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High ASC expression is associated with Gastric Cancer.
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ASC has a role in the regulation of renal fibrosis and endoplasmic reticulum stress after unilateral ureter obstruction, strongly indicating that ASC could serve as an attractive target in the treatment of chronic kidney disease
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both Nlrp3(-/-) and Asc(-/-) mice showed a strongly improved host defense, as reflected by a markedly reduced mortality rate accompanied by diminished bacterial growth and dissemination.
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Cl(-) channel-dependent formation of dynamic ASC oligomers and inflammasome specks that remain inactive in the absence of K(+) efflux. Formed after Cl(-) efflux exclusively, ASC specks are NLRP3 dependent, reversible, and inactive, although they further prime inflammatory responses.
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we found that butyrate significantly decreased Nlrp3 inflammasome formation and activation in the carotid arterial wall of wild type mice (Asc(+/+)), which was comparable to the effect of gene deletion of the adaptor protein apoptosis-associated speck-like protein gene (Asc(-/-)).
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oligomerization of ASC creates a multitude of potential caspase-1 activation sites, thus serving as a signal amplification mechanism for inflammasome-mediated cytokine production
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Collectively, these results are consistent with a model whereby the type III secretion system apparatus of Pseudomonas aeruginosa activates the caspase-1-dependent inflammasome and caspase-3/7 through an ASC-dependent mechanism.
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ASC specks released by microglia bind to amyloid-beta and increase amyloid-beta oligomer and aggregate formation, acting as an inflammation-driven cross-seed for amyloid-beta pathology
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results suggest that although Pyk2 and FAK are involved in inflammasome activation, only Pyk2 directly phosphorylates ASC and brings ASC into an oligomerization-competent state by allowing Tyr146 phosphorylation to participate ASC speck formation and subsequent NLRP3 inflammation.
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Alendronate (ALN)-augmented IL-1beta production and cell death require Smad3 and ASC activation, and SIS3 and anti-ASC antibodies may serve as palliative agents for necrotizing inflammatory diseases caused by ALN
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These data provide evidence that the inflammasome components ASC, NLRP3 and AIM2 play a role in regulating macrophage adhesion and activation in response to surface nanotopography and chemistry.
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SGLT-2 inhibition with dapagliflozin reduces the activation of the Nlrp3/ASC inflammasome and attenuates the development of diabetic cardiomyopathy in mice with type 2 diabetes. Effects are augmentated of the by DPP4 inhibitor Saxagliptin.
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Elevations of CO2 cause oligomerization of the inflammasome components ASC, NLRP3, caspase 1, thioredoxin interacting protein, and calreticulin - a protein from endoplasmic reticulum, leading to IL-1beta synthesis. An increased production rate of MPs containing elevated amounts of IL-1beta persists for hours after short-term exposures to elevated CO2
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Our cumulative findings indicate that ASC suppresses cancer metastasis and progression via the modulation of cytoskeletal remodeling and the Src-caspase-8 signaling pathway.
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these findings suggest that p205 controls expression of Asc mRNA to regulate inflammasome responses. These findings expand on our understanding of immune-regulatory roles for the PYHIN protein family.
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this study shows that ASC-dependent Inflammasomes do not shape the commensal gut microbiota composition
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Our data identify RIPK3 and the ASC inflammasome as key tumor suppressors in AML.
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Data show that T cell-intrinsic PYD and CARD domain containing protein ASC is required for TH17-mediated experimental autoimmune encephalomyelitis (EAE).
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Data suggest that interleukin 22 (IL-22) plays a pro-inflammatory/pathogenic role in the onset of antigen-induced arthritis (AIA) through apoptosis-associated speck-like Pycard protein (ASC)-dependent stimulation of interleukin-1 beta (IL-1beta) production.
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report herein that lack of ASC does not confer preferential protection in response to P. aeruginosa acute infection and that ASC(-/-) mice are capable of producing robust amounts of IL-1beta comparable with C57BL/6 mice
