Browse our anti-PYCARD (PYCARD) Antibodies

Human PYD and CARD Domain Containing (PYCARD) interaction partners

1. results suggest that ASC, as a negative regulator of the MAVS (show MAVS Antibodies)-mediated innate immunity, may play an important role in host protection upon virus infection

2. 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.

3. ASC may be involved in tumor suppression and cell death via Bcl-2 (show BCL2 Antibodies) and phosphor Src (show SRC Antibodies).

4. Data show that in HK-2 (show HK2 Antibodies) 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 (show HK2 Antibodies) cell.

5. 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

6. ASC contributes to oral cavity squamous cell carcinoma metastasis, and high-level ASC expression is a marker for poor prognosis in OSCC patients

7. ASC CpG methylation may prove to be a primary regulator of the pathogenesis of chronic inflammatory diseases such as heart failure.

8. besides its role in the inhibition of the NF-kappaB (show NFKB1 Antibodies) pathway, NLRC3 (show NLRC3 Antibodies) interferes with the assembly and activity of the NALP3 (show NLRP3 Antibodies) inflammasome complex by competing with ASC for pro-caspase-1 (show CASP1 Antibodies) binding

9. ASC Induces Apoptosis via Activation of Caspase-9 (show CASP9 Antibodies) by Enhancing Gap Junction-Mediated Intercellular Communication.(

10. These data revealed that cross-linking of ASC(PYD) filaments via ASC(CARD) mediates the assembly of ASC foci.

Mouse (Murine) PYD and CARD Domain Containing (PYCARD) interaction partners

1. Cl(-) channel-dependent formation of dynamic ASC (show STS Antibodies) oligomers and inflammasome specks that remain inactive in the absence of K(+) efflux. Formed after Cl(-) efflux exclusively, ASC (show STS Antibodies) specks are NLRP3 (show NLRP3 Antibodies) dependent, reversible, and inactive, although they further prime inflammatory responses.

2. we found that butyrate significantly decreased Nlrp3 (show NLRP3 Antibodies) inflammasome formation and activation in the carotid arterial wall of wild type mice (Asc (show STS Antibodies)(+/+)), which was comparable to the effect of gene deletion of the adaptor protein apoptosis-associated speck-like protein gene (Asc (show STS Antibodies)(-/-)).

3. oligomerization of ASC (show STS Antibodies) creates a multitude of potential caspase-1 (show CASP1 Antibodies) activation sites, thus serving as a signal amplification mechanism for inflammasome-mediated cytokine production

4. Collectively, these results are consistent with a model whereby the type III secretion system apparatus of Pseudomonas aeruginosa activates the caspase-1 (show CASP1 Antibodies)-dependent inflammasome and caspase-3 (show CASP3 Antibodies)/7 through an ASC (show STS Antibodies)-dependent mechanism.

5. ASC (show STS Antibodies) 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

6. results suggest that although Pyk2 (show PTK2B Antibodies) and FAK (show PTK2 Antibodies) are involved in inflammasome activation, only Pyk2 (show PTK2B Antibodies) directly phosphorylates ASC (show STS Antibodies) and brings ASC (show STS Antibodies) into an oligomerization-competent state by allowing Tyr146 phosphorylation to participate ASC (show STS Antibodies) speck formation and subsequent NLRP3 (show NLRP3 Antibodies) inflammation.

7. Alendronate (ALN (show TTC21B Antibodies))-augmented IL-1beta (show IL1B Antibodies) production and cell death require Smad3 (show SMAD3 Antibodies) and ASC (show STS Antibodies) activation, and SIS3 and anti-ASC (show STS Antibodies) antibodies may serve as palliative agents for necrotizing inflammatory diseases caused by ALN (show TTC21B Antibodies)

8. These data provide evidence that the inflammasome components ASC (show STS Antibodies), NLRP3 (show NLRP3 Antibodies) and AIM2 (show AIM2 Antibodies) play a role in regulating macrophage adhesion and activation in response to surface nanotopography and chemistry.

9. SGLT-2 (show SLC5A2 Antibodies) inhibition with dapagliflozin reduces the activation of the Nlrp3 (show NLRP3 Antibodies)/ASC (show STS Antibodies) inflammasome and attenuates the development of diabetic cardiomyopathy in mice with type 2 diabetes. Effects are augmentated of the by DPP4 (show DPP4 Antibodies) inhibitor Saxagliptin.

10. Elevations of CO2 cause oligomerization of the inflammasome components ASC (show STS Antibodies), NLRP3 (show NLRP3 Antibodies), caspase 1 (show CASP1 Antibodies), thioredoxin interacting protein (show TXNIP Antibodies), and calreticulin (show CALR Antibodies) - a protein from endoplasmic reticulum, leading to IL-1beta (show IL1B Antibodies) synthesis. An increased production rate of MPs containing elevated amounts of IL-1beta (show IL1B Antibodies) persists for hours after short-term exposures to elevated CO2