ArticleThe Journal of biological chemistry2016
Identification of Glycosylation Sites Essential for Surface Expression of the CaVα2δ1 Subunit and Modulation of the Cardiac CaV1.2 Channel Activity.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- The Potential Role of Calcium Channels in Pulmonary Hypertension.BioMed research international · 2026Review
- Integrated Multiomics Reveals Alterations in Paucimannose and Complex Type N-Glycans in Cardiac Tissue of Patients with COVID-19.Molecular & cellular proteomics : MCP · 2025Article
- Protein glycosylation in cardiovascular health and disease.Nature reviews. Cardiology · 2024Review
- Brain α2δ-1-Bound NMDA Receptors Drive Calcineurin Inhibitor-Induced Hypertension.Circulation research · 2023Article
- Acute phosphatidylinositol 4,5 bisphosphate depletion destabilizes sarcolemmal expression of cardiac L-type CaProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Glycans and Carbohydrate-Binding/Transforming Proteins in Axon Physiology.Advances in neurobiology · 2023Article
- Gabapentin Disrupts Binding of Perlecan to the αBiomolecules · 2022Article
- Sympathetic Stimulation Upregulates the CaCells · 2022Article
- α2δ-1 switches the phenotype of synaptic AMPA receptors by physically disrupting heteromeric subunit assembly.Cell reports · 2021Article
- α2δ-1 Upregulation in Primary Sensory Neurons Promotes NMDA Receptor-Mediated Glutamatergic Input in Resiniferatoxin-Induced Neuropathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Importance of evaluating protein glycosylation in pluripotent stem cell-derived cardiomyocytes for research and clinical applications.Pflugers Archiv : European journal of physiology · 2021Review
- The life cycle of voltage-gated CaNeuronal signaling · 2021Review
- Post-Translational Modification of Cav1.2 and its Role in Neurodegenerative Diseases.Frontiers in pharmacology · 2021Review
- Glycobiology and schizophrenia: a biological hypothesis emerging from genomic research.Molecular psychiatry · 2020Review
- Different functions of two putative Drosophila αScientific reports · 2020Article
- Ionomycin ameliorates hypophosphatasia via rescuing alkaline phosphatase deficiency-mediated L-type CaBone research · 2020Article
- Increased α2δ-1-NMDA receptor coupling potentiates glutamatergic input to spinal dorsal horn neurons in chemotherapy-induced neuropathic pain.Journal of neurochemistry · 2019Article
- Reduced myocyte complex N-glycosylation causes dilated cardiomyopathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- A three-way inter-molecular network accounts for the CaThe Journal of biological chemistry · 2018Article
- Stroke-Like Episodes and Cerebellar Syndrome in Phosphomannomutase Deficiency (PMM2-CDG): Evidence for Hypoglycosylation-Driven Channelopathy.International journal of molecular sciences · 2018Article
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Authors and funding
7 authors.
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Abstract
Alteration in the L-type current density is one aspect of the electrical remodeling observed in patients suffering from cardiac arrhythmias. Changes in channel function could result from variations in the protein biogenesis, stability, post-translational modification, and/or trafficking in any of the regulatory subunits forming cardiac L-type Ca(2+) channel complexes. CaVα2δ1 is potentially the most heavily N-glycosylated subunit in the cardiac L-type CaV1.2 channel complex. Here, we show that enzymatic removal of N-glycans produced a 50-kDa shift in the mobility of cardiac and recombinant CaVα2δ1 proteins. This change was also observed upon simultaneous mutation of the 16 Asn sites. Nonetheless, the mutation of only 6/16 sites was sufficient to significantly 1) reduce the steady-state cell surface fluorescence of CaVα2δ1 as characterized by two-color flow cytometry assays and confocal imaging; 2) decrease protein stability estimated from cycloheximide chase assays; and 3) prevent the CaVα2δ1-mediated increase in the peak current density and voltage-dependent gating of CaV1.2. Reversing the N348Q and N812Q mutations in the non-operational sextuplet Asn mutant protein partially restored CaVα2δ1 function. Single mutation N663Q and double mutations N348Q/N468Q, N348Q/N812Q, and N468Q/N812Q decreased protein stability/synthesis and nearly abolished steady-state cell surface density of CaVα2δ1 as well as the CaVα2δ1-induced up-regulation of L-type currents. These results demonstrate that Asn-663 and to a lesser extent Asn-348, Asn-468, and Asn-812 contribute to protein stability/synthesis of CaVα2δ1, and furthermore that N-glycosylation of CaVα2δ1 is essential to produce functional L-type Ca(2+) channels.
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