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Article

Mutant GNAS drives pancreatic tumourigenesis by inducing PKA-mediated SIK suppression and reprogramming lipid metabolism.

Nature cell biology - 1 Jul 2018

Patra Krushna C, Kato Yasutaka, Mizukami Yusuke, Widholz Sebastian, Boukhali Myriam, Revenco Iulia, Grossman Elizabeth A, Ji Fei, Sadreyev Ruslan I, Liss Andrew S, Screaton Robert A, Sakamoto Kei, Ryan David P, Mino-Kenudson Mari, Castillo Carlos Fernandez-Del, Nomura Daniel K, Haas Wilhelm, Bardeesy Nabeel

Abstract excerpt

G protein αs (GNAS) mediates receptor-stimulated cAMP signalling, which integrates diverse environmental cues with intracellular responses. GNAS is mutationally activated in multiple tumour types, although its oncogenic mechanisms remain elusive. We explored this question in pancreatic tumourigenesis where concurrent GNAS and KRAS mutations characterize pancreatic ductal adenocarcinomas (PDAs) arising from...

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Share to Carcinoma, Pancreatic Ductal
Share to Cellular Reprogramming

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Cyclic AMP-Dependent Protein Kinases

Share to Enzyme Repression

Share to GTP-Binding Protein alpha Subunits, Gs

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Source

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Identifiers

PMID: 29941929
DOI: 10.1038/s41556-018-0122-3
PMCID: PMC6044476

Genes

GNAS
KRAS

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Mutant GNAS drives pancreatic tumourigenesis by inducing PKA-mediated SIK suppression and reprogramming lipid metabolism.PMID 29941929Read ↗

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Mutant GNAS limits tumor aggressiveness in established pancreatic cancer via antagonizing the KRAS-pathway.Semantic proximity Read ↗

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Oncogenic GNAS uses PKA-dependent and independent mechanisms to induce cell proliferation in human pancreatic ductal and acinar organoidsSemantic proximity Read ↗

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