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Vishva M. Dixit

Researcher at Genentech

Publications -  358
Citations -  106948

Vishva M. Dixit is an academic researcher from Genentech. The author has contributed to research in topics: Apoptosis & Signal transduction. The author has an hindex of 145, co-authored 355 publications receiving 96471 citations. Previous affiliations of Vishva M. Dixit include University of Michigan & Human Genome Sciences.

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Journal ArticleDOI

Death receptors: signaling and modulation

Avi Ashkenazi, +1 more
- 28 Aug 1998 - 
TL;DR: Apoptosis is a cell suicide mechanism that enables metazoans to control cell number in tissues and to eliminate individual cells that threaten the animal's survival.
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Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Lorenzo Galluzzi, +186 more
TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
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FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death--inducing signaling complex.

TL;DR: This work utilized nano-electrospray tandem mass spectrometry to identify CAP3 and CAP4, components of the CD95 (Fas/APO-1) death-inducing signaling complex, and found a novel 55 kDa protein, designated FLICE, which has homology to both FADD and the ICE/CED-3 family of cysteine proteases.
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Cryopyrin activates the inflammasome in response to toxins and ATP

TL;DR: It is shown that cryopyrin-deficient macrophages cannot activate caspase-1 in response to Toll-like receptor agonists plus ATP, the latter activating the P2X7 receptor to decrease intracellular K+ levels.
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FADD, a novel death domain-containing protein, interacts with the death domain of fas and initiates apoptosis

TL;DR: Findings suggest that FADD may play an important role in the proximal signal transduction of Fas, a mutant of Fas possessing enhanced killing activity, but not the functionally inactive mutants Fas-LPR and Fas-FD8.