Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.7.49 (
reverse transcriptase
)
31,746
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The flavin-containing monooxygenases (FMOs) are a family of five microsomal enzymes important for the oxidative metabolism of environmental toxicants, natural products, and therapeutics. With the exception of
FMO5
, the
FMO
are encoded within a single gene cluster on human chromosome 1q23-25. As part of the human genome effort, an
FMO
-like gene, FMO6, was identified between
FMO3
and
FMO2
(GenBank accession no. AL021026). Sequence analysis of this putative
FMO
family member revealed nothing that would a priori argue against a functional gene and encoded protein. When FMO6 expression was examined by
reverse transcriptase
coupled polymerase chain reaction DNA amplification, transcripts were identified in 8 of 11 human liver samples, but 0 of 4 kidney biopsy samples. However, in all cases, the observed transcripts were shorter than predicted. Sequence analysis revealed skipping of exon 4, exons 3 and 4, and/or the use of alternative splice donor or acceptor sites in introns 3, 4, 6, and 8, resulting in nine unique transcripts. Based on an analysis of possible open reading frames, none of these transcripts would encode a functional
FMO
enzyme. Taking advantage of the high sequence identity between
FMO3
and FMO6, it is posited that the loss of binding sites for the serine-arginine-rich splicing factor protein family within exons 3 and 4 contributes to the exon skipping events, although the most commonly observed alternative splice event results from a 21-bp insertion immediately 3' to the predicted FMO6 intron 8 splice acceptor site, diminishing the efficiency of this site.
...
PMID:Alternative processing of the human FMO6 gene renders transcripts incapable of encoding a functional flavin-containing monooxygenase. 1213 Jun 84