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Cloning and characterization of human and mouse homologs of the Drosophila calcium-activated potassium channel gene, slowpoke

Pallanck, Leo, Ganetzky, Barry·1994·Human Molecular Genetics

Abstract

Potassium channels play important roles in a wide variety of physiological processes. Although several genes encoding voltage-activated potassium channels have been analyzed at the molecular level, no calcium-activated potassium channel gene has yet been characterized in humans. In an effort to provide the foundation for functional analysis of such polypeptides we report the cloning of mouse and human homologs of the Drosophila melanogaster calcium-activated potassium channel gene, slowpoke. Both the human and mouse genes encode polypeptides that have more than 50% amino acid identifies with their Drosophila counterpart. In addition, like the Drosophila slowpoke gene, both the mouse and human genes generate multiple transcripts by alternative splicing. The human gene maps to chromosome 10 based on the results of polymerase chain reaction analysis of genomic DNA from human-hamster hybrid cell lines. Because calcium-activated potassium channels participate in wide variety of cellular functions including neuromuscular communication, secretion and cellular immunity, their continued analysis promises to have broad biological and medical significance.

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Metadata

Authors
Pallanck, L., & Ganetzky, B.
Venue
Human Molecular Genetics
Published
1994
Volume
3
Issue
8
Pages
1239-1243
ISSN
  • 0964-6906 (ISSN-L)
  • 1460-2083
OpenAlex
W2058612305
Cited by
179
References
0
FWCI
4.53
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Cloning and characterization of human and mouse homologs of the Drosophila calcium-activated potassium channel gene, slowpoke. https://app.cochat.ai/papers/10.1093/hmg/3.8.1239
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Pallanck, L., & Ganetzky, B. (1994). Cloning and characterization of human and mouse homologs of the Drosophila calcium-activated potassium channel gene, slowpoke. Human Molecular Genetics. https://doi.org/10.1093/hmg/3.8.1239

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