| First Author | Attali B | Year | 1993 |
| Journal | J Biol Chem | Volume | 268 |
| Issue | 32 | Pages | 24283-9 |
| PubMed ID | 8226976 | Mgi Jnum | J:15498 |
| Mgi Id | MGI:63618 | Doi | 10.1016/s0021-9258(20)80523-7 |
| Citation | Attali B, et al. (1993) Multiple mRNA isoforms encoding the mouse cardiac Kv1-5 delayed rectifier K+ channel. J Biol Chem 268(32):24283-9 |
| abstractText | The mouse Kv1-5 K+ channel cDNA has been cloned from heart. This channel was highly expressed in heart and, to a lesser extent, in other tissues, including brain and thymus. Two alternatively spliced isoforms were found. The longer form encoded a 602-amino acid protein, while in the short form (Kv1-5 delta 5'), the first 200 amino acids lying upstream the transmembrane segment S1 were deleted. RNase protection experiments showed that both Kv1-5 mRNA isoforms are present in the mouse tissues examined, the longer form being predominant. The short mRNA (Kv1-5 delta 5') arose by an unusual splicing event within the exonic sequence. An additional short cDNA clone (Kv1-5 delta 3') that codes for a carboxyl-terminal truncated protein has been isolated. The gene coding sequence contained a single exon and has been mapped on human chromosome 12 (p13) and on mouse chromosome 6 (band F). Expression in Xenopus oocytes revealed that the long (Kv1-5) and the amino-terminal deleted (Kv1-5 delta 5') isoforms elicited similar K+ currents with a drastically decreased efficacy for Kv1-5 delta 5'. The carboxyl-terminal truncated Kv1-5 delta 3' clone was not functional but inhibited the expression of the long isoform. |
