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Background  Inward rectifier potassium channels (IRK) contribute to the normal function of skeletal and cardiac muscle cells. The chick inward rectifier K +  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  cIRK1  promoter that enhance or inhibit expression of the gene in different cell types.    Results  We cloned and characterized the 5'-flanking region of  cIRK1 .  cIRK1  contains two exons with splice sites in the 5'-untranslated region, a structure similar to mouse and human orthologs.  cIRK1  has multiple transcription initiation sites, a feature also seen in mouse. However, while the chicken and mouse promoter regions share many regulatory motifs,  cIRK1  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  cIRK1  regulatory domains by comparing promoter activities in expressing (Qm7) and non-expressing (DF1) cells using  in vitro  transcription assays.    Conclusion  While multiple transcription initiation sites and the combinatorial function of several domains in activating  cIRK1  expression are similar to those seen in  mKir2.1 , the  cIRK1  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  cIRK1  transcriptional mechanisms. The control elements identified here may provide clues to the tissue-specific expression of this K +  channel.

Characterization of the chicken inward rectifier K+ channel IRK1/Kir2.1 gene