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Article

Gatekeeper mutations activate FGF receptor tyrosine kinases by destabilizing the autoinhibited state.

Proceedings of the National Academy of Sciences of the United States of America - 21 Feb 2023

Besch Alida, Marsiglia William M, Mohammadi Moosa, Zhang Yingkai, Traaseth Nathaniel J

Abstract excerpt

Many types of human cancers are being treated with small molecule ATP-competitive inhibitors targeting the kinase domain of receptor tyrosine kinases. Despite initial successful remission, long-term treatment almost inevitably leads to the emergence of drug resistance mutations at the gatekeeper residue hindering the access of the inhibitor to a hydrophobic pocket at the back of the ATP-binding cleft. In addition...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 36791110
DOI: 10.1073/pnas.2213090120
PMCID: PMC9974468

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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