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

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

1. Activation of PAD4 by membranolytic insults that result in high levels of intracellular calcium (higher than physiological neutrophil activation) leads to rapid citrullination of p47(phox)/NCF1 and p67(phox)/NCF2, as well as their dissociation from PAD4

2. Required histone citrullination by PAD-4.

3. these findings lead us to conclude that although PAD4 together with CR3-mediated ROS production is required for NET formation in response to A. fumigatus, PAD4-dependent NETosis is not required for A. fumigatus killing either in vitro or during infection.

4. PADI4mediated EMT transition is proposed to represent a novel mechanism underlying the epigenetic and phenotypic alterations in lung cancer cells, and the PADI4 associated signaling pathway may be a therapeutic target for treating lung cancer in a clinical setting.

5. High PADI4 expression is associated with esophageal squamous cell carcinoma tumor growth.

6. these data argue against a major role for PAD4 in neutrophil extracellular trap formation, host defense, or organ injury during pneumonia-derived sepsis

7. Chronic gingival inflammation is associated with increased local citrullination and PAD2 and PAD4 expression in periodontitis.

8. Our findings suggest that PAD4-mediated RGG citrullination plays a key role in protein solubility and amyotrophic lateral sclerosis pathogenesis

9. Study reveals the potential for PAD4-dependant citrullination to drive the progression of CRC liver metastasis.

10. rs1635564 polymorphism is a candidate risk factor for systemic lupus erythematosus, particularly with renal involvement

11. In most rheumatoid arthritis patients, PAD2 and PAD4 are equally efficient in generating citrullinated target sites for anti-citrullinated protein antibodies (ACPAs) in fibrinogen and ENO1. The binding of autoantibodies to histone H3 was generally higher after citrullination with PAD4 than with PAD2. Citrullinated human serum albumin is not a target for ACPAs.

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

13. 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.

14. 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.

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

16. 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).

17. 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.

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

19. 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

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

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

1. Data suggest that mixed lineage kinase domain-like (MLKL) activation leads to loss of intracellular architecture and chromatin decondensation, but peptidylarginine deiminase 4 (PAD4) is only required for the externalization of neutrophil extracellular trap (NET).

2. Our data support the notion that NETs promote atherosclerosis and that the use of specific PAD4 inhibitors may have therapeutic benefits in this potentially devastating condition.

3. Renal proximal tubular PAD4 appears to contribute to ischemic acute kidney injury by promoting renal tubular apoptosis, whereas myeloid-cell PAD4 is preferentially involved in promoting neutrophil infiltration to the kidney and inflammation after renal ischemia/reperfusion.

4. these findings lead us to conclude that although PAD4 together with CR3-mediated ROS production is required for NET formation in response to A. fumigatus, PAD4-dependent NETosis is not required for A. fumigatus killing either in vitro or during infection.

5. these data argue against a major role for PAD4 in neutrophil extracellular trap formation, host defense, or organ injury during pneumonia-derived sepsis

6. Our findings suggest that PAD4-mediated RGG citrullination plays a key role in protein solubility and amyotrophic lateral sclerosis pathogenesis

7. Study reveals the potential for PAD4-dependant citrullination to drive the progression of CRC liver metastasis.

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

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

10. 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.

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

12. PADI4 exacerbates arthritis with diverse immunological modifications.

13. 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.

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

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

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

17. 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.

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

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

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