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ASC CpG methylation may prove to be a primary regulator of the pathogenesis of chronic inflammatory diseases such as heart failure.
besides its role in the inhibition of the NF-kappaB (显示 NFKB1 ELISA试剂盒) pathway, NLRC3 (显示 NLRC3 ELISA试剂盒) interferes with the assembly and activity of the NALP3 (显示 NLRP3 ELISA试剂盒) inflammasome complex by competing with ASC for pro-caspase-1 (显示 CASP1 ELISA试剂盒) binding
ASC Induces Apoptosis via Activation of Caspase-9 (显示 CASP9 ELISA试剂盒) by Enhancing Gap Junction-Mediated Intercellular Communication.(
These data revealed that cross-linking of ASC(PYD) filaments via ASC(CARD) mediates the assembly of ASC foci.
Down-regulation of mRNA expression was found in cases in which CASP8 (显示 CASP8 ELISA试剂盒), TMS1 (显示 SERINC3 ELISA试剂盒) and DAPK (显示 DAPK1 ELISA试剂盒) were hypermethylated.
loss of ASC driven tumor development is counterbalanced in the identical cell by the inhibition of pro-tumorigenic inflammation in the tumor cell itself
the deubiquitinating enzyme USP50 binds to the ASC protein and subsequently regulates the inflammasome signaling pathway.
ASC self-associates and binds NLRP3 (显示 NLRP3 ELISA试剂盒) PYD through equivalent protein regions, with higher binding affinity for the latter. These regions are located at opposite sides of the protein allowing multimeric complex formation previously shown in ASC PYD fibril assemblies.
Our data identify RIPK3 (显示 RIPK3 ELISA试剂盒) and the ASC inflammasome as key tumor suppressors in AML (显示 RUNX1 ELISA试剂盒).
The role of the danger signals ASC and HMGB1 (显示 HMGB1 ELISA试剂盒) in the Fusobacterium nucleatum infection of gingival epithelial cells.
SGLT-2 (显示 SLC5A2 ELISA试剂盒) inhibition with dapagliflozin reduces the activation of the Nlrp3 (显示 NLRP3 ELISA试剂盒)/ASC (显示 STS ELISA试剂盒) inflammasome and attenuates the development of diabetic cardiomyopathy in mice with type 2 diabetes. Effects are augmentated of the by DPP4 (显示 DPP4 ELISA试剂盒) inhibitor Saxagliptin.
Elevations of CO2 cause oligomerization of the inflammasome components ASC (显示 STS ELISA试剂盒), NLRP3 (显示 NLRP3 ELISA试剂盒), caspase 1 (显示 CASP1 ELISA试剂盒), thioredoxin interacting protein (显示 TXNIP ELISA试剂盒), and calreticulin (显示 CALR ELISA试剂盒) - a protein from endoplasmic reticulum, leading to IL-1beta (显示 IL1B ELISA试剂盒) synthesis. An increased production rate of MPs containing elevated amounts of IL-1beta (显示 IL1B ELISA试剂盒) persists for hours after short-term exposures to elevated CO2
Our cumulative findings indicate that ASC (显示 STS ELISA试剂盒) suppresses cancer metastasis and progression via the modulation of cytoskeletal remodeling and the Src (显示 SRC ELISA试剂盒)-caspase-8 (显示 CASP8 ELISA试剂盒) signaling pathway.
these findings suggest that p205 (显示 GNB2L1 ELISA试剂盒) controls expression of Asc (显示 STS ELISA试剂盒) mRNA to regulate inflammasome responses. These findings expand on our understanding of immune-regulatory roles for the PYHIN protein family.
this study shows that ASC (显示 STS ELISA试剂盒)-dependent Inflammasomes do not shape the commensal gut (显示 GUSB ELISA试剂盒) microbiota composition
Our data identify RIPK3 (显示 RIPK3 ELISA试剂盒) and the ASC (显示 STS ELISA试剂盒) inflammasome as key tumor suppressors in AML (显示 RUNX1 ELISA试剂盒).
Data show that T cell-intrinsic PYD and CARD domain containing protein ASC is required for TH17-mediated experimental autoimmune encephalomyelitis (EAE).
Data suggest that interleukin 22 (IL-22 (显示 IL22 ELISA试剂盒)) plays a pro-inflammatory/pathogenic role in the onset of antigen-induced arthritis (AIA) through apoptosis-associated speck-like Pycard protein (ASC (显示 STS ELISA试剂盒))-dependent stimulation of interleukin-1 beta (IL-1beta (显示 IL1B ELISA试剂盒)) production.
report herein that lack of ASC (显示 STS ELISA试剂盒) does not confer preferential protection in response to P. aeruginosa acute infection and that ASC (显示 STS ELISA试剂盒)(-/-) mice are capable of producing robust amounts of IL-1beta (显示 IL1B ELISA试剂盒) comparable with C57BL/6 mice
These data identify a novel non-canonical immunoregulatory function of NLRP3 (显示 NLRP3 ELISA试剂盒) and ASC (显示 STS ELISA试剂盒) in autoimmunity.
This gene encodes an adaptor protein that is composed of two protein-protein interaction domains: a N-terminal PYRIN-PAAD-DAPIN domain (PYD) and a C-terminal caspase-recruitment domain (CARD). The PYD and CARD domains are members of the six-helix bundle death domain-fold superfamily that mediates assembly of large signaling complexes in the inflammatory and apoptotic signaling pathways via the activation of caspase. In normal cells, this protein is localized to the cytoplasm\; however, in cells undergoing apoptosis, it forms ball-like aggregates near the nuclear periphery. Two transcript variants encoding different isoforms have been found for this gene.
apoptosis-associated speck-like protein containing a CARD
, caspase recruitment domain-containing protein 5
, target of methylation-induced silencing 1
, PYD and CARD domain-containing protein