The W620 Polymorphism in PTPN22 Disrupts Its Interaction With Peptidylarginine Deiminase Type 4 and Enhances Citrullination and NETosis
Abstract
A C‐to‐T single‐nucleotide polymorphism (SNP) located at position 1858 of human protein tyrosine phosphatase PTPN22 complementary DNA carries the highest risk of rheumatoid arthritis (RA) among all non‐HLA genetic variants. This C1858T SNP converts an arginine (R620) to a tryptophan (W620), but it is unclear why it has such a strong impact on RA, a disease characterized by anti–citrullinated protein antibodies. The aim of this study was to test the hypothesis that PTPN22 regulates protein citrullination.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Aug 26, 2015
- Source ID
- 10.1002/art.39215
Entities
People
- Anthony P. Nicholas
- Hui‐hsin Chang
- I‐cheng Ho
- Nishant Dwivedi
Organizations
- Harvard Medical School
- United States Department of Defense
- University of Alabama at Birmingham