Spritz R A, Ho L, Strunk K M
Department of Medical Genetics, University of Wisconsin, Madison.
J Invest Dermatol. 1994 Aug;103(2):148-50. doi: 10.1111/1523-1747.ep12392551.
KIT constitutes the cell surface transmembrane receptor protein tyrosine kinase for a growth factor variously termed steel factor (SLF), stem cell factor, mast cell growth factor, or Kit ligand. Inherited mutations of the KIT gene result in piebaldism in humans and dominant white spotting (W) in mice. Patches of hypopigmented skin and hair in these disorders represent regions lacking in melanocytes, the result of defective melanoblast differentiation, migration, proliferation, or survival during embryonic development. Here we show that incubation of normal human melanocytes with a KIT antisense oligodeoxynucleotide greatly inhibits cell proliferation in culture, whereas incubation with a KIT sense oligodeoxynucleotide has no effect. The KIT oligodeoxynucleotides also had little or no effect on cell survival.
KIT构成了一种生长因子的细胞表面跨膜受体蛋白酪氨酸激酶,该生长因子有多种名称,如Steel因子(SLF)、干细胞因子、肥大细胞生长因子或Kit配体。KIT基因的遗传性突变在人类中导致斑驳病,在小鼠中导致显性白斑(W)。这些疾病中皮肤和毛发色素减退的斑块代表黑素细胞缺乏的区域,这是胚胎发育过程中黑素母细胞分化、迁移、增殖或存活缺陷的结果。在这里我们表明,正常人黑素细胞与KIT反义寡脱氧核苷酸孵育可极大地抑制培养中的细胞增殖,而与KIT正义寡脱氧核苷酸孵育则无影响。KIT寡脱氧核苷酸对细胞存活也几乎没有影响。