作者: C. X. George , C. E. Samuel
关键词:
摘要: RNA-specific adenosine deaminase (ADAR1) catalyzes the deamination of to inosine in viral and cellular RNAs. Two size forms ADAR1 editing enzyme are known, an IFN-inducible ≈150-kDa protein a constitutively expressed N-terminally truncated ≈110-kDa protein. We have now identified alternative exon 1 structures human transcripts that initiate from unique promoters, one other IFN inducible. Cloning sequence analyses 5′-rapid amplification cDNA ends (RACE) cDNAs placenta established linkage between 2 two structures, designated herein as 1A 1B. Analysis RNA isolated untreated IFN-treated amnion cells demonstrated 1B–exon were synthesized absence not significantly altered amount by treatment. By contrast, 1A–exon Transient transfection analysis with reporter constructs led identification functional PC PI. Exon 1B initiated promoter whose activity transient assays was increased The 107-nt mapped 14.5 kb upstream 2. 201-nt 5.4 interferon-inducible PI promoter. These results suggest inducible not, transcription gene, splicing common junction generates deduced coding capacity for either (exon 1B) or interferon-induced 1A).