ArticlePloS one2013
The autoimmunity risk variant LYP-W620 cooperates with CSK in the regulation of TCR signaling.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- The phosphatases TCPTP, PTPN22, and SHP1 play unique roles in T cell phosphotyrosine maintenance and feedback regulation of the TCR.Scientific reports · 2025Article
- LYP regulates SLP76 and other adaptor proteins in T cells.Biological research · 2024Article
- SH3-domain mutations selectively disrupt Csk homodimerization or PTPN22 binding.Scientific reports · 2022Article
- Overexpression of theJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- PTPN22 phosphorylation acts as a molecular rheostat for the inhibition of TCR signaling.Science signaling · 2020Article
- Modulation of TCR Signaling by Tyrosine Phosphatases: From Autoimmunity to Immunotherapy.Frontiers in cell and developmental biology · 2020Review
- Non-receptor tyrosine kinase signaling in autoimmunity and therapeutic implications.Pharmacology & therapeutics · 2019Review
- Regulation of CD4Frontiers in immunology · 2019Review
- Protein tyrosine phosphatase non-receptor 22 and C-Src tyrosine kinase genes are down-regulated in patients with rheumatoid arthritis.Scientific reports · 2017Article
- Update on the genetic architecture of rheumatoid arthritis.Nature reviews. Rheumatology · 2017Review
- The role of PTPN22 risk variant in the development of autoimmunity: finding common ground between mouse and human.Journal of immunology (Baltimore, Md. : 1950) · 2015Review
- The role of tyrosine kinases in systemic lupus erythematosus and their potential as therapeutic targets.Expert review of clinical immunology · 2014Review
- Tyrosine phosphatase PTPN22: multifunctional regulator of immune signaling, development, and disease.Annual review of immunology · 2014Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The protein tyrosine phosphatase LYP, a key regulator of TCR signaling, presents a single nucleotide polymorphism, C1858T, associated with several autoimmune diseases such as type I diabetes, rheumatoid arthritis, and lupus. This polymorphism changes an R by a W in the P1 Pro rich motif of LYP, which binds to CSK SH3 domain, another negative regulator of TCR signaling. Based on the analysis of the mouse homologue, Pep, it was proposed that LYP and CSK bind constitutively to inhibit LCK and subsequently TCR signaling. The detailed study of LYP/CSK interaction, here presented, showed that LYP/CSK interaction was inducible upon TCR stimulation, and involved LYP P1 and P2 motifs, and CSK SH3 and SH2 domains. Abrogating LYP/CSK interaction did not preclude the regulation of TCR signaling by these proteins.
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