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Publication : Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1.

First Author  Howell GR Year  2007
Journal  BMC Genet Volume  8
Pages  45 PubMed ID  17608931
Mgi Jnum  J:123136 Mgi Id  MGI:3717273
Doi  10.1186/1471-2156-8-45 Citation  Howell GR, et al. (2007) Absence of glaucoma in DBA/2J mice homozygous for wild-type versions of Gpnmb and Tyrp1. BMC Genet 8(1):45
abstractText  ABSTRACT: BACKGROUND: The glaucomas are a common but incompletely understood group of diseases. DBA/2J mice develop a pigment liberating iris disease that ultimately causes elevated intraocular pressure and glaucoma. We have shown previously that mutations in two genes, Gpnmb and Tyrp1, initiate the iris disease. However, mechanisms involved in the subsequent IOP elevation and optic nerve degeneration remain unclear. RESULTS: Here we present new mouse strains with Gpnmb and/or Tyrp1 genes of normal function and with a DBA/2J genetic background. These strains do not develop elevated IOP or glaucoma with age. CONCLUSIONS: These strains provide much needed controls for studying pathogenic mechanisms of glaucoma using DBA/2J mice. Given the involvement of Gpnmb and/or Tyrp1 in areas such as immunology and tumor development and progression, these strains are also important in other research fields.
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