anti-Peptidyl Arginine Deiminase, Type IV (PADI4) Antibodies

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 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. our meta-analysis demonstrated that the PADI4_94 polymorphisms might contribute to RA susceptibility especially in Asian populations but not in Caucasian populations.

5. 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).

6. PADI4 interacted with SYVN1 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.

7. mRNA expression of PADI2, PADI4 and Sp1 is upregulated in rheumatoid arthritis bone marrow CD34+ cells independently of the systemic inflammation or treatment regimen.

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

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

10. PADI4 contributes to gastric tumorigenesis by upregulating CXCR2, KRT14 and TNF-alpha expression.

11. 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

12. SNPs of PADI4 may be a risk factor for airway abnormalities in RA.

13. this meta-analysis suggested that PADI4 -92C/G polymorphism may be associated with the rheumatoid arthritis incidence in the Chinese population, especially for South China. Further studies conducted on other ethnic groups are required for definite conclusions.

14. PADI4 contributes to the pathogenesis of RA by protecting FLSs from apoptosis. PADI4 suppresses p21 transcription through altering histone H3 arginine modifications on p21 promoter region.

15. Proteolysis by granzyme B enhances presentation of autoantigenic PAD4 epitopes in rheumatoid arthritis.

16. No associations were found between clinical subtypes of JIA and PADI4 allele frequency. rs2240337 in the PADI4 gene was significantly associated with anti-cyclic citrullinated peptide antibody-positivity in juvenile idiopathic arthritis.

17. The effect of the PADI4-104C/T polymorphism on RA risk in the Chinese population was evaluated in a meta-analysis. The overall analysis indicated a significant association between the PADI4-104C/T polymorphism and RA risk in the Chinese population (T vs C: OR = 1.45, 95%CI = 1.18-1.78; TT vs CC: OR = 1.49, 95%CI = 1.24-1.80; TT vs CC+CT: OR = 1.28, 95%CI = 1.08-1.51; TT+CT vs CC: OR = 1.75, 95%CI = 1.30-2.37).

18. Overexpression of PAD4 constrains the activity of EMT via suppressing Elk1 expression.

19. Our study also demonstrated that PADI4 contributes to tumor metastasis by regulating the gene expression of insulin-like growth factor 1 (IGF1) and WAS/WASL-interacting protein family member 1 (WIPF1).

20. PAD4 levels were significantly higher in patients with rheumatoid arthritis than in patients with systemic lupus erythematosis or healthy controls. Anti-PAD4 antibodies were detected in 30% of patients with rheumatoid arthritis, but not in patients with SLE, systemic sclerosis or controls.

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

1. PAD4 in neutrophils is essential for kidney NET formation and ischemic kidney injury.

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

3. 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.

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

5. PADI4 exacerbates arthritis with diverse immunological modifications.

6. 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.

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

8. PAD4 regulates the proliferation of multipotent progenitors in the bone marrow by controlling c-myc expression.

9. peptidyl-arginine deiminases inhibiion reverses protein-hypercitrullination and disease in mouse models of multiple sclerosis.

10. 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.

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

12. analysis of regulation of histone modification and chromatin structure by the p53-PADI4 pathway

13. An increase in citrullinated proteins resulting from increased PAD2 and 4 is an important change in the pathogenesis of multiple sclerosis.