Recombinant Human Type II Mitochondrial Dynein-Like GTPase Gene Sequence and Its Application

Abstract

The invention discloses the recombinant human type II mitochondrial dynein-like GTPase gene sequence and its application, the nucleotide sequence of which is shown in SEQ ID NO.:1. Also disclosed is a fusion nucleic acid comprising the nucleic acid encoding human type II mitochondrial dynein-like GTPase. Further disclosed is a recombinant expression vector comprising the above nucleic acid or fusion nucleic acid. Also disclosed is a transformant which introduces the above-mentioned nucleic acid or fusion nucleic acid into a host. The nucleic acid encoding human type II mitochondrial dynein-like GTPase of the present invention has a higher expression level, so more human type II mitochondrial dynein-like GTPase can be obtained in the mitochondria, and can better treat eye diseases such as ADOA disease.

Description

technical field [0001] The invention relates to the field of biological preparations, in particular to the recombinant human type II mitochondrial dynein-like GTPase gene sequence and its application. Background technique [0002] Autosomal dominant optic atrophy (ADOA) is the most common form of primary hereditary optic neuropathy, with an incidence rate of about 1:12 000 to 1:50 000, and the onset is insidious in childhood. It is clinically characterized by mild to moderate progressive loss of vision, color vision deficits, central visual field defects, and temporal optic disc pallor. Initially there is damage to the papillary vascular bundle, followed by ascending atrophy of the optic nerve and loss of myelin sheath of the optic nerve. [0003] ADOA is caused by mutations in genes encoding inner mitochondrial membrane proteins and loci. Foreign scholars have determined that such genes are mainly OPA1-OPA8. It has been preliminarily confirmed that about 75% of ADOA patien...

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