ArticleThe Journal of biological chemistry2007
A novel Ca(V)1.2 N terminus expressed in smooth muscle cells of resistance size arteries modifies channel regulation by auxiliary subunits.
Article in The Journal of biological chemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 56 citations in OpenAlex.
- Trial
- The psychiatric risk gene CACNA1C encodes distinct full-length isoforms in human brain, heart and aorta.Molecular psychiatry · 2026Article
- Article
- Rapid Pacing Decreases L-type CaThe Journal of membrane biology · 2023Article
- Alternative Splicing of the Flip/Flop Cassette and TARP Auxiliary Subunits Engage in a Privileged Relationship That Fine-Tunes AMPA Receptor Gating.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022Review
- Alternative Splicing at N Terminus and Domain I Modulates CaBiophysical journal · 2018Article
- Differences in L-type CaAmerican journal of physiology. Heart and circulatory physiology · 2018Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Calcium Channels in Vascular Smooth Muscle.Advances in pharmacology (San Diego, Calif.) · 2017Review
- Associations of Variants in the CACNA1A and CACNA1C Genes With Longitudinal Blood Pressure Changes and Hypertension Incidence: The GenSalt Study.American journal of hypertension · 2016Article
- Rab25 influences functional Cav1.2 channel surface expression in arterial smooth muscle cells.American journal of physiology. Cell physiology · 2016Article
- Post-transcriptional modifications and "Calmodulation" of voltage-gated calcium channel function: Reflections by two collaborators of David T Yue.Channels (Austin, Tex.) · 2016Review
- Expression of Calcium Channel Subunit Variants in Small Mesenteric Arteries of WKY and SHR.American journal of hypertension · 2015Article
- Intravascular pressure enhances the abundance of functional Kv1.5 channels at the surface of arterial smooth muscle cells.Science signaling · 2015Article
- Alternative splicing generates a novel truncated Cav1.2 channel in neonatal rat heart.The Journal of biological chemistry · 2015Article
- Cinnamaldehyde inhibits L-type calcium channels in mouse ventricular cardiomyocytes and vascular smooth muscle cells.Pflugers Archiv : European journal of physiology · 2014Article
- Eugenol dilates rat cerebral arteries by inhibiting smooth muscle cell voltage-dependent calcium channels.Journal of cardiovascular pharmacology · 2014Article
- Should pharmacologists care about alternative splicing? IUPHAR Review 4.British journal of pharmacology · 2014Review
- 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
7 authors at 1 institution in 1 country.
Funding
Abstract
Voltage-dependent L-type Ca(2+) (Ca(V)1.2) channels are the principal Ca(2+) entry pathway in arterial myocytes. Ca(V)1.2 channels regulate multiple vascular functions and are implicated in the pathogenesis of human disease, including hypertension. However, the molecular identity of Ca(V)1.2 channels expressed in myocytes of myogenic arteries that regulate vascular pressure and blood flow is unknown. Here, we cloned Ca(V)1.2 subunits from resistance size cerebral arteries and demonstrate that myocytes contain a novel, cysteine rich N terminus that is derived from exon 1 (termed "exon 1c"), which is located within CACNA1C, the Ca(V)1.2 gene. Quantitative PCR revealed that exon 1c was predominant in arterial myocytes, but rare in cardiac myocytes, where exon 1a prevailed. When co-expressed with alpha(2)delta subunits, Ca(V)1.2 channels containing the novel exon 1c-derived N terminus exhibited: 1) smaller whole cell current density, 2) more negative voltages of half activation (V(1/2,act)) and half-inactivation (V(1/2,inact)), and 3) reduced plasma membrane insertion, when compared with channels containing exon 1b. beta(1b) and beta(2a) subunits caused negative shifts in the V(1/2,act) and V(1/2,inact) of exon 1b-containing Ca(V)1.2alpha(1)/alpha(2)delta currents that were larger than those in exon 1c-containing Ca(V)1.2alpha(1)/alpha(2)delta currents. In contrast, beta(3) similarly shifted V(1/2,act) and V(1/2,inact) of currents generated by exon 1b- and exon 1c-containing channels. beta subunits isoform-dependent differences in current inactivation rates were also detected between N-terminal variants. Data indicate that through novel alternative splicing at exon 1, the Ca(V)1.2 N terminus modifies regulation by auxiliary subunits. The novel exon 1c should generate distinct voltage-dependent Ca(2+) entry in arterial myocytes, resulting in tissue-specific Ca(2+) signaling.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.