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Publication : Thyroxine treatments do not correct inner ear defects in tmprss1 mutant mice.

First Author  Hanifa S Year  2010
Journal  Neuroreport Volume  21
Issue  13 Pages  897-901
PubMed ID  20683358 Mgi Jnum  J:180548
Mgi Id  MGI:5306554 Doi  10.1097/WNR.0b013e32833dbd2d
Citation  Hanifa S, et al. (2010) Thyroxine treatments do not correct inner ear defects in tmprss1 mutant mice. Neuroreport 21(13):897-901
abstractText  Complete deficiency of a member of the type II transmembrane serine protease family, tmprss1 (also known as hepsin), is associated with severe to profound hearing loss in mice and a gross enlargement of the tectorial membrane in the cochlea. Levels of thyroxine in these mice have been shown to be significantly lower when compared with wild-type controls. As thyroxine is critical for inner ear development, we delivered thyroxine to these mice during the prenatal or postnatal stage of development. Both the treatments could not ameliorate hearing loss or correct deformities in the tectorial membrane of these mutant mice, suggesting that a deficiency in tmprss1 affects thyroxine responsiveness in the inner ear in vivo.
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