CACNA1D Membrane Protein Introduction

Introduction of CACNA1D

CACNA1D, Calcium channel, voltage-dependent, L type, alpha 1D subunit (also known as Cav1.3) is a protein that in humans is encoded by the CACNA1D gene. Cav1.3 channel is a member of the Cav1 family, which form L-type calcium currents and is sensitive to selective inhibition by dihydropyridines (DHP). It mediates the entry of calcium ions into excitable cells and is also involved in a variety of calcium-dependent processes, including muscle contraction, neurotransmitter or hormone release, gene expression, cell division cell motility, and cell death.

Basic Information of CACNA1D
Protein Name Voltage-dependent L-type calcium channel subunit alpha-1D
Gene Name CACNA1D
Aliases Calcium channel, L type, alpha-1 polypeptide, isoform 2, Voltage-gated calcium channel subunit alpha Cav1.3, CACH3, CACN4, CACNL1A2, CCHL1A2
Organism Homo sapiens (Human)
UniProt ID Q01668
Transmembrane Times 24
Length (aa) 2161

Function of CACNA1D Membrane Protein

CACNA1D is a member of voltage-sensitive calcium channels (VSCC) which mediates the entry of calcium ions into excitable cells and is also involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division, and cell death. The isoform alpha-1D gives rise to L-type calcium currents. It has been identified that Long-lasting (L-type) calcium channels are members of the 'high-voltage activated' (HVA) group. They are blocked by dihydropyridines (DHP), phenylalkylamines, benzothiazepines, and by omega-agatoxin-IIIA (omega-Aga-IIIA). They are however insensitive to omega-conotoxin-GVIA (omega-CTx-GVIA) and omega-agatoxin-IVA (omega-Aga-IVA).

Cav1.3 isoform structure. Fig.1 Cav1.3 isoform structure. (Zuccotti, 2011)

Application of CACNA1D Membrane Protein in Literature

  1. Azizan E.A., et al. Somatic mutations in ATP1A1 and CACNA1D underlie a common subtype of adrenal hypertension. Nat Genet. 2013, 45(9): 1055-60. PubMed ID: 23913004

    This article found that mutations of CACNA1D ATP1A1 and caused a shift of voltage-dependent gating to more negative voltages, suppressed inactivation or increased currents. Identification of the distinct genotype and phenotype for this subset could facilitate diagnosis.

  2. Tan G.C., et al. Aldosterone-Producing Adenomas: Histopathology-Genotype Correlation and Identification of a Novel CACNA1D Mutation. Hypertension. 2017, 70(1): 129-136. PubMed ID: 28584016

    This article found that the mutation in CACNA1D caused a hyperpolarizing shift of the voltage-dependent inactivation and activation and slowed the channel's inactivation kinetics. ATP1A1 and CACNA1D mutant adenomas had a specific histopathologic phenotype.

  3. Kabir Z.D., et al. From Gene to Behavior: L-Type Calcium Channel Mechanisms Underlying Neuropsychiatric Symptoms. Neurotherapeutics. 2017, 14(3): 588-613. PubMed ID: 28497380

    This study provided an overview of clinical studies that had evaluated LTCC blockers for BD, SCZ, and drug dependence-associated symptoms, in addition, rodent studies that had identified Cav1.2 and Cav1.3 specific molecular and cellular cascades that underlie mood (anxiety, depression), social behavior, cognition, and addiction.

  4. Pinggera A., et al. New gain-of-function mutation shows CACNA1D as recurrently mutated gene in autism spectrum disorders and epilepsy. Hum Mol Genet. 2017, 26(15): 2923-2932. PubMed ID: 28472301

    This article proved that CACNA1D could be as a new candidate autism risk gene and encouraged experimental therapy with available channel-blockers for this mutation. The additional presence of seizures and neurological abnormalities in our patient defined a novel phenotype partially overlapping with symptoms in two individuals with PASNA (congenital primary aldosteronism, seizures, and neurological abnormalities) caused by similar Cav1.3 gain-of-function mutations.

  5. Vincent P.F., et al. Different CaV1.3 Channel Isoforms Control Distinct Components of the Synaptic Vesicle Cycle in Auditory Inner Hair Cells. J Neurosci. 2017, 37(11): 2960-2975. PubMed ID: 28193694

    This article showed that this synaptic process involved long and short C-terminal isoforms of the Cav1.3 Ca2+ channel that differed in the kinetics of their Ca2+-dependent inactivation and their relative sensitivity to the L-type Ca2+ channel blocker nifedipine. The long isoforms, with slow inactivation and great sensitivity to nifedipine, mainly regulated the vesicular replenishment of the RRP; that was, the sustained or tonic exocytosis.

CACNA1D Preparation Options

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  1. Zuccotti A, et al. (2011). Structural and functional differences between L-type calcium channels: crucial issues for future selective targeting. Trends Pharmacol Sci. 32(6):366-75.

All listed customized services & products are for research use only, not intended for pharmaceutical, diagnostic, therapeutic or any in vivo human use.

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