KATs in the MYST: A New Therapeutic Vulnerability for SETBP1-Mutated Myeloid Malignancies.

Abstract excerpt

Carlson and colleagues demonstrate that SETBP1 mutations promote leukemic self-renewal by recruiting MYST acetyltransferase complexes (KAT7/KAT6A) to chromatin, where H3K14ac and H3K23ac marks are deposited on promoter sites for key stemness genes. Genetic deletion or pharmacologic inhibition of KAT7/KAT6A was shown to shut down this SETBP1-associated self-renewal program and promote myeloid differentiation of...

Topics

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• Carrier Proteins
• SETBP1 gene
• Histone Acetyltransferases
• Leukemia, Myeloid
• Mutation
• Nuclear Proteins