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© 1995 Oxford University Press

RESEARCH-ARTICLE

Characterization of the human homologue of the mouse Tg737 candidate polycystic kidney disease gene

Jeffrey J. Schrick, L.F. Onuchic1, S.T. Reeders1, J. Korenberg2, X-N. Chen2, J.H. Moyer, J.E. Wilkinson3 and Richard Woychik4,*

University of Tennessee-Oak Ridge Graduate School for Biomedical Sciences Oak Ridge, TN 37831, USA 1Yale University School of Medicine New Haven, CT 2Ahamanson Department of Pediatrics, Division of Genetics, Cedars-Sinai Medical Center, University of California Los Angeles, CA 3College of Veterinary Sciences, University of Tennessee Knoxville, TN 37923, USA 4Biology Division, Oak Ridge National Laboratory Oak Ridge, TN 37831, USA

*To whom correspondence should be addressed

Received November 21, 1994; Revised February 7, 1995; Accepted February 7, 1995

We previously identified a gene from the mutant locus in a new mouse mutation that causes recessive polycystic kidney disease. Here we describe the cloning, characterization and mapping of the homologous human gene. The human and mouse genes are 95% identical at the predicted amino acid sequence level, and both genes encode a putative protein that contains a tetratricopeptide repeat motif. The human gene, called hTg737, is expressed with a broad tissue distribution that includes the kidney and liver, and gives rise to a 2.9 kb mRNA. The gene contains 26 exons and spans a genomic region greater than 100 kb. Chromosome mapping experiments revealed that the hTg737 gene maps near the centromere on the long arm of human chromosome 13, at position 13q12.1. While this gene does not map to the primary locus that has been identified for ARPKD in humans, it may represent a candidate gene for other recessive renal disorders that have yet to be mapped.


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