Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q Exactive
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): Cell Culture, Fibroblast, Embryonic Stem Cell
SUBMITTER: Witold Szymanski
LAB HEAD: Gerhard Mittler
PROVIDER: PXD008539 | Pride | 2019-08-16
REPOSITORIES: Pride
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2015_01_AcIP_rev_1_01.raw | Raw | |||
2015_01_AcIP_rev_1_02.raw | Raw |
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Nature cell biology 20191001 10
While nuclear lamina abnormalities are hallmarks of human diseases, their interplay with epigenetic regulators and precise epigenetic landscape remain poorly understood. Here, we show that loss of the lysine acetyltransferase MOF or its associated NSL-complex members KANSL2 or KANSL3 leads to a stochastic accumulation of nuclear abnormalities with genomic instability patterns including chromothripsis. SILAC-based MOF and KANSL2 acetylomes identified lamin A/C as an acetylation target of MOF. HDA ...[more]