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Kumaravel Somasundaram

Researcher at Indian Institute of Science

Publications -  137
Citations -  12975

Kumaravel Somasundaram is an academic researcher from Indian Institute of Science. The author has contributed to research in topics: Glioma & Cell cycle. The author has an hindex of 46, co-authored 128 publications receiving 11744 citations. Previous affiliations of Kumaravel Somasundaram include Northwestern University & University of Pennsylvania.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Arrest of the cell cycle by the tumour-suppressor BRCA1 requires the cdk-inhibitor p21waf1/cip1

Kumaravel Somasundaram, +8 more
- 11 Sep 1997 - 
TL;DR: It is shown that BRCA1 transactivates expression of the cyclin-dependent kinase inhibitor p21WAF1/CIP1 in a p53-independent manner, and that B RCA1 inhibits cell-cycle progression into the S-phase following its transfection into human cancer cells.
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BRCA1 physically associates with p53 and stimulates its transcriptional activity

Hongbing Zhang, +7 more
- 02 Apr 1998 - 
TL;DR: BRCA1 increases p53-dependent transcription from the p21WAF1/CIP1 and bax promoters and interacts with p53 proteins both in vitro and in vivo, indicating that BRCA 1 and p53 may coordinately regulate gene expression in their role as tumor suppressors.
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Essential role of METTL3-mediated m(6)A modification in glioma stem-like cells maintenance and radioresistance

Abhirami Visvanathan, +6 more
- 25 Jan 2018 - 
TL;DR: The crucial role of METTL3-mediated m6A modification in GSC (neurosphere) maintenance and dedifferentiation of glioma cells is reported andMETTL3 is uncovered as a potential molecular target in GBM therapy.
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AP2 inhibits cancer cell growth and activates p21WAF1/CIP1 expression.

Yi Xin Zeng, +2 more
- 01 Jan 1997 - 
TL;DR: Overexpression of AP2 in HepG2 human hepatoblastoma and SW480 human colon adenocarcinoma cells inhibited cell division and stable colony formation, linking the differentiation-associated factor AP2 to negative cell cycle and growth control, possibly through p21 activation.