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anti-Human PYCARD Anticorps:
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Human Polyclonal PYCARD Primary Antibody pour WB - ABIN610691
Auphan, DiDonato, Rosette, Helmberg, Karin: Immunosuppression by glucocorticoids: inhibition of NF-kappa B activity through induction of I kappa B synthesis. dans Science (New York, N.Y.) 1995
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Human Polyclonal PYCARD Primary Antibody pour 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. dans PLoS ONE 2015
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Human Polyclonal PYCARD Primary Antibody pour 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. dans Nature cell biology 2004
Human Polyclonal PYCARD Primary Antibody pour 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. dans The Journal of clinical endocrinology and metabolism 2011
Human Polyclonal PYCARD Primary Antibody pour 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. dans Nature 2014
Human PYCARD Primary Antibody pour 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. dans PLoS pathogens 2015
Human Monoclonal PYCARD Primary Antibody pour FACS, IHC - ABIN4281806
Peng, French, Tillman, Morgan, French: The inflammasome in alcoholic hepatitis: Its relationship with Mallory-Denk body formation. dans Experimental and molecular pathology 2014
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 (Montrer NFKB1 Anticorps) pathway, NLRC3 (Montrer NLRC3 Anticorps) interferes with the assembly and activity of the NALP3 (Montrer NLRP3 Anticorps) inflammasome complex by competing with ASC for pro-caspase-1 (Montrer CASP1 Anticorps) binding
ASC Induces Apoptosis via Activation of Caspase-9 (Montrer CASP9 Anticorps) 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 (Montrer CASP8 Anticorps), TMS1 (Montrer SERINC3 Anticorps) and DAPK (Montrer DAPK1 Anticorps) 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 (Montrer USP50 Anticorps) binds to the ASC protein and subsequently regulates the inflammasome signaling pathway.
ASC self-associates and binds NLRP3 (Montrer NLRP3 Anticorps) 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 (Montrer RIPK3 Anticorps) and the ASC inflammasome as key tumor suppressors in AML (Montrer RUNX1 Anticorps).
The role of the danger signals ASC and HMGB1 (Montrer HMGB1 Anticorps) in the Fusobacterium nucleatum infection of gingival epithelial cells.
these findings suggest that p205 (Montrer GNB2L1 Anticorps) controls expression of Asc (Montrer STS Anticorps) 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 (Montrer STS Anticorps)-dependent Inflammasomes do not shape the commensal gut (Montrer GUSB Anticorps) microbiota composition
Our data identify RIPK3 (Montrer RIPK3 Anticorps) and the ASC (Montrer STS Anticorps) inflammasome as key tumor suppressors in AML (Montrer RUNX1 Anticorps).
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 (Montrer IL22 Anticorps)) plays a pro-inflammatory/pathogenic role in the onset of antigen-induced arthritis (AIA) through apoptosis-associated speck-like Pycard protein (ASC (Montrer STS Anticorps))-dependent stimulation of interleukin-1 beta (IL-1beta (Montrer IL1B Anticorps)) production.
report herein that lack of ASC (Montrer STS Anticorps) does not confer preferential protection in response to P. aeruginosa acute infection and that ASC (Montrer STS Anticorps)(-/-) mice are capable of producing robust amounts of IL-1beta (Montrer IL1B Anticorps) comparable with C57BL/6 mice
These data identify a novel non-canonical immunoregulatory function of NLRP3 (Montrer NLRP3 Anticorps) and ASC (Montrer STS Anticorps) in autoimmunity.
a significant role for NLRP3 (Montrer NLRP3 Anticorps) and ASC (Montrer STS Anticorps) in prion (Montrer PRNP Anticorps) pathogenesis
ASC (Montrer STS Anticorps)-driven caspase-1 (Montrer CASP1 Anticorps) autoprocessing and speck formation are dispensable for the activation of caspase-1 (Montrer CASP1 Anticorps) and the NLRP1b inflammasome.
IKKalpha (Montrer CHUK Anticorps) controls the inflammasome at the level of the adaptor molecule ASC (Montrer STS Anticorps), which interacts with IKKalpha (Montrer CHUK Anticorps) in the nucleus of resting macrophages in an IKKalpha (Montrer CHUK Anticorps) kinase-dependent manner.
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