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Kartik Venkatachalam

Researcher at University of Texas at Austin

Publications -  49
Citations -  8557

Kartik Venkatachalam is an academic researcher from University of Texas at Austin. The author has contributed to research in topics: Transient receptor potential channel & TRPML. The author has an hindex of 28, co-authored 45 publications receiving 7770 citations. Previous affiliations of Kartik Venkatachalam include University of Maryland, Baltimore & Katholieke Universiteit Leuven.

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Journal ArticleDOI

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.
Journal ArticleDOI

The cellular and molecular basis of store-operated calcium entry

Kartik Venkatachalam, +4 more
- 01 Nov 2002 - 
TL;DR: New insights are reviewed into the exchange of signals between the endoplasmic reticulum (ER) and plasma membrane that result in activation of calcium entry channels mediating crucial long-term calcium signals.
Journal ArticleDOI

Regulation of Canonical Transient Receptor Potential (TRPC) Channel Function by Diacylglycerol and Protein Kinase C

Kartik Venkatachalam, +2 more
- 01 Aug 2003 - 
TL;DR: The results reveal that each TRPC subtype is strongly inhibited by D AG-induced PKC activation, reflecting a likely universal feedback control on TRPCs, and that DAG-mediated PKC-independent activation of TRPC channels is highly subtype-specific.
Journal ArticleDOI

Membrane potential modulates plasma membrane phospholipid dynamics and K-Ras signaling

Yong Zhou, +16 more
- 21 Aug 2015 - 
TL;DR: It is shown that plasma membrane depolarization induces nanoscale reorganization of phosphatidylserine and phosphatinositol 4,5-bisphosphate but not other anionic phospholipids, and K-Ras nanoclusters set up the plasma membrane as a biological field-effect transistor, allowing membrane potential to control the gain in mitogenic signaling circuits.
Journal ArticleDOI

Motor Deficit in a Drosophila Model of Mucolipidosis Type IV due to Defective Clearance of Apoptotic Cells

Kartik Venkatachalam, +5 more
- 28 Nov 2008 - 
TL;DR: It is concluded that the neurodegeneration and motor defects result primarily from decreased clearance of apoptotic cells, and the results raise the possibility that bone marrow transplantation may limit the progression of MLIV.