Article
Cell Biology
Rachel Conrad, Daniel Kortzak, Gustavo A. Guzman, Erick Miranda-Laferte, Patricia Hidalgo
Summary: Membrane depolarization activates the Ca(V)1.2 L-type calcium channel, leading to various excitation coupling responses. The presence of Ca-V beta promotes fast transport speed along anterograde trafficking and controls the endocytic turnover of L-type calcium channels.
Article
Neurosciences
Laurent Ferron, Sydney D. Guderyan, Ethan J. Smith, Gerald W. Zamponi
Summary: The impact of Ca-v beta subunits on the plasma membrane expression of Ca(v)1.2 channels depends on their differential ability to protect the channels from degradation.
Article
Cardiac & Cardiovascular Systems
Arianne Papa, Jared Kushner, Jessica A. Hennessey, Alexander N. Katchman, Sergey Zakharov, Bi-xing Chen, Lin Yang, Ree Lu, Stephen Leong, Johanna Diaz, Guoxia Liu, Daniel Roybal, Xianghai Liao, Pedro J. del Rivero Morfin, Henry M. Colecraft, Geoffrey S. Pitt, Oliver Clarke, Veli Topkara, Manu Ben-Johny, Steven O. Marx
Summary: The study identified that the activity of Ca(V)1.2 channels is dynamically modulated by factors converging at the alpha(1C) I-II loop under different conditions, including basal conditions, beta-adrenergic stimulation, and heart failure. This has significant implications for cardiac physiology and pathophysiology.
CIRCULATION RESEARCH
(2021)
Review
Cell Biology
Amelie Vergnol, Massire Traore, France Pietri-Rouxel, Sestina Falcone
Summary: Voltage-gated calcium channels play crucial roles in regulating intracellular calcium levels and influencing various physiological processes in cells. The auxiliary CaV beta subunits, particularly their involvement in modulating Ca2+ signaling and gene expression, have been highlighted in recent research findings.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Article
Neurosciences
Alexandra Tran-Van-Minh, Michel De Waard, Norbert Weiss
Summary: Voltage-gated calcium channels are crucial for regulating brain function by allowing calcium entry into neurons. The proper functioning of these channels relies on the co-assembly of a pore-forming subunit (Ca-v alpha(1)) with ancillary subunits, with Ca-v beta playing a vital role in regulating surface expression and gating of the channels. In this study, the importance of surface charged residues in Ca-v beta(3) in the regulation of Ca(v)2.1 channels was investigated, revealing their contribution to channel gating and suggesting additional contacts beyond the known interaction between Ca-v alpha(1) and Ca-v beta.
Review
Biochemistry & Molecular Biology
Maartje Westhoff, Rose E. Dixon
Summary: During cardiac excitation-contraction coupling, the activity of Ca(V)1.2 channels plays a crucial role in regulating calcium influx, intracellular calcium concentration, and ultimately myocardial contraction. Recent studies have identified internal reservoirs of preformed Ca(V)1.2 channels that can be rapidly mobilized during acute stress to enhance sarcolemmal expression and maintain cardiac function.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Biochemistry & Molecular Biology
Ilona Uzieliene, Daiva Bironaite, Rokas Miksiunas, Edvardas Bagdonas, Raminta Vaiciuleviciute, Ali Mobasheri, Eiva Bernotiene
Summary: This study investigated the role of intracellular calcium (iCa(2+)) and its regulation through voltage-operated calcium channels (VOCC) in the chondrogenic differentiation of mesenchymal stem/stromal cells. Results showed that chondrocytes had the highest level of iCa(2+), while MenSCs had the largest iCa(2+) store capacity and proliferation ability. The expression of the CaV1.2 gene was highest in MenSCs during chondrogenic differentiation. Nifedipine, a CaV1.2 antagonist, could suppress iCa(2+) and proliferation in all cells and affect iCa(2+) stores, especially in BMMSCs.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Multidisciplinary Sciences
Taylor L. Voelker, Silvia G. del Villar, Maartje Westhoff, Alexandre D. Costa, Andrea M. Coleman, Johannes W. Hell, Mary C. Horne, Eamonn J. Dickson, Rose E. Dixon
Summary: CaV1.2 channels in the heart are affected by angiotensin II, a therapeutic target of heart failure drugs and regulator of blood pressure. Angiotensin II causes a decrease in PIP2, which leads to the suppression of CaV1.2 currents. This study found that PIP2 depletion destabilizes CaV1.2 channels and reduces their expression and function. The results suggest that PIP2 plays a crucial role in maintaining cardiac excitability and that angiotensin II-induced PIP2 depletion impairs excitation-contraction coupling.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2023)
Article
Multidisciplinary Sciences
Clemens L. Schoepf, Cornelia Ablinger, Stefanie M. Geisler, Ruslan Stanika, Marta Campiglio, Walter A. Kaufmann, Benedikt Nimmervoll, Bettina Schlick, Johannes Brockhaus, Markus Missler, Ryuichi Shigemoto, Gerald J. Obermair
Summary: The alpha(2)delta subunits in nerve cells play a critical role in the formation and organization of glutamatergic synapses, with defects leading to synaptic dysfunction and potentially neurological diseases. Each individual alpha(2)delta isoform can rescue presynaptic calcium channel trafficking and expression of synaptic proteins, suggesting a highly redundant role as synaptic organizers. These findings suggest a shift in understanding of excitatory synapse formation, highlighting the importance of presynaptic differentiation and the potential of alpha(2)delta subunits as nucleation points for synaptic organization.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2021)
Article
Cell Biology
Joerg Isensee, Marianne van Cann, Patrick Despang, Dioneia Araldi, Katharina Moeller, Jonas Petersen, Achim Schmidtko, Jan Matthes, Jon D. Levine, Tim Hucho
Summary: Depolarization activates protein kinase A type II in nociceptive neurons, leading to sensitization. This process involves calcium influx through Ca(V)1.2 channels, calpains modulation, and phosphorylation of Ca(V)1.2, ultimately resulting in local peripheral hyperalgesia.
JOURNAL OF CELL BIOLOGY
(2021)
Editorial Material
Physiology
Laurent Ferron, Gerald W. Zamponi
Summary: The specific gating effects of Timothy syndrome Ca(V)1.2 channel mutations determine the deficits in cardiovascular and nervous systems.
JOURNAL OF GENERAL PHYSIOLOGY
(2022)
Article
Allergy
Nicolas Giang, Marion Mars, Marc Moreau, Jose E. Mejia, Gregory Bouchaud, Antoine Magnan, Marine Michelet, Brice Ronsin, Geoffrey G. Murphy, Joerg Striessnig, Jean-Charles Guery, Lucette Pelletier, Magali Savignac
Summary: This study demonstrates that Ca(v)1.2 and Ca(v)1.3 in Th2 cells have non-redundant and synergistic functions, and deficiency in either one of these channels is sufficient to inhibit cardinal features of type 2 airway inflammation.
Article
Biochemistry & Molecular Biology
Guillermo Avila
Summary: Fluorofenidone (AKF-PD) is a compound that inhibits fibrosis and inflammation. It has been shown to enhance cell contractility and Ca2+ channel activity in cardiac myocytes, suggesting potential therapeutic effects for cardiac diseases.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2023)
Article
Biochemistry & Molecular Biology
Shuai Gao, Xia Yao, Jiaofeng Chen, Gaoxingyu Huang, Xiao Fan, Lingfeng Xue, Zhangqiang Li, Tong Wu, Yupeng Zheng, Jian Huang, Xueqin Jin, Yan Wang, Zhifei Wang, Yong Yu, Lei Liu, Xiaojing Pan, Chen Song, Nieng Yan
Summary: Cav1.2 channels have important functions in neuronal and physiological processes. Cryo-EM structures of human Cav1.2 in different states, including its apo form and in complex with drugs or peptides, reveal consistent inactivated conformations. The binding of certain drugs induces structural changes, such as upward movement of VSDII and dilation of the selectivity filter and its surrounding segments.
Review
Physiology
Kunal R. Shah, Xin Guan, Jiusheng Yan
Summary: Ion channels can form macromolecular signaling complexes to ensure accurate signal transduction. The BK channel limits increases in [Ca2+]i levels through K+ efflux and rapid membrane repolarization, serving as a negative feedback regulator.
FRONTIERS IN PHYSIOLOGY
(2022)