Asunto(s)
Antibacterianos/administración & dosificación , Hipertermia Inducida/métodos , Infecciones por Mycobacterium no Tuberculosas/terapia , Mycobacterium chelonae/aislamiento & purificación , Diálisis Peritoneal Ambulatoria Continua/efectos adversos , Peritonitis/microbiología , Terapia Combinada , Quimioterapia Combinada , Estudios de Seguimiento , Humanos , Fallo Renal Crónico/diagnóstico , Fallo Renal Crónico/terapia , Masculino , Persona de Mediana Edad , Infecciones por Mycobacterium no Tuberculosas/diagnóstico , Mycobacterium chelonae/efectos de los fármacos , Diálisis Peritoneal Ambulatoria Continua/métodos , Peritonitis/etiología , Peritonitis/terapia , Resultado del TratamientoRESUMEN
CLC-K1 and CLC-K2 are highly homologous kidney-specific chloride channels, but they are expressed in the different nephron segments. To understand the molecular mechanisms of kidney-specific and nephron-segment-specific expression of CLC-K channel genes, the rat ClC-K2 gene promoter was cloned and compared with that of CLC-K1. In the 1.5-kb pair 5'-flanking region of the CLC-K2 gene, no TATA box was identified around the transcriptional start site, and the proximal region (-32 to -68) was characterized by a GA-rich motif that had a significant sequence similarity to that of the previously isolated CLC-K1 gene promoter. In contrast, the distal portion did not have significant sequence similarity to that of CLC-K1. Reporter gene assay and gel-retardation analysis revealed that the GA-rich motif and the binding of a specific protein(s) to this element were indispensable for the basal promoter activity of the CLC-K2 gene. These results suggest that the GA-rich element may have an important role in the promoter activities of the kidney-specific CLC-K1 and -K2 genes, but that the GA-element alone is not sufficient for the strict regulation of nephron-segment-specific expression of CLC-K1 and CLC-K2 genes.