Broughton B C, Steingrimsdottir H, Weber C A, Lehmann A R
MRC Cell Mutation Unit, University of Sussex, Falmer, Brighton, UK.
Nat Genet. 1994 Jun;7(2):189-94. doi: 10.1038/ng0694-189.
DNA repair defects in the xeroderma pigmentosum (XP) group D complementation group can be associated with the clinical features of two quite different disorders; XP, a sun-sensitive and cancer-prone disorder, or trichothiodystrophy (TTD) which is characterized by sulphur-deficient brittle hair and a variety of other associated abnormalities, but no skin cancer. The XPD gene product, a DNA helicase, is required for nucleotide excision repair and recent evidence has demonstrated a role in transcription. We have now identified causative mutations in XPD in four TTD patients. The patients are all compound heterozygotes and the locations of the mutations enable us to suggest relationships between different domains in the gene and its roles in excision repair and transcription.
着色性干皮病D组互补群中的DNA修复缺陷可能与两种截然不同的疾病的临床特征相关;着色性干皮病,一种对阳光敏感且易患癌症的疾病,或毛发硫营养不良(TTD),其特征是毛发硫缺乏且脆弱,并伴有多种其他相关异常,但不会患皮肤癌。XPD基因产物是一种DNA解旋酶,是核苷酸切除修复所必需的,最近的证据表明它在转录中也发挥作用。我们现已在4例毛发硫营养不良患者中鉴定出XPD基因的致病突变。这些患者均为复合杂合子,突变的位置使我们能够推测该基因不同结构域之间的关系及其在切除修复和转录中的作用。