| Summary: | <p>Abstract</p> <p>Background</p> <p>Inward rectifier potassium channels (IRK) contribute to the normal function of skeletal and cardiac muscle cells. The chick inward rectifier K<sup>+ </sup>channel cIRK1/Kir2.1 is expressed in skeletal muscle, heart, brain, but not in liver; a distribution similar but not identical to that of mouse Kir2.1. We set out to explore regulatory domains of the <it>cIRK1 </it>promoter that enhance or inhibit expression of the gene in different cell types.</p> <p>Results</p> <p>We cloned and characterized the 5'-flanking region of <it>cIRK1</it>. <it>cIRK1 </it>contains two exons with splice sites in the 5'-untranslated region, a structure similar to mouse and human orthologs. <it>cIRK1 </it>has multiple transcription initiation sites, a feature also seen in mouse. However, while the chicken and mouse promoter regions share many regulatory motifs, <it>cIRK1 </it>possesses a GC-richer promoter and a putative TATA box, which appears to positively regulate gene expression. We report here the identification of several candidate cell/tissue specific <it>cIRK1 </it>regulatory domains by comparing promoter activities in expressing (Qm7) and non-expressing (DF1) cells using <it>in vitro </it>transcription assays.</p> <p>Conclusion</p> <p>While multiple transcription initiation sites and the combinatorial function of several domains in activating <it>cIRK1 </it>expression are similar to those seen in <it>mKir2.1</it>, the <it>cIRK1 </it>promoter differs by the presence of a putative TATA box. In addition, several domains that regulate the gene's expression differentially in muscle (Qm7) and fibroblast cells (DF1) were identified. These results provide fundamental data to analyze <it>cIRK1 </it>transcriptional mechanisms. The control elements identified here may provide clues to the tissue-specific expression of this K<sup>+ </sup>channel.</p>
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