Debeer Ph, Van Esch H, Huysmans C, Pijkels E, De Smet L, Van de Ven W, Devriendt K, Fryns J-P
Department of Orthopaedics, University Hospital Pellenberg, Weligerveld 1, B-3212 Pellenberg, Belgium.
Eur J Med Genet. 2005 Oct-Dec;48(4):377-87. doi: 10.1016/j.ejmg.2005.05.003.
Oculo-dento-digital dysplasia (ODDD) is an autosomal dominant disorder characterized by developmental anomalies of the face, the eyes, the limbs and the teeth. Patients with ODDD usually present with complete syndactyly of the fourth and fifth fingers (type III syndactyly), ocular changes, abnormalities of primary and permanent dentition and specific craniofacial malformations. Mutations in GJA1, a gene that encodes the gap junction protein connexin 43, are responsible for ODDD. Gap junctions are assemblies of intercellular channels that allow exchange of various ions and signaling molecules between cells. In this way, gap junctions play an important regulatory role in a variety of physiologic and developmental processes. We identified three novel and one previously described GJA1 mutation in two large ODDD families and two sporadic ODDD cases.
眼-牙-指发育不全(ODDD)是一种常染色体显性疾病,其特征为面部、眼睛、四肢和牙齿的发育异常。ODDD患者通常表现为第四和第五指完全并指(III型并指)、眼部改变、乳牙和恒牙异常以及特定的颅面畸形。编码间隙连接蛋白连接蛋白43的GJA1基因突变是导致ODDD的原因。间隙连接是细胞间通道的集合,允许各种离子和信号分子在细胞间交换。通过这种方式,间隙连接在多种生理和发育过程中发挥重要的调节作用。我们在两个大型ODDD家族和两个散发性ODDD病例中鉴定出三个新的和一个先前描述的GJA1突变。