ArticleMolecular cell2007
A phosphatase activity of Sts-1 contributes to the suppression of TCR signaling.
Article in Molecular cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
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Who cites it
75 citing papers in PubMed, 121 citations in OpenAlex.
- Suppressor of TCR signaling 2 (Sts-2) as a potential immunotherapy target and prognostic biomarker in cervical cancer.Journal of gynecologic oncology · 2026Article
- FCRL3 is an immunoregulatory receptor that restrains the activation of human memory T lymphocytes.The Journal of experimental medicine · 2026Article
- Exploring UBASH3A: from immune regulation to autoimmune diseases.Journal of translational medicine · 2025Review
- STS2 deficiency revives CD8Journal for immunotherapy of cancer · 2025Article
- Roles of TULA-family proteins in T cells and autoimmune diseases.Genes and immunity · 2025Review
- CD6 regulates CD4 T follicular helper cell differentiation and humoral immunity during murine coronavirus infection.Journal of virology · 2025Article
- Focusing on CD8Journal of experimental & clinical cancer research : CR · 2024Review
- CD6 Regulates CD4 T Follicular Helper Cell Differentiation and Humoral Immunity During Murine Coronavirus Infection.bioRxiv : the preprint server for biology · 2024Article
- Role of Tula-Family Proteins in Cell Signaling and Activation: Advances and Challenges.International journal of molecular sciences · 2024Article
- FLI1 induces erythroleukemia through opposing effects on UBASH3A and UBASH3B expression.BMC cancer · 2024Article
- Rebamipide and Derivatives are Potent, Selective Inhibitors of Histidine Phosphatase Activity of the Suppressor of T Cell Receptor Signaling Proteins.Journal of medicinal chemistry · 2024Article
- Cbl-b mitigates the responsiveness of naive CD8Science signaling · 2024Article
- How protons pave the way to aggressive cancers.Nature reviews. Cancer · 2023Review
- Inactivation of the Sts enzymes promotes resistance to lethalInfection and immunity · 2023Article
- STS-1 and STS-2, Multi-Enzyme Proteins Equipped to Mediate Protein-Protein Interactions.International journal of molecular sciences · 2023Review
- TULA Proteins in Men, Mice, Hens, and Lice: Welcome to the Family.International journal of molecular sciences · 2023Review
- The Sts Proteins: Modulators of Host Immunity.International journal of molecular sciences · 2023Review
- STS1 and STS2 Phosphatase Inhibitor Baicalein Enhances the Expansion of Hematopoietic and Progenitor Stem Cells and Alleviates 5-Fluorouracil-Induced Myelosuppression.International journal of molecular sciences · 2023Article
- T-helper cells flexibility: the possibility of reprogramming T cells fate.Frontiers in immunology · 2023Review
- TULA-Family Regulators of Platelet Activation.International journal of molecular sciences · 2022Review
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Precise signaling by the T cell receptor (TCR) is crucial for a proper immune response. To ensure that T cells respond appropriately to antigenic stimuli, TCR signaling pathways are subject to multiple levels of regulation. Sts-1 negatively regulates signaling pathways downstream of the TCR by an unknown mechanism(s). Here, we demonstrate that Sts-1 is a phosphatase that can target the tyrosine kinase Zap-70 among other proteins. The X-ray structure of the Sts-1 C terminus reveals that it has homology to members of the phosphoglycerate mutase/acid phosphatase (PGM/AcP) family of enzymes, with residues known to be important for PGM/AcP catalytic activity conserved in nature and position in Sts-1. Point mutations that impair Sts-1 phosphatase activity in vitro also impair the ability of Sts-1 to regulate TCR signaling in T cells. These observations reveal a PGM/AcP-like enzyme activity involved in the control of antigen receptor signaling.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.