| First Author | Porcellati F | Year | 1998 |
| Journal | Am J Physiol | Volume | 274 |
| Issue | 5 Pt 1 | Pages | C1215-25 |
| PubMed ID | 9612208 | Mgi Jnum | J:47719 |
| Mgi Id | MGI:1205959 | Doi | 10.1152/ajpcell.1998.274.5.C1215 |
| Citation | Porcellati F, et al. (1998) Human Na(+)-myo-inositol cotransporter gene: alternate splicing generates diverse transcripts. Am J Physiol 274(5 Pt 1):C1215-25 |
| abstractText | Na(+)-myo-inositol cotransport activity generally maintains millimolar intracellular concen-trations of myo-inositol and specifically promotes transepithelial myo-inositol transport in kidney, intestine, retina, and choroid plexus. Glucose-induced, tissue-specific myo-inositol depletion and impaired Na(+)-myo-inositol cotransport activity are implicated in the pathogenesis of diabetic complications, a process modeled in vitro in cultured human retinal pigment epithelium (RPE) cells. To explore this process at the molecular level, a human RPE cDNA library was screened with a canine Na(+)-dependent myo-inositol cotransporter (SMIT) cDNA. Overlapping cDNAs spanning 3569 nt were cloned. The resulting cDNA sequence contained a 2154-nt open reading frame, 97% identical to the canine SMIT amino acid sequence. Genomic clones containing SMIT exons suggested that the cDNA is derived from at least five exons. Hypertonic stress induced a time-dependent increase, initially in a 16-kb transcript and subsequently in 11.5-, 9.8-, 8.5-, 3.8-, and approximately 1.2-kb SMIT transcripts, that was ascribed to alternate exon splicing using exon-specific probes and direct cDNA sequencing. The human SMIT gene is a complex multiexon transcriptional unit that by alternate exon splicing generates multiple SMIT transcripts that accumulate differentially in response to hypertonic stress. |
