Takahashi M
Department of Pathology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
Cytokine Growth Factor Rev. 2001 Dec;12(4):361-73. doi: 10.1016/s1359-6101(01)00012-0.
Glial cell line-derived neurotrophic factor (GDNF) and related molecules, neurturin, artemin and persephin, signal through a unique multicomponent receptor system consisting of RET tyrosine kinase and glycosyl-phosphatidylinositol-anchored coreceptor (GFRalpha1-4). These neurotrophic factors promote the survival of various neurons including peripheral autonomic and sensory neurons as well as central motor and dopamine neurons, and have been expected as therapeutic agents for neurodegenerative diseases. In addition, it turned out that the GDNF/RET signaling plays a crucial role in renal development and regulation of spermatogonia differentiation. RET mutations cause several human diseases such as papillary thyroid carcinoma, multiple endocrine neoplasia types 2A and 2B, and Hirschsprung's disease. The mutations resulted in RET activation or inactivation by various mechanisms and the biological properties of mutant proteins appeared to be correlated with disease phenotypes. The signaling pathways activated by GDNF or mutant RET are being extensively investigated to understand the molecular mechanisms of disease development and the physiological roles of the GDNF family ligands.
胶质细胞源性神经营养因子(GDNF)及相关分子,如神经营养素、artemin和persephin,通过由RET酪氨酸激酶和糖基磷脂酰肌醇锚定的共受体(GFRalpha1 - 4)组成的独特多组分受体系统进行信号传导。这些神经营养因子可促进包括外周自主神经和感觉神经元以及中枢运动神经元和多巴胺能神经元在内的多种神经元的存活,并有望成为神经退行性疾病的治疗药物。此外,事实证明,GDNF/RET信号传导在肾脏发育和精原细胞分化调控中起关键作用。RET突变会导致多种人类疾病,如甲状腺乳头状癌、2A和2B型多发性内分泌腺瘤以及先天性巨结肠病。这些突变通过各种机制导致RET激活或失活,并且突变蛋白的生物学特性似乎与疾病表型相关。为了了解疾病发展的分子机制以及GDNF家族配体的生理作用,人们正在广泛研究由GDNF或突变型RET激活的信号通路。