ArticleThe EMBO journal2001
ShcA tyrosine phosphorylation sites can replace ShcA binding in signalling by middle T-antigen.
Article in The EMBO journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- SRC inhibition enables formation of a growth suppressive MAGI1-PP2A complex in isocitrate dehydrogenase-mutant cholangiocarcinoma.Science translational medicine · 2024Article
- The Shc1 adaptor simultaneously balances Stat1 and Stat3 activity to promote breast cancer immune suppression.Nature communications · 2017Article
- p66Molecular and cellular biology · 2016Article
- Polyomavirus middle T-antigen is a transmembrane protein that binds signaling proteins in discrete subcellular membrane sites.Journal of virology · 2011Article
- Lessons in signaling and tumorigenesis from polyomavirus middle T antigen.Microbiology and molecular biology reviews : MMBR · 2009Review
- Cellular transformation by Simian Virus 40 and Murine Polyoma Virus T antigens.Seminars in cancer biology · 2009Review
- Lessons from polyoma middle T antigen on signaling and transformation: A DNA tumor virus contribution to the war on cancer.Virology · 2009Review
- ShcA signalling is essential for tumour progression in mouse models of human breast cancer.The EMBO journal · 2008Article
- The tyrosine kinase Abl is required for Src-transforming activity in mouse fibroblasts and human breast cancer cells.Oncogene · 2007Article
- p66Shc mediates anoikis through RhoA.The Journal of cell biology · 2007Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ShcA and Grb2 are crucial components in signalling by most tyrosine kinase-associated receptors. How ever, it is not clear whether Grb2 bound directly to the receptor is equivalent to Grb2 associated via ShcA. We have used signalling stimulated by the middle T-antigen (MT) of polyoma virus to address this question. The two known Grb2-binding sites from murine ShcA, 313Y and 239/240YY, could functionally replace the MT ShcA-interacting region in transformation assays using Rat2 fibroblasts. This demonstrates that signal output from membrane-bound ShcA requires only these two sequences and the ShcA-binding site in MT does not recruit other signalling molecules. Two standard Grb2-interacting sequences, either from the EGF receptor or the ShcA 313Y region, could not replace the requirement for ShcA binding to MT, indicating an enhanced role for the ShcA 239/240YY motif. Sos1 and the docking protein Gab1 are brought into the MT complex through Grb2 association and this may be more effective using the 239/240YY sequence.
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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.