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The Ca V 1.2 channel C‐terminus fragment is a transcriptional vasodilator
Author(s) -
Bannister John P,
Leo Marie Dennis,
Naryanan Damodaran,
Nair Anitha,
Pachuau Judith,
Jaggar Jonathan H
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.870.2
Subject(s) - contractility , vasodilation , depolarization , messenger rna , vasoconstriction , myocyte , transcription (linguistics) , chemistry , microbiology and biotechnology , biology , endocrinology , gene , biochemistry , linguistics , philosophy
Arterial myocyte voltage‐dependent L‐type (Ca V 1.2) channels are essential for physiological control of vascular contractility. The Ca V 1.2 channel C‐terminus is post‐translationally cleaved, yielding a protein fragment (CCT) that contains a putative nuclear targeting sequence and can act as a transcription factor. Here, we investigated physiological functions of the CCT in myocytes of resistance‐size cerebral arteries. Immunofluorescence using a custom antibody raised to CCT identified CCT localized to both the nucleus and plasma membrane. CCT overexpression reduced Ca V 1.2 mRNA and protein, and reduced pressure and depolarization‐induced vasoconstriction. Overexpression of a CCT construct lacking the putative nuclear targeting sequence did not alter Ca V 1.2 mRNA, protein or arterial contractility. These data suggest that the CCT inhibits Ca V 1.2 transcription and is a cerebral vasodilator. NIH/NHLBI
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