The Grb2 splice variant, Grb3-3, is a negative regulator of RAS activation

Caroline Seiler; Amy K. Stainthorp; Sophie Ketchen; Christopher M. Jones; Kate Marks; Philip Quirke; John E. Ladbury

doi:10.1038/s42003-022-03985-7

Communications Biology (Sep 2022)

The Grb2 splice variant, Grb3-3, is a negative regulator of RAS activation

Caroline Seiler,
Amy K. Stainthorp,
Sophie Ketchen,
Christopher M. Jones,
Kate Marks,
Philip Quirke,
John E. Ladbury

Affiliations

Caroline Seiler: School of Molecular and Cellular Biology, University of Leeds
Amy K. Stainthorp: School of Molecular and Cellular Biology, University of Leeds
Sophie Ketchen: School of Molecular and Cellular Biology, University of Leeds
Christopher M. Jones: School of Molecular and Cellular Biology, University of Leeds
Kate Marks: University of Leeds School of Medicine, Leeds Institute of Medical Research, Pathology and Data Analytics, University of Leeds
Philip Quirke: University of Leeds School of Medicine, Leeds Institute of Medical Research, Pathology and Data Analytics, University of Leeds
John E. Ladbury: School of Molecular and Cellular Biology, University of Leeds

DOI: https://doi.org/10.1038/s42003-022-03985-7
Journal volume & issue: Vol. 5, no. 1
pp. 1 – 12

Abstract

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The Grb2 splice variant Grb3-3 results in decreased activation of the Ras-MAPK pathway due competition with Grb2 for SOS binding, with reduced Grb3-3 levels observed in tumour tissue suggestive of a mechanism for enhancing Ras pathway activity.

Published in Communications Biology

ISSN: 2399-3642 (Online)
Publisher: Nature Portfolio
Country of publisher: United Kingdom
LCC subjects: Science: Biology (General)
Website: https://www.nature.com/commsbio/

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