ArticleOncogene2005
Cooperation and selectivity of the two Grb2 binding sites of p52Shc in T-cell antigen receptor signaling to Ras family GTPases and Myc-dependent survival.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- CSF1R-CAR T cells induce CSF1R signaling and can promote target cell proliferation.Science signaling · 2025Article
- A streamlined tandem tip-based workflow for sensitive nanoscale phosphoproteomics.Communications biology · 2023Article
- Current understanding of CTLA-4: from mechanism to autoimmune diseases.Frontiers in immunology · 2023Review
- ShcA regulates thymocyte proliferation through specific transcription factors and a c-Abl-dependent signaling axis.Molecular and cellular biology · 2015Article
- microRNAs regulate cell-to-cell variability of endogenous target gene expression in developing mouse thymocytes.PLoS genetics · 2015Article
- TRIM31 is downregulated in non-small cell lung cancer and serves as a potential tumor suppressor.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- The ShcA SH2 domain engages a 14-3-3/PI3'K signaling complex and promotes breast cancer cell survival.Oncogene · 2012Article
- Molecular basis of signaling specificity of insulin and IGF receptors: neglected corners and recent advances.Frontiers in endocrinology · 2012Article
- Amelioration of central cardiovascular regulatory dysfunction by tropomyocin receptor kinase B in a mevinphos intoxication model of brain stem death.British journal of pharmacology · 2011Article
- Adaptor protein Shc acts as an immune-regulator for the LPS-stimulated maturation of bone marrow-derived dendritic cells.BMC immunology · 2011Article
- Recruitment of Pyk2 to SHPS-1 signaling complex is required for IGF-I-dependent mitogenic signaling in vascular smooth muscle cells.Cellular and molecular life sciences : CMLS · 2010Article
- Glycoprotein capture and quantitative phosphoproteomics indicate coordinated regulation of cell migration upon lysophosphatidic acid stimulation.Molecular & cellular proteomics : MCP · 2010Article
- The PTB domain of ShcA couples receptor activation to the cytoskeletal regulator IQGAP1.The EMBO journal · 2010Article
- Intraflagellar transport is required for polarized recycling of the TCR/CD3 complex to the immune synapse.Nature cell biology · 2009Article
- The adaptor protein Shc plays a key role during early B cell development.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- p66shc negatively regulates insulin-like growth factor I signal transduction via inhibition of p52shc binding to Src homology 2 domain-containing protein tyrosine phosphatase substrate-1 leading to impaired growth factor receptor-bound protein-2 membrane recruitment.Molecular endocrinology (Baltimore, Md.) · 2008Article
- P-selectin activates integrin-mediated colon carcinoma cell adhesion to fibronectin.Experimental cell research · 2006Article
- ShcA mediates the dominant pathway to extracellular signal-regulated kinase activation during early thymic development.Molecular and cellular biology · 2006Article
- Direct inhibition of T-lymphocyte activation by anthrax toxins in vivo.Infection and immunity · 2005Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shc proteins participate in a variety of processes regulating cell proliferation, survival and apoptosis. The two ubiquitously expressed isoforms, p52Shc/p46Shc, couple tyrosine kinase receptors to Ras by recruiting Grb2/Sos complexes to a membrane-proximal localization. Tyrosine residues 239/240 and 317 become phosphorylated following receptor engagement and, as such, form two Grb2 binding sites, which have been proposed to be differentially coupled to Myc-dependent survival and to fos-dependent proliferation, respectively. Here, we have addressed the individual function of YY239/240 and Y317 in T-cell antigen receptor (TCR) signaling. We show that p52Shc is phosphorylated on both YY239/240 and Y317 following TCR engagement. Mutation of either YY239/240 or Y317 results in impaired interaction with Grb2 and inhibition of Ras/MAP kinase activation and CD69 induction, supporting a role for both Grb2 binding sites in this function. Substitution of either YY239/240 or Y317 also results in a defective activation of Rac and the coupled stress kinases JNK and p38. Furthermore, mutation of Y317 or, to a larger extent, of YY239/240, results in increased activation-induced cell death, which in cells expressing the FF239/240 mutant is accompanied by impaired TCR-dependent c-myc transcription. The data underline a pleiotropic and nonredundant role of Shc, mediated by both YY239/240 and Y317, in T-cell activation and survival.
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