anti-Calcium Channel, Voltage-Dependent, T Type, alpha 1G Subunit (CACNA1G) Antibodies

Human Calcium Channel, Voltage-Dependent, T Type, alpha 1G Subunit (CACNA1G) interaction partners

1. 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.

2. 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.

3. Here we show that T-type channels Cav3.1 and Cav3.2 (show CACNA1H Antibodies) 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

4. Cacna1g exclusively expressed in serosal PDGFRalpha+ cells is a new pathological marker for gastrointestinal diseases.

5. Electrophysiological studies showed a significant increase in Cd(2 (show CD2 Antibodies)+) and manganese (Mn(2+)) currents through the CaV3.1 mutants as well as a reduction in the inhibitory effect of Cd(2 (show CD2 Antibodies)+) on the Ca(2 (show CA2 Antibodies)+) current.

6. 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

7. CACNA1G variant is associated with differential antiepileptic drug response in childhood absence epilepsy.

8. 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.

9. 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.

10. A Recurrent Mutation in CACNA1G Alters Cav3.1 T-Type Calcium-Channel Conduction and Causes Autosomal-Dominant Cerebellar Ataxia.

Mouse (Murine) Calcium Channel, Voltage-Dependent, T Type, alpha 1G Subunit (CACNA1G) interaction partners

1. Membrane-protein extraction and use of an intracellular protein (show CKAP2 Antibodies)-transport inhibitor showed that GDF-15 (show GDF15 Antibodies) promoted CaV3.1 and CaV3.3 (show CACNA1I Antibodies) alpha-subunit (show POLG Antibodies) expression by trafficking to the membrane.

2. Cacna1g exclusively expressed in serosal PDGFRalpha+ cells is a new pathological marker for gastrointestinal diseases.

3. Data, including data from studies using knockout mice, suggest that acetylcholine- (Ach (show FGFR3 Antibodies)-)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 (show FGFR3 Antibodies)-induced vasorelaxation/vasodilatation.

4. These results provide support for Cacna1g as an epilepsy modifier gene and suggest that modulation of Cav3.1 may be an effective therapeutic strategy.

5. 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.

6. 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

7. 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.

8. 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.

9. CaV3.1 and CaV3.2 (show CACNA1H Antibodies) are substrates for EHD3 (show EHD3 Antibodies)-dependent protein trafficking in heart

10. 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.

Cow (Bovine) Calcium Channel, Voltage-Dependent, T Type, alpha 1G Subunit (CACNA1G) interaction partners

1. CaV3.1 structural analysis and comparison to CaV1.2 (show CACNA1C Antibodies) channel