2.1.1.370: [histone H3]-lysine4 N-dimethyltransferase
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For detailed information about [histone H3]-lysine4 N-dimethyltransferase, go to the full flat file.
Reaction
2 S-adenosyl-L-methionine + = 2 S-adenosyl-L-homocysteine +
Synonyms
MEL, NSD3, PFM13, PRDM16, WHISTLE, WHSC1L1
ECTree
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General Information
General Information on EC 2.1.1.370 - [histone H3]-lysine4 N-dimethyltransferase
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physiological function
Nsd3 dimethylates H3K4 and additionally di-, and tri-methylates histones H3K27. Overexpression of Nsd3 represses transcription of the SV40 promoter
physiological function
loss of Prdm3 or Prdm16 in zebrafish causes craniofacial defects including hypoplasia of the craniofacial cartilage elements, undefined posterior ceratobranchials, and decreased mineralization of the parasphenoid. Prdm3 and Prdm16 compensate for each other as well as a Prdm1a. Combinatorial loss of Prdm1a, Prdm3, and Prdm16 alleles results in severe hypoplasia of the anterior cartilage elements, abnormal formation of the jaw joint, complete loss of the posterior ceratobranchials, and clefting of the ethmoid plate. Loss of Prdm3 and Prdm16 reduces methylation of histone 3 lysine 9 (repression) and histone 3 lysine 4 (activation) in zebrafish
physiological function
PRDM16 is a histone H3 K9 methyltransferase on chromatin. Mutation in the N-terminal PR-domain of PRDM16 completely abolishes the intrinsic enzymatic activity of PRDM16. The methyltransferase activity of PRDM16 is required for specific suppression of mixed lineage leukemia leukemogenesis both in vitro and in vivo. PRDM16 directly activates the SNAG family transcription factor GFI1b, which in turn down regulates the HOXA gene cluster. Knockdown GFI1b represses PRDM16-mediated tumor suppression while GFI1b overexpression mimics PRDM16 overexpression. Silencing PRDM16 by DNA methylation is concomitant with mixed lineage leukemia MLL-AF9 induced leukemic transformation