ArticleMolecular and cellular biology2005
Removal of C-terminal SRC kinase from the immune synapse by a new binding protein.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- G3BP1 is a SWI/SNF-bound regulator of transcription that modulates activation of STATs.Bioscience reports · 2026Article
- PTPN22 phosphorylation acts as a molecular rheostat for the inhibition of TCR signaling.Science signaling · 2020Article
- PAG--a multipurpose transmembrane adaptor protein.Oncogene · 2014Review
- G3BP1, G3BP2 and CAPRIN1 are required for translation of interferon stimulated mRNAs and are targeted by a dengue virus non-coding RNA.PLoS pathogens · 2014Article
- DUSP3/VHR is a pro-angiogenic atypical dual-specificity phosphatase.Molecular cancer · 2014Article
- Hepatitis C virus co-opts Ras-GTPase-activating protein-binding protein 1 for its genome replication.Journal of virology · 2011Article
- Regulation of T cell receptor signaling by activation-induced zinc influx.The Journal of experimental medicine · 2011Article
- Autoimmune-associated PTPN22 R620W variation reduces phosphorylation of lymphoid phosphatase on an inhibitory tyrosine residue.The Journal of biological chemistry · 2010Article
- Identification of a Sam68 ribonucleoprotein complex regulated by epidermal growth factor.The Journal of biological chemistry · 2009Article
- An adaptor role for cytoplasmic Sam68 in modulating Src activity during cell polarization.Molecular and cellular biology · 2009Article
- Identification of c-Src tyrosine kinase substrates using mass spectrometry and peptide microarrays.Journal of proteome research · 2008Article
- Distinct structural features of caprin-1 mediate its interaction with G3BP-1 and its induction of phosphorylation of eukaryotic translation initiation factor 2alpha, entry to cytoplasmic stress granules, and selective interaction with a subset of mRNAs.Molecular and cellular biology · 2007Article
- A molecular-properties-based approach to understanding PDZ domain proteins and PDZ ligands.Genome research · 2006Article
- Lipid raft targeting of hematopoietic protein tyrosine phosphatase by protein kinase C theta-mediated phosphorylation.Molecular and cellular biology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
The Csk tyrosine kinase negatively regulates the Src family kinases Lck and Fyn in T cells. Engagement of the T-cell antigen receptor results in a removal of Csk from the lipid raft-associated transmembrane protein PAG/Cbp. Instead, Csk becomes associated with an approximately 72-kDa tyrosine-phosphorylated protein, which we identify here as G3BP, a phosphoprotein reported to bind the SH3 domain of Ras GTPase-activating protein. G3BP reduced the ability of Csk to phosphorylate Lck at Y505 by decreasing the amount of Csk in lipid rafts. As a consequence, G3BP augmented T-cell activation as measured by interleukin-2 gene activation. Conversely, elimination of endogenous G3BP by RNA interference increased Lck Y505 phosphorylation and reduced TCR signaling. In antigen-specific T cells, endogenous G3BP moved into a intracellular location adjacent to the immune synapse, but deeper inside the cell, upon antigen recognition. Csk colocalization with G3BP occurred in this "parasynaptic" location. We conclude that G3BP is a new player in T-cell-antigen receptor signaling and acts to reduce the amount of Csk in the immune synapse.
Indexed as
Identifiers
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.