Alfonso Palacín Pilar, Pocoví Miguel
Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Instituto de Salud Carlos III, Spain.
Med Clin (Barc). 2011 Sep;137 Suppl 1:17-22. doi: 10.1016/S0025-7753(11)70012-4.
Gaucher's disease (GD) results from a deficiency of the lysosomal enzyme glucocerebrosidase and, in very rare occasions, a deficiency of its activator, the saposin C. The complexity of identification and characterization of mutations in the gene of glucocerebrosidase (GBA1) is caused by a great amount of mutated alleles, the existence of a highly homologous pseudogene and its location in a very rich zone in genes, which promotes the presence of complex alleles. Although genotype-phenotype correlations in EG are not completely established, there are a series of generalities, as the mutation c.1226A>G (N370S) is often associated with a certain degree of neuroprotection and the homozygosity for the c.1448T>C (L444P) mutation presents with neurological symptoms.
戈谢病(GD)是由溶酶体酶葡萄糖脑苷脂酶缺乏引起的,在极少数情况下,也可由其激活剂鞘脂激活蛋白C缺乏导致。葡萄糖脑苷脂酶(GBA1)基因突变的鉴定和特征分析较为复杂,这是由于存在大量突变等位基因、一个高度同源的假基因以及该基因位于基因丰富区域,从而导致复杂等位基因的出现。尽管GD的基因型与表型之间的相关性尚未完全确立,但仍有一系列普遍规律,例如突变c.1226A>G(N370S)通常与一定程度的神经保护相关,而c.1448T>C(L444P)突变的纯合子则表现出神经症状。