| Literature DB >> 22230121 |
Pilar Alfonso Palacín1, Miguel Pocoví.
Abstract
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.Entities:
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Year: 2011 PMID: 22230121 DOI: 10.1016/S0025-7753(11)70012-4
Source DB: PubMed Journal: Med Clin (Barc) ISSN: 0025-7753 Impact factor: 1.725