Gal A, Li Y, Thompson D A, Weir J, Orth U, Jacobson S G, Apfelstedt-Sylla E, Vollrath D
Institut für Humangenetik, Universitäts-Krankenhaus Eppendorf, Hamburg, Germany.
Nat Genet. 2000 Nov;26(3):270-1. doi: 10.1038/81555.
Mutation of a receptor tyrosine kinase gene, Mertk, in the Royal College of Surgeons (RCS) rat results in defective phagocytosis of photoreceptor outer segments by the retinal pigment epithelium (RPE) and retinal degeneration. We screened the human orthologue, MERTK, located at 2q14.1 (ref. 10), in 328 DNA samples from individuals with various retinal dystrophies and found three mutations in three individuals with retinitis pigmentosa (RP). Our findings are the first conclusive evidence implicating the RPE phagocytosis pathway in human retinal disease.
皇家外科学院(RCS)大鼠中,受体酪氨酸激酶基因Mertk发生突变,导致视网膜色素上皮(RPE)对光感受器外段的吞噬功能缺陷以及视网膜变性。我们对位于2q14.1的人类同源基因MERTK(参考文献10),在328份来自患有各种视网膜营养不良个体的DNA样本中进行了筛查,在三名患有色素性视网膜炎(RP)的个体中发现了三个突变。我们的研究结果是首次确凿证据,表明RPE吞噬途径与人类视网膜疾病有关。