ArticleOncogene2001
Key role of Shc signaling in the transforming pathway triggered by Ret/ptc2 oncoprotein.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- ERK Signaling in Thyroid Cancer: Lineage Suppression, Epigenetic Reprogramming, and Theranostic Reversal.Cancers · 2026Review
- Ret signaling in ureteric bud epithelial cells controls cell movements, cell clustering and bud formation.Development (Cambridge, England) · 2021Article
- Kinase gene fusions: roles and therapeutic value in progressive and refractory papillary thyroid cancer.Journal of cancer research and clinical oncology · 2021Review
- Targeting the Shc-EGFR interaction with indomethacin inhibits MAP kinase pathway signalling.Cancer letters · 2019Article
- Proteomic detection of a large amount of SCGFα in the stroma of GISTs after imatinib therapy.Journal of translational medicine · 2011Article
- Screening for PTB domain binding partners and ligand specificity using proteome-derived NPXY peptide arrays.Molecular and cellular biology · 2006Article
- Induction of a proinflammatory program in normal human thyrocytes by the RET/PTC1 oncogene.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Disruption of the Shc/Grb2 complex during abelson virus transformation affects proliferation, but not apoptosis.Journal of virology · 2005Article
- Differential requirement of Tyr1062 multidocking site by RET isoforms to promote neural cell scattering and epithelial cell branching.Oncogene · 2004Article
- Article
- Nuclear envelope irregularity is induced by RET/PTC during interphase.The American journal of pathology · 2003Article
- RET/PTC-induced dedifferentiation of thyroid cells is mediated through Y1062 signaling through SHC-RAS-MAP kinase.Oncogene · 2003Article
- Article
- Biological activity of the thyroid TRK-T3 oncogene requires signalling through Shc.British journal of cancer · 2002Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RET/PTC oncogenes, generated by chromosomal rearrangements in papillary thyroid carcinomas, are constitutively activated versions of protoRET, a gene encoding two protein isoforms of a transmembrane tyrosine kinase receptor. By using Ret/ptc2 short isoform (iso9), we have previously demonstrated that Tyr586 (Tyr1062 of protoRet) is the docking site for both the PTB and the SH2 domains of Shc. To determine the relevance of this interaction for the transforming activity of Ret/ptc oncogenes, we have generated and characterized novel Ret/ptc mutants unable to activate Shc: Ret/ptc2 long isoform (iso51)-Y586F and both isoforms of Ret/ptc2-N583A. These mutants neither activate Shc nor transform NIH3T3 cells. Since Tyr1062 shows features of a multifunctional docking site, we have used a Shc mutant (Shc Y317F) to directly assess Shc role. We have demonstrated that in our cell system Shc Y317F behaves like a dominant interfering mutant on the activation of the Grb2-Sos pathway by endogenous Shc triggered by Ret/ptc2. A strong reduction of the transforming activity of Ret/ptc2 in presence of this mutant was also demonstrated. Our data suggest that Shc activation play a key role in the transforming pathways triggered by Ret/ptc oncoproteins. Moreover, we have shown that coexpression of the Shc-Y317F mutant with Ret/ptc2 specifically causes apoptosis, and that the surviving cells lose the long-term expression of one of the two genes.
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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.