Davies A F, Mirza G, Flinter F, Ragoussis J
Division of Medical and Molecular Genetics, Guy's Hospital, King's College, London, UK.
J Med Genet. 1999 Sep;36(9):708-10.
The FKHL7 gene has been implicated in the pathogenesis of glaucoma/autosomal dominant iridogoniodysgenesis (IGDA) (IRID1). This has been supported by mutations in some glaucoma and IGDA patients and the development of anterior eye chamber anomalies in patients with 6p deletions affecting the 6p25 region. We report a case with anterior eye chamber anomalies and an interstitial deletion of 6p24-p25 that does not include the FKHL7 gene, suggesting the possible additional involvement of another locus, within 6p24-6p25, in anterior eye chamber development. A candidate gene is AP-2alpha, which is contained within the deleted segment and plays a role in anterior eye chamber development.
FKHL7基因与青光眼/常染色体显性虹膜角膜内皮发育异常(IGDA)(IRID1)的发病机制有关。一些青光眼和IGDA患者的突变以及6p25区域发生6p缺失的患者出现眼前房异常,均支持这一观点。我们报告了1例伴有眼前房异常及6p24 - p25间质性缺失(不包括FKHL7基因)的病例,提示6p24 - 6p25区域内可能有另一个基因座参与眼前房发育。一个候选基因是AP - 2α,它包含在缺失片段内且在眼前房发育中起作用。