Preferential inhibition of the oncogenic form of RasH by mutations in the GAP binding/"effector" domain.

doi:10.1016/0092-8674(91)90246-u

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Article

Preferential inhibition of the oncogenic form of RasH by mutations in the GAP binding/"effector" domain.

Cell - 8 Feb 1991

Farnsworth C L, Marshall M S, Gibbs J B, Stacey D W, Feig L A

Abstract excerpt

The double mutation, D33H/P34S, reduced the transforming activity of oncogenic RasH proteins, G12V and Q61L, 400- and 20-fold, respectively. Remarkably, this same mutation did not reduce the transforming activity of normal RasH, nor did it impair the ability of the protein to restore a functional...

Topics

Animals
Cell Line
Cell Transformation, Neoplastic
GTP-Binding Proteins
GTPase-Activating Proteins
Guanosine Diphosphate
Guanosine Triphosphate
In Vitro Techniques
Mice
Microinjections
Mutation
Proteins
Proto-Oncogene Proteins p21(ras)
Signal Transduction
Structure-Activity Relationship
ras GTPase-Activating Proteins

Source

Open in PubMed

Identifiers

PMID: 1899358
DOI: 10.1016/0092-8674(91)90246-u

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026. Prepared record publication-1899358-2026-08-30.1. Manifest publication-graph-cohort-2026-08-30.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 30 Aug 2026.

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