Dominant Gα mutations in human disease: unifying mechanisms and treatment strategies.

doi:10.1038/s44321-025-00274-8

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Back to search

Article

Dominant Gα mutations in human disease: unifying mechanisms and treatment strategies.

EMBO molecular medicine - 1 Sept 2025

Katanaev Vladimir L, Solis Gonzalo P

Abstract excerpt

Sixteen Gα-subunits transduce hundreds of G protein-coupled receptors and control countless cellular activities. Mutations in respective GNA genes underlie developmental, oncological, metabolic, neurological, and other pathologies. In addition to classical loss-of-function (LOF) and gain-of-function (GOF) mutations (the former represented by gene deletions/truncations, the latter by specific GTP...

Topics

Humans
GTP-Binding Protein alpha Subunits
Mutation
Mutation, Missense

Source

Open in PubMed Open full text

Identifiers

PMID: 40745211
DOI: 10.1038/s44321-025-00274-8
PMCID: PMC12423288

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026.

Community interpretation

Discuss the evidence

Ask a question, add context or challenge an interpretation. Community activity is separate from scientific evidence strength.

discussions

replies

Citations encouraged

Claims remain attributable.

No discussion yet

Be the first to add a careful, cited interpretation.

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics