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. These findings reveal spectrin (alpha/beta) / ankyrin B cytoskeletal and signaling proteins as key regulators of T-type calcium channels expressed in the nervous system.

2. 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.

3. 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.

4. Here we show that T-type channels Cav3.1 and Cav3.2 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

5. In gastric cancer, expression of all the CACNA (1G, 1H, 1I) genes was associated with overall survival (OS) among stage I-IV patients. By combining the three potential biomarkers, a TTCC signature was developed, which retained a significant association with OS both in stage IV and stage I-III patients. Alterations in CACNA gene expression are linked to tumour prognosis.

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

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

8. 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

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

10. CaV3.1, CaV3.2 and CaV3.3 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.

11. 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.

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

13. 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

14. 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.

15. Ethanol affects CaV3.2 but not CaV3.1 nor CaV3.3 channel isoforms.

16. Cd(2) carried sizable inward currents through Ca(v)3.1 channels (210 +/- 20 pA at -60 mV with 2 mM Cd(2)).

17. Ca(V)3.1 channels represent a likely pathway for Fe(2) entry into cells.

18. The abnormal mRNA expressions of T-type channel alpha1H and alpha1G may be one of the causes of declined semen quality and infertility in varicocele patients.

19. Augmentation of CaV3.1 currents by Ras-ERK activation is associated with enhanced trafficking of channels to the plasma membrane.

20. Cav3.1 channels may contribute to the repression of tumor proliferation and the promotion of apoptosis mediated via Cav3.1-specific calcium signals

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

1. FMOD affected the expressions of the Cav1.1 and Cav3.1 genes. FMOD regulates calcium channel activity. The mRNA expressions of Cav1.1 and Cav3.1 increased during muscle regeneration.

2. Membrane-protein extraction and use of an intracellular protein-transport inhibitor showed that GDF-15 promoted CaV3.1 and CaV3.3 alpha-subunit expression by trafficking to the membrane.

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

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

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

6. 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.

7. GluA4 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

8. 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 by central nervous system-infiltrating Th1 and Th17 cells.

9. 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.

10. Results suggest that alpha1G T-type calcium channel plays a modulatory role in the duration and frequency of hippocampal seizures as well as the epileptogenicity of kainic acid-induced temporal lobe epilepsy in mice, mostly during acute periods

11. CaV3.1 and CaV3.2 are substrates for EHD3-dependent protein trafficking in heart

12. This study reported on the cloning and characterization of a proximal promoter region and initiated the analysis of transcription factors that control CaV 3.1 channel expression using the murine Cacna1g gene as a model.

13. Ca(v)3.1-dependent synaptic depression at thalamocortical projections contributes to mechanisms of forward suppression in the auditory cortex

14. Suggest that T-type Ca(2+) channels play an important role in infranodal escape automaticity.

15. CaV 3.1 channels are important for the myogenic tone at low arterial pressure, which is potentially relevant under resting conditions in vivo mice.

16. Ca(v)3.1 is required for vascular smooth muscle proliferation during neointimal formation, and blocking of Ca(v)3.1 may be beneficial for preventing restenosis.

17. Activation of Cav3.1 T-type channel subunit during wake-like states is a major determinant for single and multiple spike occurrence during tonic firing and for the robustness of the thalamocortical transfer of sensory inputs.

18. Elimination of Cav3.1 expression leads to impaired cardiac function and enhanced arrhythmia vulnerability post-myocardial infarction.

19. this study suggests that the CaV3.1 T-type Ca2+ channel plays a role in modulating motor function under pathological condition.

20. Cav3.2 may contribute to the development of the outflow tract from the secondary heart field in the embryonic heart, whereas Cav3.1 may be involved in the development of the cardiac conduction-system together with Cav3.2.

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

1. CaV3.1 structural analysis and comparison to CaV1.2 channel