PubMed:9843038 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PubMed/sourceid/9843038","sourcedb":"PubMed","sourceid":"9843038","source_url":"http://www.ncbi.nlm.nih.gov/pubmed/9843038","text":"Identification of a novel mutation of the CPO gene in a Japanese hereditary coproporphyria family.\nHereditary coproporphyria (HCP) is an autosomal dominant disease characterized by a deficiency of coproporphyrinogen oxidase (CPO) caused by a mutation in the CPO gene. Only 11 mutations of the gene have been reported in HCP patients. We report another mutation in a Japanese family. Polymerase chain reaction-single strand conformational polymorphism and direct sequence analyses demonstrated a C to T substitution in exon 1 of the CPO gene at nucleotide position 85, which lies in the putative presequence for targeting to mitochondria. This mutation changes the codon for glutamine to a termination codon at amino acid position 29. MaeI restriction analysis showed two other carriers in the family. The C-T mutation is located within a recently proposed putative alternative translation initiation codon (TIC-1), supporting that TIC-1 is the real TIC rather than 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