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1997 Oxford University Press 12251231Human Molecular Genetics, 1997, Vol. 6, No. 8 Characterization of unconventional MYO6, the human
 

Summary:  1997 Oxford University Press 12251231Human Molecular Genetics, 1997, Vol. 6, No. 8
Characterization of unconventional MYO6, the human
homologue of the gene responsible for deafness in
Snell's waltzer mice
Karen B. Avraham1,*, Tama Hasson2, Tama Sobe1, Binaifer Balsara3, Joseph R. Testa3,
Anne B. Skvorak4, Cynthia C. Morton4,5, Neal G. Copeland6 and Nancy A. Jenkins6
1Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel,
2Departments of Biology and Pathology, Yale University, New Haven, CT 06511, USA, 3Department of Medical
Oncology, Fox Chase Cancer Center, Philadelphia, PA 19111, USA, 4Department of Pathology and 5Department
of Obstetrics, Gynecology and Reproductive Biology, Brigham and Women's Hospital and Harvard Medical
School, Boston, MA 02115, USA and 6Mammalian Genetics Laboratory, ABL-Basic Research Program,
NCI-Frederick Cancer Research and Development Center, Frederick, MD 21702, USA
Received February 25, 1997; Revised and Accepted May 8, 1997 DDBJ/EMBL/GenBank accession no. U90236
Deafness is the most common form of sensory
impairment in humans. Mutations in unconventional
myosins have been found to cause deafness in humans
and mice. The mouse recessive deafness mutation,
Snell's waltzer, contains an intragenic deletion in an
unconventional myosin, myosin VI (locus designation,
Myo6). The requirement for Myo6 for proper hearing in

  

Source: Avraham, Karen - Department of Human Genetics and Molecular Medicine, Tel Aviv University

 

Collections: Biology and Medicine