Abstract：
FGF5 functions as a negative regulator of the hair cycle in mammals. It is expressed in the outer root sheath of hair follicles during the late anagen phase of the hair cycle. It functions as a signaling molecule, mediating the transition of the anagen growth phase to catagen regression phase of the hair cycle. Spontaneous and engineered FGF5 mutations in mammalian animal models result in long hair phenotypes. In humans, inherited FGF5 mutations result in trichomegaly (long eyelashes). Knockdown of fgf5 in zebrafish embryos results in inner ear alterations. Alterations in FGF5 expression are also associated with various human pathologies.
摘要：
FGF5在哺乳动物中作为毛发周期的负调节因子起作用。在毛发周期的生长期后期，它在毛囊的外根鞘中表达。它起信号分子的作用,介导毛发周期的生长期向退步期的过渡。哺乳动物动物模型中的自发和工程化FGF5突变导致长发表型。在人类中,遗传的FGF5突变导致毛眼肿大（长睫毛）。斑马鱼胚胎中fgf5的敲除导致内耳改变。FGF5表达的改变也与各种人类病理有关。
