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Two isoforms of the kidney androgen-regulated protein are encoded by two alleles of a single gene in OFl mice

Published online by Cambridge University Press:  14 April 2009

E. Melanitou
Affiliation:
Institut Pasteur, Unité de Génétique et Biochimie du Développement, Département d'Immunologie, 25 rue du Dr Roux, 75724 Paris Cedex 15, France
D. Tronik
Affiliation:
Institut Pasteur, Unité de Génétique et Biochimie du Développement, Département d'Immunologie, 25 rue du Dr Roux, 75724 Paris Cedex 15, France
F. Rougeon*
Affiliation:
Institut Pasteur, Unité de Génétique et Biochimie du Développement, Département d'Immunologie, 25 rue du Dr Roux, 75724 Paris Cedex 15, France
*
* Corresponding author.

Summary

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Two cDNA clones coding for two forms of the mouse kidney androgen-regulated protein (KAP) distinguished by their electrophoretic mobilities on SDS gel electrophoresis have been isolated from libraries prepared from strains of mice having one (BALB/c) or two (OFl) forms of the KAP protein. The corresponding mRNAs have identical sizes, as well as identical sequences in their 5' non-translated regions. The size difference observed between the two proteins is due to two point mutations in the coding region of the KAP mRNA, leading to two amino-acid changes one of which resulted in the substitution of a glycine for a glutamic acid. As shown by in vitro transcription/translation experiments, these two amino-acid differences are responsible for the shift in the apparent molecular weight of the protein on SDS gels. Both forms of the protein are more abundant in males than in females.

In vitro translation of kidney RNAs isolated from six different strains and species of mice revealed the presence of other forms of the KAP protein, characterized by small variations of their molecular weights. Southern blot analysis data are consistent with the presence of only one kap gene in the mouse genome. A restriction fragment length polymorphism has been observed, which does not correlate with the protein polymorphism, indicating the presence of another allele in the OF1 mouse genome.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1992

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