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PADI4 is a member of a gene family which encodes enzymes responsible for the conversion of arginine residues to citrulline residues. Zusätzlich bieten wir Ihnen PADI4 Kits (15) und PADI4 Proteine (13) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 109 products:
Human Polyclonal PADI4 Primary Antibody für ELISA, WB - ABIN250318
Wang, Wysocka, Sayegh, Lee, Perlin, Leonelli, Sonbuchner, McDonald, Cook, Dou, Roeder, Clarke, Stallcup, Allis, Coonrod: Human PAD4 regulates histone arginine methylation levels via demethylimination. in Science (New York, N.Y.) 2004
Show all 2 Pubmed References
Cow (Bovine) Polyclonal PADI4 Primary Antibody für WB - ABIN2785937
Costenbader, Chang, De Vivo, Plenge, Karlson: Genetic polymorphisms in PTPN22, PADI-4, and CTLA-4 and risk for rheumatoid arthritis in two longitudinal cohort studies: evidence of gene-environment interactions with heavy cigarette smoking. in Arthritis research & therapy 2008
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.
PADI4 contributes to the pathogenesis of RA by protecting FLSs from apoptosis. PADI4 suppresses p21 (zeige CDKN1A Antikörper) transcription through altering histone H3 (zeige HIST3H3 Antikörper) arginine modifications on p21 (zeige CDKN1A Antikörper) promoter region.
Proteolysis by granzyme B (zeige Gzmb Antikörper) enhances presentation of autoantigenic PAD4 epitopes in rheumatoid arthritis.
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.
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).
Overexpression of PAD4 constrains the activity of EMT (zeige ITK Antikörper) via suppressing Elk1 (zeige ELK1 Antikörper) expression.
Our study also demonstrated that PADI4 contributes to tumor metastasis by regulating the gene expression of insulin-like growth factor 1 (IGF1 (zeige IGF1 Antikörper)) and WAS/WASL-interacting protein family member 1 (WIPF1 (zeige WIPF1 Antikörper)).
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.
This meta-analysis showed that the PADI4 -94G/A variants may influence RA risk in the Chinese population.
The results highlight an association between PAD4 and DNA hypermethylation in acute promyelocytic leukemia (zeige PML Antikörper) and demonstrate that targeting PAD4 or regulating its downstream effectors may be a promising strategy to control differentiation in the clinic.
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.
a role for NETs in cardiac fibrosis and conclude that PAD4 regulates age-related organ fibrosis and dysfunction.
PADI4 exacerbates arthritis with diverse immunological modifications.
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.
Padi4 is part of the pluripotency transcriptional network, binding to regulatory elements of key stem-cell genes and activating their expression
PAD4 regulates the proliferation of multipotent progenitors in the bone marrow by controlling c-myc (zeige MYC Antikörper) expression.
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.
PAD4 is dispensable in this effector phase model of arthritis
analysis of regulation of histone modification and chromatin structure by the p53 (zeige TP53 Antikörper)-PADI4 pathway
An increase in citrullinated proteins resulting from increased PAD2 and 4 is an important change in the pathogenesis of multiple sclerosis.
This gene is a member of a gene family which encodes enzymes responsible for the conversion of arginine residues to citrulline residues. This gene may play a role in granulocyte and macrophage development leading to inflammation and immune response.
peptidyl arginine deiminase, type IV
, protein-arginine deiminase type-4-like
, HL-60 PAD
, PADI-H protein
, peptidyl arginine deiminase, type V
, protein-arginine deiminase type IV
, protein-arginine deiminase type-4
, PAD type IV
, peptidylarginine deiminase IV
, peptidyl arginine deiminase, type 4
, peptidylarginine deiminase type alpha