BALB/cByJ mice

Bauer, A. K. Dwyer-Nield, L. D. Hankin, J. A. Murphy, R. C. Malkinson, A. M. The lung tumor promoter, butylated hydroxytoluene (BHT), causes chronic inflammation in promotion-sensitive BALB/cByJ mice but not in promotion-resistant CXB4 mice. 

Figure 1. Molecular structure of the mouse short-chain acyl-CoA dehydrogenase gene including the deletion mutation found in BALB/cByJ mice. Adapted and redrawn from previous publications."- A. The fine genomic structure of the deletion mutation, b. Molecular structure of the approximately normal size Acads mRNA from the mutant allele. This consists of an RNA copy of the deleted gene sequence with no splicing, c. Molecular structure of the short Acads mRNA from the mutant allele. This consists of a missplked mRNA from exon 8 to a cryptic splice site in exon 10.

Prochazka, M. Letter, E.H. (1986) Mouse News Lett, 78, 31. A null activity variant found at the butyryl CoA dehydrogenase (Bcd-l) locus in BALB/cByJ mice. 

Armstrorig, D.L., Masiowski, M.L. Wood, PA (1993) A r. J. Med Genet, 47, 884-892. Pathologic characterization of short-chain acyl-CoA dehydrogenase deficiency in BALB/cByJ mice. 

Hinsdale, M.F., KeUy, C.L. Wood, PA (1993) Genomics 16, 605-611. Null allele at bcd-l locus in BALB/cByJ mice is due to a deletion in the short-chain acyl-CoA dehydrogenase gene and results in missplicing ofmRNA. 

Wood, P.A., Hinsdale, M.E. Kelly, C.L. (1993) Mouse Genome 91, 342-344. Molecular detection of the Bcd-1 null allele in BALB/cByJ mice by polymerase chain reaction A simple assay for genetic monitoring. 

Rao, K.V.R. Qureshi, I.A. (1997) Can. J. Physiol. Pharmacol., 75, 423-4360. Decompensation of hepatic and cerebral acyl-CoA metabolism in BALB/cByJ mice by chronic riboflavin deficiency restoration by acetyl-L-camitine. 

Brigand RA, Rotman HL, Yutanawihoonchai W, Leon O, Nolan TJ, Schad GA, Abraham D. Strongyloides stercoralis role of antibody and complement in immunity to the third stage larvae in BALB/cByJ mice. Exp Parasitol 1996 82 279-289. 

---