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Article

FOXL2 posttranslational modifications mediated by GSK3β determine the growth of granulosa cell tumours.

Nature communications - 1 Jan 2014

Kim Jae-Hong, Kim Yong-Hak, Kim Hong-Man, Park Ho-Oak, Ha Nam-Chul, Kim Tae Heon, Park Mira, Lee Kangseok, Bae Jeehyeon

Abstract excerpt

Approximately 97% of patients with ovarian granulosa cell tumours (GCTs) bear the C134W mutation in FOXL2; however, the pathophysiological mechanism of this mutation is unknown. Here we report how this mutation affects GCT development. Sequential posttranslational modifications of the C134W mutant occur where hyperphosphorylation at serine 33 (S33) by GSK3β induces MDM2-mediated ubiquitination and proteasomal...

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Source

Identifiers

PMID: 24390485
DOI: 10.1038/ncomms3936

Genes

FOXL2
MDM2

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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FOXL2 posttranslational modifications mediated by GSK3β determine the growth of granulosa cell tumours.PMID 24390485Read ↗

The Oncogenic FOXL2 C134W Mutation Is a Key Driver of Granulosa Cell Tumors.Semantic proximity Read ↗

FOXO1 mitigates the SMAD3/FOXL2 <sup>C134W</sup> Transcriptomic Effect in a Model of Human Adult Granulosa Cell TumorSemantic proximity Read ↗

FOXO1 mitigates the SMAD3/FOXL2C134W transcriptomic effect in a model of human adult granulosa cell tumor.Semantic proximity Read ↗

Impact of FOXL2 mutations on signaling in ovarian granulosa cell tumors.Semantic proximity Read ↗

SMAD3 Activation: A Converging Point of Dysregulated TGF-Beta Superfamily Signaling and Genetic Aberrations in Granulosa Cell Tumor Development?Semantic proximity Read ↗

Identification and Validation of Differential Phosphorylation Sites of the Nuclear FOXL2 Protein as Potential Novel Biomarkers for Adult-Type Granulosa Cell Tumors.Semantic proximity Read ↗

Mutant FOXL2C134W Hijacks SMAD4 and SMAD2/3 to Drive Adult Granulosa Cell Tumors.Semantic proximity Read ↗

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