| Literature DB >> 25411247 |
Satoshi Ito1, Sayuri Horikawa1, Tateki Suzuki2, Hiroki Kawauchi2, Yoshikazu Tanaka3, Takeo Suzuki1, Tsutomu Suzuki4.
Abstract
Human N-acetyltransferase 10 (NAT10) is known to be a lysine acetyltransferase that targets microtubules and histones and plays an important role in cell division. NAT10 is highly expressed in malignant tumors, and is also a promising target for therapies against laminopathies and premature aging. Here we report that NAT10 is an ATP-dependent RNA acetyltransferase responsible for formation of N(4)-acetylcytidine (ac(4)C) at position 1842 in the terminal helix of mammalian 18 S rRNA. RNAi-mediated knockdown of NAT10 resulted in growth retardation of human cells, and this was accompanied by high-level accumulation of the 30 S precursor of 18 S rRNA, suggesting that ac(4)C1842 formation catalyzed by NAT10 is involved in rRNA processing and ribosome biogenesis.Entities:
Keywords: Acetyl Coenzyme A (Acetyl-CoA); Acetyltransferase; RNA Modification; Ribosomal RNA Processing (rRNA Processing); Ribosome Assembly
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Year: 2014 PMID: 25411247 PMCID: PMC4276842 DOI: 10.1074/jbc.C114.602698
Source DB: PubMed Journal: J Biol Chem ISSN: 0021-9258 Impact factor: 5.157