Click here to close Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly. We suggest using a current version of Chrome, FireFox, or Safari.
XB-ART-21996
J Biol Chem 1993 Nov 15;26832:24283-9.
Show Gene links Show Anatomy links

Multiple mRNA isoforms encoding the mouse cardiac Kv1-5 delayed rectifier K+ channel.

Attali B , Lesage F , Ziliani P , Guillemare E , Honoré E , Waldmann R , Hugnot JP , Mattéi MG , Lazdunski M , Barhanin J .


???displayArticle.abstract???
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.

???displayArticle.pubmedLink??? 8226976
???displayArticle.link??? J Biol Chem