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Primary structure and functional expression from complementary DNA of a brain calcium channel

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Abstract

The primary structure of a voltage-dependent cal-cium channel from rabbit brain has been deduced by cloning and sequencing the complementary DNA. Calcium channel activity expressed from the cDNA is dramatically increased by coexpression of the α2 and β subunits, known to be associated with the dihydropyridine receptor. This channel is a high voltage-activated calcium channel that is insensitive both to nifedipine and to ω-conotoxin. We suggest that it is expressed predominantly in cerebellar Purkinje cells and granule cells.

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Author notes

  1. Thomas Friedrich

    Present address: BASF AG, ZHB/P A30, D-6700, Ludwigshafen, Germany

  2. Shosaku Numa: To whom correspondence should be addressed.

Authors and Affiliations

  1. Departments of Medical Chemistry and Molecular Genetics, Kyoto University Faculty of Medicine, Kyoto, 606

    Yasuo Mori, Thomas Friedrich, Man-Suk Kim, Atsushi Mikami, Junichi Nakai, Keiji Imoto, Tsutomu Tanabe & Shosaku Numa

  2. Institut für Medizinische Biochemie, Medizinische Fakultät, Universität des Saarlandes, D-6650, Homburg/Saar, Germany

    Peter Ruth, Eva Bosse, Franz Hofmann & Veit Flockerzi

  3. Division of Behavior and Neurobiology, National Institute for Basic Biology, Okazaki, 444, Japan

    Teiichi Furuichi & Katsuhiko Mikoshiba

  4. Division of Regulation of Macromolecular Function, Institute for Protein Research, Osaka University, Suita, 565, Japan

    Katsuhiko Mikoshiba

Authors
  1. Yasuo Mori
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  2. Thomas Friedrich
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  3. Man-Suk Kim
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  4. Atsushi Mikami
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  5. Junichi Nakai
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  6. Peter Ruth
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  7. Eva Bosse
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  8. Franz Hofmann
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  9. Veit Flockerzi
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  10. Teiichi Furuichi
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  11. Katsuhiko Mikoshiba
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  12. Keiji Imoto
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  13. Tsutomu Tanabe
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  14. Shosaku Numa
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Mori, Y., Friedrich, T., Kim, MS. et al. Primary structure and functional expression from complementary DNA of a brain calcium channel. Nature 350, 398–402 (1991). https://doi.org/10.1038/350398a0

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  • DOI: https://doi.org/10.1038/350398a0

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