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抗Human PYCARD 抗体:
抗Mouse (Murine) PYCARD 抗体:
抗Rat (Rattus) PYCARD 抗体:
Human Polyclonal PYCARD Primary Antibody for WB - ABIN610691
Auphan, DiDonato, Rosette, Helmberg, Karin: Immunosuppression by glucocorticoids: inhibition of NF-kappa B activity through induction of I kappa B synthesis. in Science (New York, N.Y.) 1995
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Human Polyclonal PYCARD Primary Antibody for ICC, IF - ABIN4281803
Yao, Carlson, Sun, Ma, Wolf, Minei, Zang: Mitochondrial ROS Induces Cardiac Inflammation via a Pathway through mtDNA Damage in a Pneumonia-Related Sepsis Model. in PLoS ONE 2015
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Human PYCARD Primary Antibody for ELISA, WB - ABIN645848
Ansari, Dutta, Veettil, Dutta, Iqbal, Kumar, Roy, Chikoti, Singh, Chandran: Herpesvirus Genome Recognition Induced Acetylation of Nuclear IFI16 Is Essential for Its Cytoplasmic Translocation, Inflammasome and IFN-β Responses. in PLoS pathogens 2015
Human Polyclonal PYCARD Primary Antibody for IHC (p), IHC - ABIN257733
Ohtsuka, Ryu, Minamishima, Macip, Sagara, Nakayama, Aaronson, Lee: ASC is a Bax adaptor and regulates the p53-Bax mitochondrial apoptosis pathway. in Nature cell biology 2004
Human Monoclonal PYCARD Primary Antibody for FACS, IHC - ABIN4281806
Peng, French, Tillman, Morgan, French: The inflammasome in alcoholic hepatitis: Its relationship with Mallory-Denk body formation. in Experimental and molecular pathology 2014
Human Polyclonal PYCARD Primary Antibody for WB - ABIN4281797
Siraj, Hussain, Al-Rasheed, Ahmed, Bavi, Alsobhi, Al-Nuaim, Uddin, Al-Kuraya: Demethylation of TMS1 gene sensitizes thyroid cancer cells to TRAIL-induced apoptosis. in The Journal of clinical endocrinology and metabolism 2011
Human Polyclonal PYCARD Primary Antibody for IHC, IHC (fro) - ABIN4281795
Doitsh, Galloway, Geng, Yang, Monroe, Zepeda, Hunt, Hatano, Sowinski, Muñoz-Arias, Greene: Cell death by pyroptosis drives CD4 T-cell depletion in HIV-1 infection. in Nature 2014
ASC contributes to oral cavity squamous cell carcinoma metastasis, and high-level ASC expression is a marker for poor prognosis in OSCC patients
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 抗体) pathway, NLRC3 (显示 NLRC3 抗体) interferes with the assembly and activity of the NALP3 (显示 NLRP3 抗体) inflammasome complex by competing with ASC for pro-caspase-1 (显示 CASP1 抗体) binding
ASC Induces Apoptosis via Activation of Caspase-9 (显示 CASP9 抗体) 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 抗体), TMS1 (显示 SERINC3 抗体) and DAPK (显示 DAPK1 抗体) 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 (显示 USP50 抗体) binds to the ASC protein and subsequently regulates the inflammasome signaling pathway.
ASC self-associates and binds NLRP3 (显示 NLRP3 抗体) 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 抗体) and the ASC inflammasome as key tumor suppressors in AML (显示 RUNX1 抗体).
SGLT-2 (显示 SLC5A2 抗体) inhibition with dapagliflozin reduces the activation of the Nlrp3 (显示 NLRP3 抗体)/ASC (显示 STS 抗体) inflammasome and attenuates the development of diabetic cardiomyopathy in mice with type 2 diabetes. Effects are augmentated of the by DPP4 (显示 DPP4 抗体) inhibitor Saxagliptin.
Elevations of CO2 cause oligomerization of the inflammasome components ASC (显示 STS 抗体), NLRP3 (显示 NLRP3 抗体), caspase 1 (显示 CASP1 抗体), thioredoxin interacting protein (显示 TXNIP 抗体), and calreticulin (显示 CALR 抗体) - a protein from endoplasmic reticulum, leading to IL-1beta (显示 IL1B 抗体) synthesis. An increased production rate of MPs containing elevated amounts of IL-1beta (显示 IL1B 抗体) persists for hours after short-term exposures to elevated CO2
Our cumulative findings indicate that ASC (显示 STS 抗体) suppresses cancer metastasis and progression via the modulation of cytoskeletal remodeling and the Src (显示 SRC 抗体)-caspase-8 (显示 CASP8 抗体) signaling pathway.
these findings suggest that p205 (显示 GNB2L1 抗体) controls expression of Asc (显示 STS 抗体) 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 抗体)-dependent Inflammasomes do not shape the commensal gut (显示 GUSB 抗体) microbiota composition
Our data identify RIPK3 (显示 RIPK3 抗体) and the ASC (显示 STS 抗体) inflammasome as key tumor suppressors in AML (显示 RUNX1 抗体).
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 抗体)) 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 抗体))-dependent stimulation of interleukin-1 beta (IL-1beta (显示 IL1B 抗体)) production.
report herein that lack of ASC (显示 STS 抗体) does not confer preferential protection in response to P. aeruginosa acute infection and that ASC (显示 STS 抗体)(-/-) mice are capable of producing robust amounts of IL-1beta (显示 IL1B 抗体) comparable with C57BL/6 mice
These data identify a novel non-canonical immunoregulatory function of NLRP3 (显示 NLRP3 抗体) and ASC (显示 STS 抗体) 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