V. Dixit

Publications405
h-index151
Citations104,501
Highly Influential Citations4,893
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Death receptors: signaling and modulation.
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. Certain cells have unique…
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Cryopyrin activates the inflammasome in response to toxins and ATP
TLDR
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.
View on Springer
Non-canonical inflammasome activation targets caspase-11
TLDR
It is shown, with C57BL/6 Casp11 gene-targeted mice, that caspase-11 is critical for casp enzyme-1 activation and IL-1β production in macrophages infected with Escherichia coli, Citrobacter rodentium or Vibrio cholerae, and a unique pro-inflammatory role for casingase- 11 in the innate immune response to clinically significant bacterial infections is highlighted.
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FADD, a novel death domain-containing protein, interacts with the death domain of fas and initiates apoptosis
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Mechanisms and Functions of Inflammasomes
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Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling
TLDR
It is shown that gasdermin D is essential for caspase-11-dependent pyroptosis and interleukin-1β maturation and a key mediator of the host response against Gram-negative bacteria.
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An antagonist decoy receptor and a death domain-containing receptor for TRAIL.
TLDR
Ectopic expression of TRID protected mammalian cells from TRAIL-induced apoptosis, which is consistent with a protective role.
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The Receptor for the Cytotoxic Ligand TRAIL
TLDR
The DR4-TRAIL axis defines another receptor-ligand pair involved in regulating cell suicide and tissue homeostasis.
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Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf
TLDR
Interestingly, cell death triggered by stimuli that engage caspase-1 was ablated in macrophages lacking either ASC or Ipaf, suggesting a coupling between the inflammatory and cell death pathways.
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De-ubiquitination and ubiquitin ligase domains of A20 downregulate NF-κB signalling
TLDR
A novel ubiquitin ligase domain is defined and two sequential mechanisms by which A20 downregulates NF-κB signalling are identified, both of which participate in mediating a distinct regulatory effect.
View on Nature
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