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Interactive cloning with the SH3 domain of N-src identifies a new brain specific ion channel protein, with homology to eag and cyclic nucleotide-gated channels.

TitleInteractive cloning with the SH3 domain of N-src identifies a new brain specific ion channel protein, with homology to eag and cyclic nucleotide-gated channels.
Publication TypeJournal Article
Year of Publication1997
AuthorsSantoro B, Grant SG, Bartsch D, Kandel ER
JournalProc Natl Acad Sci U S A
Volume94
Issue26
Pagination14815-20
Date Published1997 Dec 23
ISSN0027-8424
KeywordsAmino Acid Sequence, Animals, Brain, Cloning, Molecular, Cyclic Nucleotide-Gated Cation Channels, Ether-A-Go-Go Potassium Channels, Genes, src, Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels, Ion Channel Gating, Ion Channels, Mice, Molecular Sequence Data, Nerve Tissue Proteins, Nucleotides, Cyclic, Organ Specificity, Potassium Channels, Sequence Alignment, src Homology Domains
Abstract

We have isolated a novel cDNA, that appears to represent a new class of ion channels, by using the yeast two-hybrid system and the SH3 domain of the neural form of Src (N-src) as a bait. The encoded polypeptide, BCNG-1, is distantly related to cyclic nucleotide-gated channels and the voltage-gated channels, Eag and H-erg. BCNG-1 is expressed exclusively in the brain, as a glycosylated protein of approximately 132 kDa. Immunohistochemical analysis indicates that BCNG-1 is preferentially expressed in specific subsets of neurons in the neocortex, hippocampus, and cerebellum, in particular pyramidal neurons and basket cells. Within individual neurons, the BCNG-1 protein is localized to either the dendrites or the axon terminals depending on the cell type. Southern blot analysis shows that several other BCNG-related sequences are present in the mouse genome, indicating the emergence of an entire subfamily of ion channel coding genes. These findings suggest the existence of a new type of ion channel, which is potentially able to modulate membrane excitability in the brain and could respond to regulation by cyclic nucleotides.

Alternate JournalProc. Natl. Acad. Sci. U.S.A.
PubMed ID9405696
PubMed Central IDPMC25120