The autoimmunity risk variant LYP-W620 cooperates with CSK in the regulation of TCR signaling.
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, whic...
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Public Library of Science (PLoS)
2013-01-01
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Online Access: | http://europepmc.org/articles/PMC3554717?pdf=render |
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author | María Luisa de la Puerta Antonio G Trinidad María del Carmen Rodríguez José María de Pereda Mariano Sánchez Crespo Yolanda Bayón Andrés Alonso |
author_facet | María Luisa de la Puerta Antonio G Trinidad María del Carmen Rodríguez José María de Pereda Mariano Sánchez Crespo Yolanda Bayón Andrés Alonso |
author_sort | María Luisa de la Puerta |
collection | DOAJ |
description | 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. |
first_indexed | 2024-12-21T19:17:13Z |
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institution | Directory Open Access Journal |
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language | English |
last_indexed | 2024-12-21T19:17:13Z |
publishDate | 2013-01-01 |
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spelling | doaj.art-12163d7910a543449746a13f71d307362022-12-21T18:53:02ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0181e5456910.1371/journal.pone.0054569The autoimmunity risk variant LYP-W620 cooperates with CSK in the regulation of TCR signaling.María Luisa de la PuertaAntonio G TrinidadMaría del Carmen RodríguezJosé María de PeredaMariano Sánchez CrespoYolanda BayónAndrés AlonsoThe 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.http://europepmc.org/articles/PMC3554717?pdf=render |
spellingShingle | María Luisa de la Puerta Antonio G Trinidad María del Carmen Rodríguez José María de Pereda Mariano Sánchez Crespo Yolanda Bayón Andrés Alonso The autoimmunity risk variant LYP-W620 cooperates with CSK in the regulation of TCR signaling. PLoS ONE |
title | The autoimmunity risk variant LYP-W620 cooperates with CSK in the regulation of TCR signaling. |
title_full | The autoimmunity risk variant LYP-W620 cooperates with CSK in the regulation of TCR signaling. |
title_fullStr | The autoimmunity risk variant LYP-W620 cooperates with CSK in the regulation of TCR signaling. |
title_full_unstemmed | The autoimmunity risk variant LYP-W620 cooperates with CSK in the regulation of TCR signaling. |
title_short | The autoimmunity risk variant LYP-W620 cooperates with CSK in the regulation of TCR signaling. |
title_sort | autoimmunity risk variant lyp w620 cooperates with csk in the regulation of tcr signaling |
url | http://europepmc.org/articles/PMC3554717?pdf=render |
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