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Article

Converging mechanism of UM171 and KBTBD4 neomorphic cancer mutations.

Nature - 1 Mar 2025

Xie Xiaowen, Zhang Olivia, Yeo Megan J R, Lee Ceejay, Tao Ran, Harry Stefan A, Payne N Connor, Nam Eunju, Paul Leena, Li Yiran, Kwok Hui Si, Jiang Hanjie, Mao Haibin, Hadley Jennifer L, Lin Hong, Batts Melissa, Gosavi Pallavi M, D'Angiolella Vincenzo, Cole Philip A, Mazitschek Ralph, Northcott Paul A, Zheng Ning, Liau Brian B

Abstract excerpt

Cancer mutations can create neomorphic protein-protein interactions to drive aberrant function1,2. As a substrate receptor of the CULLIN3-RING E3 ubiquitin ligase complex, KBTBD4 is recurrently mutated in medulloblastoma3, the most common embryonal brain tumour in children4. These mutations impart gain-of-function to KBTBD4 to induce aberrant degradation of the transcriptional corepressor CoREST5. However, their...

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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

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Identifiers

PMID: 39939763
DOI: 10.1038/s41586-024-08533-3
PMCID: PMC11882451

Genes

HDAC1

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