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J. Biol. Chem., Vol. 268, Issue 32, 24283-24289, Nov, 1993
B Attali, F Lesage, P Ziliani, E Guillemare, E Honore, R Waldmann, JP Hugnot, MG Mattei, M Lazdunski and J Barhanin
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.
Multiple mRNA isoforms encoding the mouse cardiac Kv1-5 delayed rectifier K+ channel
Institut de Pharmacologie Moleculaire et Cellulaire, Valbonne, France.
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