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Publication : Genetic regulation of aromatic amine N-acetylation in inbred mice.

First Author  Glowinski IB Year  1982
Journal  J Biol Chem Volume  257
Issue  3 Pages  1424-30
PubMed ID  6976963 Mgi Jnum  J:6685
Mgi Id  MGI:55159 Doi  10.1016/s0021-9258(19)68210-4
Citation  Glowinski IB, et al. (1982) Genetic regulation of aromatic amine N-acetylation in inbred mice. J Biol Chem 257(3):1424-30
abstractText  A survey among 20 inbred mouse strains revealed large variation (up to approximately 20-fold) for the N-acetylation of p-aminobenzoic acid by blood N-acetyltransferase and for the aromatic amine carcinogen benzidine by both liver and blood N-acetyltransferase. Of 20 strains surveyed, three are classified as slow acetylators (A/J, AHe/J, and X/Gf) and 17 are classified as rapid acetylators (AuSsJ, Castaneous, ST/bJ, C57BL/6J, Molossinus, SF, SWR/J, 129/SV, RF/J, RIII/2J, IsCam, SJL/J, Balb/cJ, C3H/HeJ, CBA/J, AKR/J, and DBA/J). The rapid acetylator strains possessed approximately 10 times greater liver benzidine N-acetyltransferase specific activity than the slow acetylator strains. Intercross and backcross matings of A/J and C57BL/6J mice indicate that a single gene with two major alleles is responsible for differences in N-acetyltransferase activity in blood for p-aminobenzoic acid or the alternate aromatic amine carcinogen aminofluorene, and in liver for aminofluorene. Analysis of 11 recombinant inbred strains derived from matings of A/J with C57BL/6J mice support this conclusion and demonstrate the existence of minor modifying genes that segregate independently of the major N-acetyltransferase gene.
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