Peptidyl Arginine Deiminase, Type IV (PADI4) ELISA Kits

Human Peptidyl Arginine Deiminase, Type IV (PADI4) interaction partners

1. Molecular interplay between the dimer interface and the substrate-binding site of human PAD4 has been reported.

2. PADI4 may be closely associated with hypoxiainduced autophagy, and the inhibition of hypoxiainduced autophagy by PADI4 knockdown may contribute to an increase in the apoptosis of RAFLS.

3. MiRNA-146a rs2910164 and IRAK1 (show IRAK1 ELISA Kits) rs3027898 polymorphisms were a risk factor for predisposition to Rheumatoid Arthritis in Egyptian Population in codominant and dominant tested inheritance models, while, the miRNA-499 rs3746444 and PADI4 rs1748033 polymorphisms were a risk factor in codominant and recessive one.

4. Meta-analysis indicated a significantly increased association between PADI -104C/T polymorphism and rheumatoid arthritis (RA) in Chinese and Japanese populations (which were the majority of included populations in the analysis).

5. PADI4 interacted with SYVN1 (show SYVN1 ELISA Kits) directly and that overexpression of PADI4 suppressed the ubiquitination of proteins. Thus, a reduction in ER stress induced by PADI4 may abrogate the initiation of chronic RA by suppressing the proliferative signals of RA synoviocytes.

6. mRNA expression of PADI2 (show PADI2 ELISA Kits), PADI4 and Sp1 (show PSG1 ELISA Kits) is upregulated in rheumatoid arthritis bone marrow CD34 (show CD34 ELISA Kits)+ cells independently of the systemic inflammation or treatment regimen.

7. this study in a Southern Mexican population suggests that PADI4 individual polymorphisms and the related susceptibility haplotype (GTG (show GGT1 ELISA Kits)) are also genetic risk markers for rheumatoid arthritis

8. The T allele of PADI4 rs2240340 is associated with Rheumatoid Arthritis in Asians.

9. PADI4 contributes to gastric tumorigenesis by upregulating CXCR2 (show CXCR2 ELISA Kits), KRT14 (show KRT14 ELISA Kits) and TNF-alpha (show TNF ELISA Kits) expression.

10. In this case-control study with sufficient sample size to detect associations, we observed that PADI4 SNPS rs11203367 and rs874881 do not significantly determine RA susceptibility

Mouse (Murine) Peptidyl Arginine Deiminase, Type IV (PADI4) interaction partners

1. PADi4 is critical for neutrophil extracellular traps formation, but is dispensable for generalized citrullination

2. sFlt-1 overexpression in Padi4(-/-) mice resulted in dramatically lower inflammatory and thrombotic response, which was accompanied by significant reduction in pregnancy losses. Inhibition of NETosis may serve as a novel target in disorders of impaired placentation.

3. a role for NETs in cardiac fibrosis and conclude that PAD4 regulates age-related organ fibrosis and dysfunction.

4. PADI4 exacerbates arthritis with diverse immunological modifications.

5. Selective inhibition of peptidylarginine deiminase IV with Cl-amidine blocked NET formation, reduced atherosclerotic lesion area, and delayed time to carotid artery thrombosis in a photochemical injury model.

6. Padi4 is part of the pluripotency transcriptional network, binding to regulatory elements of key stem-cell genes and activating their expression

7. PAD4 regulates the proliferation of multipotent progenitors in the bone marrow by controlling c-myc (show MYC ELISA Kits) expression.

8. PAD4-mediated chromatin decondensation in the neutrophil is crucial for pathological venous thrombosis and present neutrophil activation and PAD4 as potential drug targets for deep vein thrombosis.

9. PAD4 is dispensable in this effector phase model of arthritis

10. analysis of regulation of histone modification and chromatin structure by the p53 (show TP53 ELISA Kits)-PADI4 pathway