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• W2090824775 endingPage "375" @default.
• W2090824775 startingPage "366" @default.
• W2090824775 abstract "Within the family of voltage-gated calcium channels (VGCCs), L-type channels (L-VGCCs) represent a well-established therapeutic target for calcium channel blockers, which are widely used to treat hypertension and myocardial ischemia. L-VGCCs outside the cardiovascular system also control key physiological processes such as neuronal plasticity, sensory cell function (e.g. in the inner ear and retina) and endocrine function (e.g. in pancreatic beta cells and adrenal chromaffin cells). Research into L-VGCCs was stimulated by the discovery that the known L-VGCC isoforms (CaV1.1, CaV1.2, CaV1.3 and CaV1.4) possess different biophysical properties. However, no L-VGCC-isoform-selective drugs have yet been identified. In this review, we examine CaV1.2 and CaV1.3 isoforms at the level of genetic structure, splice variants, post-translational modifications and functional protein coupling. We discuss candidate CaV1.2- and CaV1.3-specific characteristics as future therapeutic targets in individual organs. Within the family of voltage-gated calcium channels (VGCCs), L-type channels (L-VGCCs) represent a well-established therapeutic target for calcium channel blockers, which are widely used to treat hypertension and myocardial ischemia. L-VGCCs outside the cardiovascular system also control key physiological processes such as neuronal plasticity, sensory cell function (e.g. in the inner ear and retina) and endocrine function (e.g. in pancreatic beta cells and adrenal chromaffin cells). Research into L-VGCCs was stimulated by the discovery that the known L-VGCC isoforms (CaV1.1, CaV1.2, CaV1.3 and CaV1.4) possess different biophysical properties. However, no L-VGCC-isoform-selective drugs have yet been identified. In this review, we examine CaV1.2 and CaV1.3 isoforms at the level of genetic structure, splice variants, post-translational modifications and functional protein coupling. We discuss candidate CaV1.2- and CaV1.3-specific characteristics as future therapeutic targets in individual organs. α1 pore-forming subunit of L-type voltage gated Ca2+ channels (L-VGCCs), encoded by CACNA1. a voltage range that is more negative than the activation voltage for a predominant depolarizing mechanism. mechanism that operates by combinatorial inclusion or exclusion of alternatively spliced exons, insertion of one or more base pairs or alternative 3′ and 5′ ends. Ca2+-dependent intrinsic feedback mechanism that limits its own Ca2+ influx. L-VGCC mechanisms that respond to membrane depolarization by conformational changes, controlling channel opening and closing. intrinsic gating modulator located in the C terminus of L-VGCCs. CTM prevents or reduces CDI and shifts the activation voltage range to more positive potentials. defined as the capability of a given cell type or tissue to generate action potentials by its own intrinsic electrical properties, without the need for an external physiological trigger. also known as upstate transition, indicates the period during which a neuron (or an excitable cell) can fire single or bursts of action potentials. although not strictly defined in function, they interact and/or bind with multiple members of a signaling pathway, tethering them into complexes. a DNA sequence variation occurring when a single nucleotide in the genome differs between members of a species or paired chromosomes in an individual. the intrinsic property of the heart to develop a mechanical force, such as contraction. Drugs, neurotransmitters and ion channels can increase or decrease contractility, leading to positive or negative inotropism, respectively." @default.
• W2090824775 created "2016-06-24" @default.
• W2090824775 creator A5004536401 @default.
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• W2090824775 date "2011-06-01" @default.
• W2090824775 modified "2023-10-16" @default.
• W2090824775 title "Structural and functional differences between L-type calcium channels: crucial issues for future selective targeting" @default.
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