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N6AMT1 / HEMK2 Protein

N-6 adenine-specific DNA methyltransferase 1 (putative) / HemK methyltransferase family member 2

N6AMT1 / HEMK2 Products

N6AMT1 / HEMK2 Protein, Recombinant

Molecule Species Description //For Detailed Info. and Price------CLICK! Cat. No
N6AMT1/HEMK2 Human N6AMT1/HEMK2 Protein, Recombinant 12399-H08E

N6AMT1 / HEMK2 Alternative Names

N6AMT1, HEMK2, PRED28, C21orf127, HEMK2, MGC19995, MTQ2, N6AMT [Homo sapiens]

N6amt1, HEMK2, 5830445C04Rik, Hemk2, MGC106447, Pred28 [Mus musculus]

N6AMT1 / HEMK2 Background

N6AMT1 (N-6 adenine-specific DNA methyltransferase 1), also known as HEMK2 (HemK methyltransferase family member 2), a putative methyltransferase, is a member of the HemK family. HemK family is a widespread family of putative proteins encoded in genomes from bacteria to human. HemK contains two domains: a putative substrate binding domain at the N terminus consisting of a five helix bundle and a seven-stranded catalytic domain at the C terminus that harbors the binding site for AdoHcy. The two domains are linked by a beta-hairpin. Structure-guided sequence analysis of the HemK family revealed 11 invariant residues functioning in methyl-donor binding and catalysis of methyl transfer. N6AMT1 has a significant role in determining susceptibility to arsenic toxicity and carcinogenicity because of its specific activity in methylating MMAIII to DMA and other unknown mechanisms.

N6AMT1 / HEMK2 Related Studies

  1. Ren X, et al. (2011) Involvement of N-6 adenine-specific DNA methyltransferase 1 (N6AMT1) in arsenic biomethylation and its role in arsenic-induced toxicity. Environ Health Perspect. 119(6): 771-7.
  2. Yang Z, et al. (2004) Structural characterization and comparative phylogenetic analysis of Escherichia coli HemK, a protein (N5)-glutamine methyltransferase. J Mol Biol. 340(4): 695-706.
  3. Bujnicki JM, et al. (1999) Is the HemK family of putative S-adenosylmethionine-dependent methyltransferases a "missing" zeta subfamily of adenine methyltransferases? A hypothesis. IUBMB Life. 48(3): 247-9.