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Chromosomal Localization of the Human and Mouse Hyaluronan Synthase Genes
Authors:Andrew P. Spicer  Michael F. Seldin  Anne S. Olsen  Nicholas Brown  Dan E. Wells  Norman A. Doggett  Naoki Itano  Koji Kimata  Joji Inazawa  John A. McDonald
Affiliation:aDepartment of Biochemistry and Molecular Biology, Mayo Clinic Scottsdale, 13400 East Shea Boulevard, Scottsdale, Arizona, 85259;bRowe Program in Genetics, Departments of Biological Chemistry and Medicine, University of California Davis, Davis, California, 95616;cHuman Genome Center, Lawrence Livermore National Laboratory, Livermore, California, 94550;dDepartment of Biology and Institute for Molecular Biology, University of Houston, Houston, Texas, 77204;eLife Sciences Division and Center for Human Genome Studies, Los Alamos National Laboratory, Los Alamos, New Mexico, 87545;fInstitute for Molecular Science of Medicine, Aichi Medical University, Nagakute, Aichi, 480-11, Japan;gDepartment of Hygiene, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto, 602, Japan
Abstract:We have recently identified a new vertebrate gene family encoding putative hyaluronan (HA) synthases. Three highly conserved related genes have been identified, designatedHAS1, HAS2,andHAS3in humans andHas1, Has2,andHas3in the mouse. All three genes encode predicted plasma membrane proteins with multiple transmembrane domains and approximately 25% amino acid sequence identity to theStreptococcus pyogenesHA synthase, HasA. Furthermore, expression of any oneHASgene in transfected mammalian cells leads to high levels of HA biosynthesis. We now report the chromosomal localization of the threeHASgenes in human and in mouse. The genes localized to three different positions within both the human and the mouse genomes.HAS1was localized to the human chromosome 19q13.3–q13.4 boundary andHas1to mouse Chr 17.HAS2was localized to human chromosome 8q24.12 andHas2to mouse Chr 15.HAS3was localized to human chromosome 16q22.1 andHas3to mouse Chr 8. The map position forHAS1reinforces the recently reported relationship between a small region of human chromosome 19q and proximal mouse chromosome 17.HAS2mapped outside the predicted critical region delineated for the Langer–Giedion syndrome and can thus be excluded as a candidate gene for this genetic syndrome.
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