein and Promotes Their Degradation by Proteasomes
Nihar Ranjan Jana,Priyanka Dikshit,Anand Goswami,Svetlana Kotliarova,Shigeo Murata,Keiji Tanaka,Nobuyuki Nukina +6 more
TL;DR: It is demonstrated that CHIP (C terminus of Hsp70-interacting protein) co-immunoprecipitates with the polyglutamine-expanded huntingtin or ataxin-3 and associates with their aggregates and suppressive effect is more prominent when CHIP is overexpressed along with Hsc70.
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Glycogen synthase kinase-3 inhibition induces glioma cell death through c-MYC, nuclear factor-κB, and glucose regulation
Svetlana Kotliarova,Sandra Pastorino,Lara C. Kovell,Yuri Kotliarov,Hua Song,Wei Zhang,Rolanda Bailey,Dragan Maric,Jean C. Zenklusen,Jeongwu Lee,Howard A. Fine +10 more
TL;DR: It is shown that multiple small molecular inhibitors of GSK3 activity and genetic down-regulation of G SK3alpha/beta significantly inhibit glioma cell survival and clonogenicity and may be an important therapeutic target for gliomas.
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Ataxin-3, the MJD1 gene product, interacts with the two human homologs of yeast DNA repair protein RAD23, HHR23A and HHR23B
TL;DR: The results suggest that this interaction is associated with the normal function of ataxin-3 and that some functional abnormality of the HHR23 proteins might exist in MJD.