Institut fuer Humangenetik, Philipps-Universitaet, Marburg, Germany.
Hum Mutat. 2013 Apr;34(4):587-94. doi: 10.1002/humu.22275. Epub 2013 Mar 8.
Missense mutations affecting membrane-bound transcription factor protease site 2 (MBTPS2) have been associated with Ichthyosis Follicularis with Atrichia and Photophobia (IFAP) syndrome with or without BRESHECK syndrome, with keratosis follicularis spinulosa decalvans, and Olmsted syndrome. This metalloprotease activates, by intramembranous trimming in conjunction with the protease MBTPS1, regulatory factors involved in sterol control of transcription and in cellular stress response. In this study, 11 different MBTPS2 missense mutations detected in patients from 13 unrelated families were correlated with the clinical phenotype, with their effect on cellular growth in media without lipids, and their potential role for sterol control of transcription. Seven variants were novel [c.774C>G (p.I258M); c.758G>C (p.G253A); c.686T>C (p.F229S); c.1427T>C (p.L476S); c.1430A>T (p.D477V); c.1499G>A (p.G500D); c.1538T>C (p.L513P)], four had previously been reported in unrelated sibships [c.261G>A (p.M87I); c.1286G>A (p.R429H); c.1424T>C (p.F475S); c.1523A>G (p.N508S)]. In the enzyme, the mutations cluster in transmembrane domains. Amino-acid exchanges near the active site are more detrimental to functionality of the enzyme and, clinically, associated with more severe phenotypes. In male patients, a genotype-phenotype correlation begins to emerge, linking the site of the mutation in MBTPS2 with the clinical outcome described as IFAP syndrome with or without BRESHECK syndrome, keratosis follicularis spinulosa decalvans, X-linked, Olmsted syndrome, or possibly further X-linked traits with an oculocutaneous component.
错义突变影响膜结合转录因子蛋白酶位点 2(MBTPS2)与滤泡性鱼鳞病伴无发和畏光(IFAP)综合征有关,伴有或不伴有 BRESHECK 综合征、滤泡性棘状角化不良、Olmsted 综合征。这种金属蛋白酶通过与蛋白酶 MBTPS1 的跨膜修剪激活参与固醇转录调控和细胞应激反应的调节因子。在这项研究中,在来自 13 个无关家族的患者中检测到 11 种不同的 MBTPS2 错义突变,与临床表型相关,与无脂质的细胞生长相关,与固醇转录调控的潜在作用相关。七种变体是新的[c.774C>G(p.I258M); c.758G>C(p.G253A); c.686T>C(p.F229S); c.1427T>C(p.L476S); c.1430A>T(p.D477V); c.1499G>A(p.G500D); c.1538T>C(p.L513P)],四个先前在无关的兄弟姐妹中报道过[c.261G>A(p.M87I); c.1286G>A(p.R429H); c.1424T>C(p.F475S); c.1523A>G(p.N508S)]。在酶中,突变聚集在跨膜结构域中。靠近活性位点的氨基酸交换对酶的功能更具危害性,并且在临床上与更严重的表型相关。在男性患者中,基因型-表型相关性开始显现,将 MBTPS2 中的突变位点与描述为 IFAP 综合征伴或不伴 BRESHECK 综合征、滤泡性棘状角化不良、X 连锁、Olmsted 综合征的临床结果联系起来,或者可能与具有眼皮肤成分的进一步 X 连锁特征相关。