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Cold Spring Harb Perspect Med. 2017 Jan 3;7(1). pii: a026443. doi: 10.1101/cshperspect.a026443.

Oncogenic Mechanisms of Histone H3 Mutations.

Author information

1
Laboratory of Chromatin Biology and Epigenetics, The Rockefeller University, New York, New York 10065.

Abstract

Recurrent missense mutations in histone H3 were recently reported in pediatric gliomas and soft tissue tumors. Strikingly, these mutations only affected a minority of the total cellular H3 proteins and occurred at or near lysine residues at positions 27 and 36 on the amino-terminal tail of H3 that are subject to well-characterized posttranslational modifications. Here we review recent progress in elucidating the mechanisms by which these mutations perturb the chromatin landscape in cells through their effects on chromatin-modifying machinery, particularly through inhibition of specific histone lysine methyltransferases. One common feature of histone mutations is their ability to arrest cells in a primitive state refractory to differentiation induction, highlighting the importance of studying these mutations in their proper developmental context.

PMID:
27864305
PMCID:
PMC5204328
DOI:
10.1101/cshperspect.a026443
[Indexed for MEDLINE]
Free PMC Article

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