A dominant-negative mutant of mSOS1 inhibits insulin-induced Ras activation and reveals Ras-dependent and -independent insulin signaling pathways.

doi:10.1128/MCB.15.1.379

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Article

A dominant-negative mutant of mSOS1 inhibits insulin-induced Ras activation and reveals Ras-dependent and -independent insulin signaling pathways.

Molecular and cellular biology - 1 Jan 1995

Sakaue M, Bowtell D, Kasuga M

Abstract excerpt

The role of the Grb2-SOS complex in insulin signal transduction was investigated with a deletion mutant of mSOS1 that lacks the guanine nucleotide exchange domain of the wild-type protein. Cells over-expressing either wild-type (CHO-IR/SOS cells) or mutant (CHO-IR/delta SOS cells) mSOS1 were established by transfection of Chinese hamster ovary cells that express human insulin receptors (CHO-IR cells) with the...

Topics

Animals
CHO Cells
Calcium-Calmodulin-Dependent Protein Kinases
Cell Division
Cricetinae
DNA
Enzyme Activation
Genes, Dominant
Glycogen Synthase
Guanine Nucleotide Exchange Factors
Insulin

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Mice

Mutation

Protein Serine-Threonine Kinases

Proteins

Proto-Oncogene Proteins p21(ras)

Receptor, Insulin

Ribosomal Protein S6 Kinases

Source

Open in PubMed Open full text

Identifiers

PMID: 7799946
DOI: 10.1128/MCB.15.1.379
PMCID: PMC231974

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 29 Aug 2026. Prepared record publication-7799946-2026-08-29.1. Manifest publication-graph-cohort-2026-08-29.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 29 Aug 2026.

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