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Molecular Pharmacology

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Abstract

Molecular genetic basis of rapid and slow acetylation in mice.

K J Martell, K P Vatsis and W W Weber
Molecular Pharmacology August 1991, 40 (2) 218-227;
K J Martell
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K P Vatsis
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W W Weber
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Abstract

The molecular genetic basis of N-acetylation polymorphism has been investigated in inbred mouse models of the human acetylation polymorphism. Two genomic clones, Nat1 and Nat2, were isolated from a C57BL/6J (B6) mouse (rapid acetylator) genomic library. The Nat1 and Nat2 genes both have intronless coding regions of 870 nucleotides and display greater than 47% deduced amino acid similarity with human, rabbit, and chicken N-acetyltransferases. Amplification of Nat1 and Nat2 from A/J (A) mouse (slow acetylator) genomic DNA by the polymerase chain reaction and subsequent sequencing revealed that Nat1 was identical in B6 and A mice, whereas Nat2 contained a single nucleotide change from adenine in B6 to thymine in A mice. This nucleotide substitution changes the deduced amino acid at position 99 from asparagine in B6 to isoleucine in A mice. Hydropathy analysis revealed that this amino acid change alters the hydropathy of the flanking peptide segment in NAT2 from hydrophilic in the B6 mouse to hydrophobic in the A mouse. The amino acid change occurs in a region of the gene where no polymorphism has yet been reported in human or rabbit NAT2 and may represent an important structural domain for N-acetyltransferase activity. Nat1 and Nat2 have the same 5' to 3' orientation in the B6 mouse; the two genes are separated by approximately 9 kilobases, with Nat1 located 5' of Nat2.

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Molecular Pharmacology
Vol. 40, Issue 2
1 Aug 1991
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Abstract

Molecular genetic basis of rapid and slow acetylation in mice.

K J Martell, K P Vatsis and W W Weber
Molecular Pharmacology August 1, 1991, 40 (2) 218-227;

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Abstract

Molecular genetic basis of rapid and slow acetylation in mice.

K J Martell, K P Vatsis and W W Weber
Molecular Pharmacology August 1, 1991, 40 (2) 218-227;
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