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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. Additionally we are shipping CACNA1G Proteins (4) and many more products for this protein.
Showing 10 out of 86 products:
Human Monoclonal CACNA1G Primary Antibody for ICC, IF - ABIN2483301
Perez-Reyes: Molecular physiology of low-voltage-activated t-type calcium channels. in Physiological reviews 2002
Human Polyclonal CACNA1G Primary Antibody for FACS, IF (p) - ABIN680608
Lu, Long, Zhou, Xu, Hu, Li: Mibefradil reduces blood glucose concentration in db/db mice. in Clinics (São Paulo, Brazil) 2014
Dog (Canine) Polyclonal CACNA1G Primary Antibody for IHC, WB - ABIN2776348
Ogino, Kawasaki, Kirkner, Kraft, Loda, Fuchs: Evaluation of markers for CpG island methylator phenotype (CIMP) in colorectal cancer by a large population-based sample. in The Journal of molecular diagnostics : JMD 2007
CaV3.1, CaV3.2 (show CACNA1H Antibodies) and CaV3.3 (show CACNA1I Antibodies) 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 (show USP14 Antibodies).
CaV3.1 channel is required for the generation of a given set of thalamocortical rhythms during unconsciousness. Further, that thalamocortical resonant neuronal activity supported by this channel is important for the control of vigilance states
CaV3.1 downregulation is a major initiating factor for the increased production of the toxic Ab peptide, then the CaV3.1 T-type calcium channel represents a novel target for preventative therapeutics in Alzheimer's disease.
Ethanol affects CaV3.2 (show CACNA1H Antibodies) but not CaV3.1 nor CaV3.3 (show CACNA1I Antibodies) channel isoforms.
Cd(2 (show CD2 Antibodies)) carried sizable inward currents through Ca(v)3.1 channels (210 +/- 20 pA at -60 mV with 2 mM Cd(2 (show CD2 Antibodies))).
Ca(V)3.1 channels represent a likely pathway for Fe(2) entry into cells.
Augmentation of CaV3.1 currents by Ras-ERK (show EPHB2 Antibodies) activation is associated with enhanced trafficking of channels to the plasma membrane.
Cav3.1 channels may contribute to the repression of tumor proliferation and the promotion of apoptosis mediated via Cav3.1-specific calcium signals
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 (show GRIA4 Antibodies) 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 (show CSF2 Antibodies) by central nervous system-infiltrating Th1 (show HAND1 Antibodies) 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 (show CACNA1H Antibodies) are substrates for EHD3 (show EHD3 Antibodies)-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 (show CA5A Antibodies) 3.1 channel expression using the murine Cacna1g gene as a model.
Ca(v)3.1-dependent synaptic depression at thalamocortical projections contributes to mechanisms of forward suppression in the auditory cortex
Suggest that T-type Ca(2 (show CA2 Antibodies)+) channels play an important role in infranodal escape automaticity.
CaV (show CA5A Antibodies) 3.1 channels are important for the myogenic tone at low arterial pressure, which is potentially relevant under resting conditions in vivo mice.
CaV3.1 structural analysis and comparison to CaV1.2 (show CACNA1C Antibodies) 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