Yokoi Norihide, Fujiwara Yuuka, Wang He-Yao, Kitao Mai, Hayashi Chihiro, Someya Tomohiro, Kanamori Masao, Oiso Yutaka, Tajima Naoko, Yamada Yuichiro, Seino Yutaka, Ikegami Hiroshi, Seino Susumu
Division of Cellular and Molecular Medicine, Department of Physiology and Cell Biology, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan.
Biochem Biophys Res Commun. 2008 Mar 28;368(1):37-42. doi: 10.1016/j.bbrc.2008.01.032. Epub 2008 Jan 15.
Casitas B-lineage lymphoma b (Cblb) is a negative regulator of T-cell activation and dysfunction of Cblb in rats and mice results in autoimmunity. In particular, a nonsense mutation in Cblb has been identified in a rat model of autoimmune type 1 diabetes. To clarify the possible involvement of CBLB mutation in type 1 diabetes in humans, we performed mutation screening of CBLB and characterized functional properties of the mutations in Japanese subjects. Six missense mutations (A155V, F328L, N466D, K837R, T882A, and R968L) were identified in one diabetic subject each, excepting N466D. Of these mutations, F328L showed impaired suppression of T-cell activation and was a loss-of-function mutation. These data suggest that the F328L mutation is involved in the development of autoimmune diseases including type 1 diabetes, and also provide insight into the structure-function relationship of CBLB protein.
Casitas B 细胞系淋巴瘤b(Cblb)是T细胞活化的负调节因子,大鼠和小鼠中Cblb功能异常会导致自身免疫。特别是,在1型自身免疫性糖尿病大鼠模型中已鉴定出Cblb的一个无义突变。为了阐明CBLB突变在人类1型糖尿病中的可能作用,我们对日本受试者进行了CBLB突变筛查并对突变的功能特性进行了表征。除N466D外,在每位糖尿病受试者中均鉴定出六个错义突变(A155V、F328L、N466D、K837R、T882A和R968L)。在这些突变中,F328L表现出对T细胞活化抑制受损,是一个功能丧失突变。这些数据表明F328L突变与包括1型糖尿病在内的自身免疫性疾病的发生有关,也为CBLB蛋白的结构-功能关系提供了见解。