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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 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 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 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 Polyclonal PYCARD Primary Antibody for ELISA, ICC - ABIN6264533
Wang, Zhang, Meng, Wang, Li, Liu, Liu: Ozone protects the rat lung from ischemia-reperfusion injury by attenuating NLRP3-mediated inflammation, enhancing Nrf2 antioxidant activity and inhibiting apoptosis. in European journal of pharmacology 2018
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
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 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
results suggest that ASC, as a negative regulator of the MAVS (显示 MAVS 抗体)-mediated innate immunity, may play an important role in host protection upon virus infection
PYCARD gene and its transcript variant may play a critical and regulative role in the inflflammatory response of primary gout patients with different phases and Chinese medicine syndromes.
ASC may be involved in tumor suppression and cell death via Bcl-2 (显示 BCL2 抗体) and phosphor Src (显示 SRC 抗体).
Data show that in HK-2 (显示 HK2 抗体) cells and unilateral nephrectomy model, ASC expression level is significantly augmented after treatment with contrast media. Its silencing attenuates contrast-induced apoptosis in HK-2 (显示 HK2 抗体) cell.
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
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.
both Nlrp3 (显示 NLRP3 抗体)(-/-) and Asc (显示 STS 抗体)(-/-) mice showed a strongly improved host defense, as reflected by a markedly reduced mortality rate accompanied by diminished bacterial growth and dissemination.
Cl(-) channel-dependent formation of dynamic ASC (显示 STS 抗体) oligomers and inflammasome specks that remain inactive in the absence of K(+) efflux. Formed after Cl(-) efflux exclusively, ASC (显示 STS 抗体) specks are NLRP3 (显示 NLRP3 抗体) dependent, reversible, and inactive, although they further prime inflammatory responses.
we found that butyrate significantly decreased Nlrp3 (显示 NLRP3 抗体) inflammasome formation and activation in the carotid arterial wall of wild type mice (Asc (显示 STS 抗体)(+/+)), which was comparable to the effect of gene deletion of the adaptor protein apoptosis-associated speck-like protein gene (Asc (显示 STS 抗体)(-/-)).
oligomerization of ASC (显示 STS 抗体) creates a multitude of potential caspase-1 (显示 CASP1 抗体) activation sites, thus serving as a signal amplification mechanism for inflammasome-mediated cytokine production
Collectively, these results are consistent with a model whereby the type III secretion system apparatus of Pseudomonas aeruginosa activates the caspase-1 (显示 CASP1 抗体)-dependent inflammasome and caspase-3 (显示 CASP3 抗体)/7 through an ASC (显示 STS 抗体)-dependent mechanism.
ASC (显示 STS 抗体) 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
results suggest that although Pyk2 (显示 PTK2B 抗体) and FAK (显示 PTK2 抗体) are involved in inflammasome activation, only Pyk2 (显示 PTK2B 抗体) directly phosphorylates ASC (显示 STS 抗体) and brings ASC (显示 STS 抗体) into an oligomerization-competent state by allowing Tyr146 phosphorylation to participate ASC (显示 STS 抗体) speck formation and subsequent NLRP3 (显示 NLRP3 抗体) inflammation.
Alendronate (ALN (显示 TTC21B 抗体))-augmented IL-1beta (显示 IL1B 抗体) production and cell death require Smad3 (显示 SMAD3 抗体) and ASC (显示 STS 抗体) activation, and SIS3 and anti-ASC (显示 STS 抗体) antibodies may serve as palliative agents for necrotizing inflammatory diseases caused by ALN (显示 TTC21B 抗体)
These data provide evidence that the inflammasome components ASC (显示 STS 抗体), NLRP3 (显示 NLRP3 抗体) and AIM2 (显示 AIM2 抗体) play a role in regulating macrophage adhesion and activation in response to surface nanotopography and chemistry.
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.
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