ArticleThe Journal of biological chemistry2011
Truncation of murine CaV1.2 at Asp-1904 results in heart failure after birth.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Sympathetic Nervous System Regulation of Cardiac Calcium Channels.Handbook of experimental pharmacology · 2023Article
- Adrenergic Regulation of Calcium Channels in the Heart.Annual review of physiology · 2022Review
- Cardiac CaV1.2 channels require β subunits for β-adrenergic-mediated modulation but not trafficking.The Journal of clinical investigation · 2019Article
- An African loss-of-function CACNA1C variant p.T1787M associated with a risk of ventricular fibrillation.Scientific reports · 2018Article
- Identification of a novel cAMP dependent protein kinase A phosphorylation site on the human cardiac calcium channel.Scientific reports · 2017Article
- Protein kinase C enhances plasma membrane expression of cardiac L-type calcium channel, CaChannels (Austin, Tex.) · 2017Article
- PMEnvironmental pollution (Barking, Essex : 1987) · 2017Article
- Proteolytic cleavage and PKA phosphorylation of αProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Protein kinase A regulates C-terminally truncated CaThe Journal of physiology · 2017Article
- The PDZ motif of the α1C subunit is not required for surface trafficking and adrenergic modulation of CaV1.2 channel in the heart.The Journal of biological chemistry · 2015Article
- Ion channel engineering: perspectives and strategies.Journal of molecular biology · 2015Review
- Regulation of Cardiac Calcium Channels in the Fight-or-Flight Response.Current molecular pharmacology · 2015Review
- Counteracting Protein Kinase Activity in the Heart: The Multiple Roles of Protein Phosphatases.Frontiers in pharmacology · 2015Review
- Basal and β-adrenergic regulation of the cardiac calcium channel CaV1.2 requires phosphorylation of serine 1700.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- L-type CaWiley interdisciplinary reviews. Membrane transport and signaling · 2014Article
- Trafficking highways to the intercalated disc: new insights unlocking the specificity of connexin 43 localization.Cell communication & adhesion · 2014Review
- Phosphorylation sites required for regulation of cardiac calcium channels in the fight-or-flight response.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Manipulating L-type calcium channels in cardiomyocytes using split-intein protein transsplicing.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- β-adrenergic regulation of the L-type Ca2+ channel does not require phosphorylation of α1C Ser1700.Circulation research · 2013Article
- Truncation of murine CaV1.2 at Asp 1904 increases CaV1.3 expression in embryonic atrial cardiomyocytes.Pflugers Archiv : European journal of physiology · 2013Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The carboxyl-terminal intracellular tail of the L-type Ca(2+) channel CaV1.2 modulates various aspects of channel activity.For example, deletion of the carboxyl-terminal sequence at Ser-1905 increased CaV1.2 currents in an expression model. To verify this finding in an animal model, we inserted three stop codons at the corresponding Asp-1904 in the murine CaV1.2 gene. Mice homozygous for the Stop mutation (Stop/Stop mice)were born at a Mendelian ratio but died after birth. Stop/Stop hearts showed reduced beating frequencies and contractions.Surprisingly, Stop/Stop cardiomyocytes displayed reduced IBa and a minor expression of the CaV1.2Stop protein. In contrast,expression of the CaV1.2Stop protein was normal in pooled smooth muscle samples from Stop/Stop embryos. As the CaV1.2 channel exists in a cardiac and smooth muscle splice variant, HK1 and LK1, respectively, we analyzed the consequences of the deletion of the carboxyl terminus in the respective splice variant using the rabbit CaV1.2 clone expressed in HEK293 cells.HEK293 cells transfected with the HK1Stop channel showed a reduced IBa and CaV1.2 expression. Treatment with proteasome inhibitors increased the expression of HK1Stop protein and IBa in HEK293 cells and in Stop/Stop cardiomyocytes indicating that truncation of CaV1.2 containing the cardiac exon 1a amino terminus results in proteasomal degradation of the translated protein. In contrast, HEK293 cells transfected with the LK1Stop channel had normal IBa and CaV1.2 expression. These findings indicate that absence of the carboxyl-terminal tail differentially determines the fate of the cardiac and smooth muscle splice variant of the CaV1.2 channel in the mouse.
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