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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. Zusätzlich bieten wir Ihnen CACNA1G Antikörper (120) und CACNA1G Proteine (4) und viele weitere Produktgruppen zu diesem Protein an.
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 (zeige CACNA1H ELISA Kits) 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 (zeige CD2 ELISA Kits)+) and manganese (Mn(2+)) currents through the CaV3.1 mutants as well as a reduction in the inhibitory effect of Cd(2 (zeige CD2 ELISA Kits)+) on the Ca(2 (zeige CA2 ELISA Kits)+) 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 (zeige CACNA1H ELISA Kits) and CaV3.3 (zeige CACNA1I ELISA Kits) 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.
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
Data, including data from studies using knockout mice, suggest that acetylcholine- (Ach (zeige FGFR3 ELISA Kits)-)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 (zeige FGFR3 ELISA Kits)-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 (zeige GRIA4 ELISA Kits) 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 (zeige CSF2 ELISA Kits) by central nervous system-infiltrating Th1 (zeige HAND1 ELISA Kits) 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 (zeige CACNA1H ELISA Kits) are substrates for EHD3 (zeige EHD3 ELISA Kits)-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 (zeige CA5A ELISA Kits) 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
CaV3.1 structural analysis and comparison to CaV1.2 (zeige CACNA1C ELISA Kits) 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