Human Na1-myo- inositol cotransporter gene: alternate splicing generates di- verse transcripts. Am. J. Physiol. 274 (Cell Physiol. 43): C1215±C1225, 1998.ÐNa1-myo-inositol cotransport activity generally maintains millimolar intracellular concentrations of myo-inositol and speci®cally promotes transepithelial myo- inositol transport in kidney, intestine, retina, and choroid plexus. Glucose-induced, tissue-speci®c myo-inositol deple- tion and impaired Na1-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 molecu- lar level, a human RPE cDNA library was screened with a canine Na1-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 ®ve 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 ,1.2-kb SMIT transcripts, that was ascribed to alternate exon splicing using exon-speci®c 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

Human Na + myo-inositol cotransporter gene: alternate spicing generates diverse transcripts

PORCELLATI, Francesca;
1998

Abstract

Human Na1-myo- inositol cotransporter gene: alternate splicing generates di- verse transcripts. Am. J. Physiol. 274 (Cell Physiol. 43): C1215±C1225, 1998.ÐNa1-myo-inositol cotransport activity generally maintains millimolar intracellular concentrations of myo-inositol and speci®cally promotes transepithelial myo- inositol transport in kidney, intestine, retina, and choroid plexus. Glucose-induced, tissue-speci®c myo-inositol deple- tion and impaired Na1-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 molecu- lar level, a human RPE cDNA library was screened with a canine Na1-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 ®ve 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 ,1.2-kb SMIT transcripts, that was ascribed to alternate exon splicing using exon-speci®c 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
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11391/1038997
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