Browse our anti-PYCARD (PYCARD) Antibodies

Human PYD and CARD Domain Containing (PYCARD) interaction partners

1. 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.

2. 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

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

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

5. 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 inflammasome complex by competing with ASC for pro-caspase-1 (show CASP1 Antibodies) binding

6. ASC Induces Apoptosis via Activation of Caspase-9 by Enhancing Gap Junction-Mediated Intercellular Communication.(

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

8. Down-regulation of mRNA expression was found in cases in which CASP8 (show CASP8 Antibodies), TMS1 (show SERINC3 Antibodies) and DAPK (show DAPK1 Antibodies) were hypermethylated.

9. loss of ASC driven tumor development is counterbalanced in the identical cell by the inhibition of pro-tumorigenic inflammation in the tumor cell itself

10. the deubiquitinating enzyme USP50 (show USP50 Antibodies) binds to the ASC protein and subsequently regulates the inflammasome signaling pathway.

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

1. 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

2. 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.

3. 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)

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

5. SGLT-2 (show SLC5A2 Antibodies) inhibition with dapagliflozin reduces the activation of the Nlrp3/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.

6. Elevations of CO2 cause oligomerization of the inflammasome components ASC (show STS Antibodies), NLRP3, 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

7. Our cumulative findings indicate that ASC (show STS Antibodies) suppresses cancer metastasis and progression via the modulation of cytoskeletal remodeling and the Src (show SRC Antibodies)-caspase-8 (show CASP8 Antibodies) signaling pathway.

8. these findings suggest that p205 (show GNB2L1 Antibodies) controls expression of Asc (show STS Antibodies) mRNA to regulate inflammasome responses. These findings expand on our understanding of immune-regulatory roles for the PYHIN protein family.

9. this study shows that ASC (show STS Antibodies)-dependent Inflammasomes do not shape the commensal gut (show GUSB Antibodies) microbiota composition

10. Our data identify RIPK3 (show RIPK3 Antibodies) and the ASC (show STS Antibodies) inflammasome as key tumor suppressors in AML (show RUNX1 Antibodies).