ArticleBritish journal of cancer2002
Biological activity of the thyroid TRK-T3 oncogene requires signalling through Shc.
Article in British journal of cancer, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 28 citations in OpenAlex.
- TRK-T3 condensate organization drives growth signaling.Life science alliance · 2026Article
- Pyrazolo[1,5-Molecules (Basel, Switzerland) · 2024Review
- Design, synthesis and biological evaluation of pyrazolo[3,4-RSC medicinal chemistry · 2023Article
- Efficacy and safety of larotrectinib in patients with TRK fusion-positive thyroid carcinoma.European journal of endocrinology · 2022Article
- Development of small-molecule tropomyosin receptor kinase (TRK) inhibitors forActa pharmaceutica Sinica. B · 2021Review
- Insights into Current Tropomyosin Receptor Kinase (TRK) Inhibitors: Development and Clinical Application.Journal of medicinal chemistry · 2019Article
- TRKing down an old oncogene in a new era of targeted therapy.Cancer discovery · 2015Review
- Article
- An in vivo functional genetic screen reveals a role for the TRK-T3 oncogene in tumor progression.Oncogene · 2004Article
- Article
- Oncogenic targeting of an activated tyrosine kinase to the Golgi apparatus in a glioblastoma.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The thyroid TRK-T3 oncogene, produced by a chromosomal translocation, is a chimeric, constitutively activated version of the NTRK1/NGF receptor and it is able to transform NIH3T3 cells and differentiate PC12 cells. TRK-T3 oncoprotein triggers multiple signal transduction pathways. Among others, TRK-T3 binds and phosphorylates the Shc and SNT1/FRS2 adaptor proteins both involved in coupling the receptor tyrosine kinase to the mitogen-activated protein kinase pathway by recruiting Grb2/SOS. We were interested in defining the role of Shc in the oncogenesis by TRK-T3. The mutation of TRK-T3 tyrosine 291, docking site for both Shc and FRS2, abrogates the oncogene biological activity. To directly explore the role of Shc we used the ShcY317F mutant, which carries the mutation of a tyrosine residue involved in Grb2 recruitment. We demonstrated that the ShcY317F mutant exerts an inhibitory effect on TRK-T3 transforming activity. Such effect can be modulated by the amount of ShcY317F protein and affects the viability of cells expressing TRK-T3 by means of a mechanism involving apoptosis. Our results indicate a definitive role of the adaptor protein Shc in TRK-T3 transforming activity.
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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.