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Photo of Brajendra Tripathi using confocal microscope

Brajendra Tripathi, Ph.D.

  • Center for Cancer Research
  • National Cancer Institute

RESEARCH SUMMARY

Dr. Tripathi has an abiding interest in the clinical applications of basic research. His current research is mainly focused on how tumor suppressor proteins, which are downregulated or inactivated in several cancer types by distinct mechanisms, can be stabilized and reactivated and exploited for cancer treatment. Specifically, Dr. Tripathi and colleagues are exploring functions of the tumor suppressor protein Deleted in Liver Cancer 1 (DLC1) and the kinases and methyltransferases that regulate its functions in normal physiology and in cancer.

Areas of Expertise

Cancer Biology
Cell Biology And Cell Imaging
Small GTPases Signaling
Oncogenes And Tumor Suppressor Genes Regulation
Protein Kinases And Post-translational Modifications

News

Dr. Tripathi is featured in the ‘People and Ideas’ section of the Journal of Cell Biology.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6781442/

Dr. Tripathi and colleagues research is featured in the special issue “Cancer Cell Biology 2020” of the Journal of Cell Biology: SRC targets the tumor suppressor DLC1: Interaction between DLC1 and tumor promoting kinase SRC reveals a possible new treatment route for DLC1-positive tumors.

Covers

Journal cover for Journal Cell Biology December 8, 2014

CDK5 Opens Up DLC1

Published Date

Tripathi et al. reveal that the serine/threonine kinase CDK5 phosphorylates the tumor suppressor DLC1 (red), switching it from a closed to an open conformation and thereby promoting its Rho-GAP activity, its ability to bind tensin and talin, and its localization to focal adhesions (green). Colocalization (yellow) of DLC1 protein with the focal adhesion protein Vinculin. Nuclei are labeled blue.

Citation

Brajendra K. Tripathi*, Xiaolan Qian, Philipp Mertins, Dunrui Wang, Alex G. Papageorge, Steven Carr, and Douglas R. Lowy* (2014Journal of Cell Biology. 207(5): 627-642. doi: 10.1083/jcb.201405105

Publications

Selected Recent Publications

Inhibition of cytoplasmic EZH2 induces antitumor activity through stabilization of the DLC1 tumor suppressor protein.

Brajendra K. Tripathi*, Meghan Anderman, Disha Bhargava, Luciarita Boccuzzi, Xiaolan Qian, Dunrui Wang, Marian E. Durkin, Alex G. Papageorge, Fernando J. de Miguel, Katerina Politi, Kylie J. Walters, James H. Doroshow and Douglas R. Lowy*
Nature Communications . Article number: 6941: 2021.
Full-Text Article
[ Journal Article ]

SRC and ERK cooperatively phosphorylate DLC1 and attenuate its Rho-GAP and tumor suppressor functions

Brajendra K. Tripathi*, Meghan Anderman, Xiaolan Qian, Ming Zhou, Dunrui Wang, Alex G. Papageorge, and Douglas R. Lowy*
Journal of Cell Biology. 218(9): 3060-3076, 2019.
Full-Text Article
[ Journal Article ]

Receptor tyrosine kinase activation of RhoA is mediated by AKT phosphorylation of DLC1

Brajendra K. Tripathi*, Tiera Grant, Xiaolan Qian, Ming Zhou, Philipp Mertins, Dunrui Wang, Alex G. Papageorge, Sergey G. Tarasov, Kent W. Hunter, Steven Carr, and Douglas R. Lowy*
Journal of Cell Biology. 216(12): 4255-4270, 2017.
Full-Text Article
[ Journal Article ]

An Apela RNA-Containing Negative Feedback Loop Regulates p53-Mediated Apoptosis in Embryonic Stem Cells

Li M, Gou H, Brajendra K. Tripathi, Huang J, Jiang S, Dubois W, Waybright T, Lei M, Shi J, Zhou M, Huang J
Cell Stem Cell. 16(6): 669-683, 2015.
Full-Text Article
[ Journal Article ]

CDK5 is a major regulator of the tumor suppressor DLC1

Brajendra K. Tripathi*, Xiaolan Qian, Philipp Mertins, Dunrui Wang, Alex G. Papageorge, Steven Carr, and Douglas R. Lowy*
Journal of Cell Biology. 207(5): 627-642, 2014.
Full-Text Article