V
Vivek M. Rangnekar
Researcher at University of Kentucky
Publications - 122
Citations - 6467
Vivek M. Rangnekar is an academic researcher from University of Kentucky. The author has contributed to research in topics: Apoptosis & Cancer cell. The author has an hindex of 46, co-authored 113 publications receiving 6058 citations. Previous affiliations of Vivek M. Rangnekar include Markey Cancer Center & The Graduate Center, CUNY.
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Journal ArticleDOI
The Cyclooxygenase-2 Inhibitor Celecoxib Induces Apoptosis by Blocking Akt Activation in Human Prostate Cancer Cells Independently of Bcl-2
TL;DR: The data demonstrate that inhibition of Akt activation may play a crucial role in the induction of apoptosis by celecoxib, supported by studies showing that overexpression of constitutively active Akt protects PC-3 cells from Celecoxib-induced apoptosis.
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Par-4 is a mediator of neuronal degeneration associated with the pathogenesis of Alzheimer disease.
Qing Guo,Weiming Fu,Jun Xie,Hong Luo,Stephen F. Sells,James W. Geddes,Vimala Bondada,Vivek M. Rangnekar,Mark P. Mattson +8 more
TL;DR: It is reported here that Par-4 expression is increased in vulnerable neurons in AD brain and is induced in cultured neurons undergoing apoptosis, and mitochondrial dysfunction and apoptosis exacerbated, in cells expressing presenilin-1 mutations associated with early-onset inherited AD.
Journal Article
Commonality of the gene programs induced by effectors of apoptosis in androgen-dependent and -independent prostate cells
Stephen F. Sells,D. P. Wood,S. S. Joshi-Barve,Sumathi Muthukumar,R. J. Jacob,S. A. Crist,S. Humphreys,Vivek M. Rangnekar +7 more
TL;DR: Together, par-1, -3, -4, and -5 represent an apoptosis response gene program common to both androgen-dependent and -independent prostate cells, and are predicted to be important components of diverse effector-driven apoptotic pathways.
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The Tumor Suppressor Par-4 Activates an Extrinsic Pathway for Apoptosis
Ravshan Burikhanov,Yanming Zhao,Anindya Goswami,Shirley Qiu,Steven R. Schwarze,Vivek M. Rangnekar +5 more
TL;DR: Interestingly, extracellular Par-4 induced apoptosis by binding to the stress response protein, glucose-regulated protein-78 (GRP78), expressed at the surface of cancer cells, and activates an extrinsic pathway involving cell surface GRP78 receptor for induction of apoptosis.
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Suppression of PTEN Expression by NF-κB Prevents Apoptosis
TL;DR: PTEN, a novel target whose suppression is critical for antiapoptosis by NF-κB, is reported here that the tumor suppressor PTEN, which functions as a negative regulator of phosphatidylinositol (PI)-3 kinase/Akt-mediated cell survival pathway, is down regulated by p65 but not by p50.