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anti-Human PYCARD Antibodies:
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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
Show all 7 Pubmed References
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
Show all 4 Pubmed References
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
Show all 2 Pubmed References
Human Polyclonal PYCARD Primary Antibody for ELISA, WB - ABIN546787
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 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 IF, IHC - ABIN6686098
Wang, Gong, Chen, Xiong, Zhou, Huang, Kong: NLRP3 inflammasome sequential changes in Staphylococcus aureus-induced mouse model of acute rhinosinusitis. in International journal of molecular sciences 2015
Human Polyclonal PYCARD Primary Antibody for IHC, WB - ABIN6672582
Deng, Zou, Xiong, Wang, Engelhardt, Ye, Yan, Qiu: Human Parvovirus Infection of Human Airway Epithelia Induces Pyroptotic Cell Death by Inhibiting Apoptosis. in Journal of virology 2017
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
For the first time, using single-molecule Forster resonance energy transfer, this work studied the relative positions of the CARD and PYD domains of full-length ASC. An unexpectedly large conformational change occurred upon ASC fibrillation, suggesting that the CARD domain folds back onto the PYD domain.
High ASC expression is associated with Gastric Cancer.
Cryo-EM structures of ASC and NLRC4 CARD filaments reveal a unified mechanism of nucleation and activation of caspase-1.
ASC specks as a putative biomarker of pyroptosis in myelodysplastic syndromes
results suggest that ASC, as a negative regulator of the MAVS-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 and phosphor Src.
Data show that in HK-2 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 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 pathway, NLRC3 interferes with the assembly and activity of the NALP3 inflammasome complex by competing with ASC for pro-caspase-1 binding
ASC Induces Apoptosis via Activation of Caspase-9 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, TMS1 and DAPK 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 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 and the ASC inflammasome as key tumor suppressors in AML.
The role of the danger signals ASC and HMGB1 in the Fusobacterium nucleatum infection of gingival epithelial cells.
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
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.
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.
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(-/-)).
oligomerization of ASC creates a multitude of potential caspase-1 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-dependent inflammasome and caspase-3/7 through an ASC-dependent mechanism.
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.
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
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.
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.
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
Our cumulative findings indicate that ASC suppresses cancer metastasis and progression via the modulation of cytoskeletal remodeling and the Src-caspase-8 signaling pathway.
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.
this study shows that ASC-dependent Inflammasomes do not shape the commensal gut microbiota composition
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) 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.
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
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