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Voltage-sensitive calcium channels mediate the entry of calcium ions into excitable cells, and are 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.
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Mammalian Monoclonal CACNA1G Primary Antibody pour ISt, IHC - ABIN1304582
Curran, Musa, Kline, Makara, Little, Higgins, Hund, Band, Mohler: Eps15 Homology Domain-containing Protein 3 Regulates Cardiac T-type Ca2+ Channel Targeting and Function in the Atria. dans The Journal of biological chemistry 2015
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Human Polyclonal CACNA1G Primary Antibody pour IF (p), IHC (p) - ABIN680608
Lu, Long, Zhou, Xu, Hu, Li: Mibefradil reduces blood glucose concentration in db/db mice. dans Clinics (São Paulo, Brazil) 2014
Cow (Bovine) Polyclonal CACNA1G Primary Antibody pour ELISA - ABIN4286741
Ernst, Zhang, Yoo, Ernst, Noebels: Genetic enhancement of thalamocortical network activity by elevating alpha 1g-mediated low-voltage-activated calcium current induces pure absence epilepsy. dans The Journal of neuroscience : the official journal of the Society for Neuroscience 2009
Human Polyclonal CACNA1G Primary Antibody pour IHC, IHC (p) - ABIN4286744
Strandberg, Cui, Rath, Liu, Silverman, Liu, Siragam, Ackerley, Su, Yan, Capecchi, Biavati, Accorroni, Yuen, Quattrone, Lung, Jaeggi, Backx, Deber, Hamilton: Congenital heart block maternal sera autoantibodies target an extracellular epitope on the α1G T-type calcium channel in human fetal hearts. dans PLoS ONE 2013
Human Polyclonal CACNA1G Primary Antibody pour IHC, IHC (p) - ABIN4286742
Borahay, Kilic, Yallampalli, Snyder, Hankins, Al-Hendy, Boehning: Simvastatin potently induces calcium-dependent apoptosis of human leiomyoma cells. dans The Journal of biological chemistry 2014
T-type channel calcium influx invokes a novel dynamic interaction between CaM and Cav3.1 channels to trigger a signaling cascade that leads to alphaCaMKII activation.
human Cav3.1, Cav3.2, and Cav3.3 T-type channels specifically associate with CaM at helix 2 of the gating brake in the I-II linker of the channels.
Here we show that T-type channels Cav3.1 and Cav3.2 (Montrer CACNA1H Anticorps) are present in the lung and PASMCs from iPAH patients and control subjects. The blockade of T-type channels by the specific blocker, TTA-A2, prevents cell cycle progression and PASMCs growth
Cacna1g exclusively expressed in serosal PDGFRalpha+ cells is a new pathological marker for gastrointestinal diseases.
Electrophysiological studies showed a significant increase in Cd(2 (Montrer CD2 Anticorps)+) and manganese (Mn(2+)) currents through the CaV3.1 mutants as well as a reduction in the inhibitory effect of Cd(2 (Montrer CD2 Anticorps)+) on the Ca(2 (Montrer CA2 Anticorps)+) current.
The results of this study provide support for Cacna1g as a genetic modifier in a mouse model of Dravet syndrome and suggest that Cav3.1 may be a potential molecular target for therapeutic intervention in patients
CACNA1G variant is associated with differential antiepileptic drug response in childhood absence epilepsy.
CaV3.1, CaV3.2 (Montrer CACNA1H Anticorps) and CaV3.3 (Montrer CACNA1I Anticorps) channels, are best recognized for their negative voltage of activation and inactivation thresholds that allow them to operate near the resting membrane potential of neurons.
In 2 families with autosomal dominant SCA, a CACNA1G mutation p.Arg1715His was found at S4 of repeat IV, the voltage sensor of the CaV3.1 which shifted it toward a positive potential.
A Recurrent Mutation in CACNA1G Alters Cav3.1 T-Type Calcium-Channel Conduction and Causes Autosomal-Dominant Cerebellar Ataxia.
Membrane-protein extraction and use of an intracellular protein (Montrer CKAP2 Anticorps)-transport inhibitor showed that GDF-15 (Montrer GDF15 Anticorps) promoted CaV3.1 and CaV3.3 (Montrer CACNA1I Anticorps) alpha-subunit (Montrer POLG Anticorps) expression by trafficking to the membrane.
Data, including data from studies using knockout mice, suggest that acetylcholine- (Ach (Montrer FGFR3 Anticorps)-)induced vasorelaxation/vasodilatation of intrapulmonary arteries is reduced in pulmonary hypertension, but is still dependent on Cav3.1 activity; thus, Cav3.1 contributes to intrapulmonary vascular reactivity by controlling calcium signaling in arterial endothelium and Ach (Montrer FGFR3 Anticorps)-induced vasorelaxation/vasodilatation.
These results provide support for Cacna1g as an epilepsy modifier gene and suggest that modulation of Cav3.1 may be an effective therapeutic strategy.
Localized Cav3.1 knockdown in the medial septum selectively enhanced object exploration, whereas the null mutant (KO) mice showed enhanced-object exploration as well as open-field exploration.
GluA4 (Montrer GRIA4 Anticorps) subunits are required to produce an EPSC-triggerable postsynaptic action potentials after the presynaptic action potential, while Cav3.1 expression is needed to establish the driver function of L5B-POm synapses at hyperpolarized membrane potentials
Mice deficient for CaV3.1 were resistant to the induction of experimental autoimmune encephalomyelitis and had reduced productions of the granulocyte-macrophage colony-stimulating factor (Montrer CSF2 Anticorps) by central nervous system-infiltrating Th1 (Montrer HAND1 Anticorps) and Th17 cells.
Cross-frequency coupling between low-frequency and gamma rhythms was pronounced in wild-type but not in CaV3.1 knockouts, suggesting that the presence of CaV3.1 channels is a key element in the pathophysiology of trigeminal neuropathic pain.
CaV3.1 and CaV3.2 (Montrer CACNA1H Anticorps) are substrates for EHD3 (Montrer EHD3 Anticorps)-dependent protein trafficking in heart
This study reported on the cloning and characterization of a proximal promoter region and initiated the analysis of transcription factors that control CaV (Montrer CA5A Anticorps) 3.1 channel expression using the murine Cacna1g gene as a model.
CaV3.1 structural analysis and comparison to CaV1.2 (Montrer CACNA1C Anticorps) channel
Voltage-sensitive calcium channels mediate the entry of calcium ions into excitable cells, and are 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. This gene encodes a T-type, low-voltage activated calcium channel. The T-type channels generate currents that are both transient, owing to fast inactivation, and tiny, owing to small conductance. T-type channels are thought to be involved in pacemaker activity, low-threshold calcium spikes, neuronal oscillations and resonance, and rebound burst firing. Many alternatively spliced transcript variants encoding different isoforms have been described for this gene.
voltage-dependent calcium channel alpha 1G subunit
, calcium channel, voltage-dependent, T type, alpha 1G subunit
, calcium channel voltage-dependent T type Cav3.1, alpha 1g subunit
, voltage-dependent T-type calcium channel subunit alpha-1G
, voltage-gated calcium channel subunit alpha Cav3.1
, calcium channel, voltage-dependent, alpha 1G subunit