Browse our anti-CACNA1H (CACNA1H) Antibodies

Human Calcium Channel, Voltage-Dependent, T Type, alpha 1H Subunit (CACNA1H) interaction partners

1. These findings reveal spectrin (alpha/beta) / ankyrin B (show ANK2 Antibodies) cytoskeletal and signaling proteins as key regulators of T-type calcium channels expressed in the nervous system.

2. In colonic biopsies, the Cav3.2 mRNA level was significantly higher in the irritable bowel syndrome group compared to controls.

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 (show CACNA1G Antibodies) 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. Our data establish Stac1 (show STAC Antibodies) as an important modulator of T-type channel expression and provide new insights into the molecular mechanisms underlying the trafficking of T-type channels to the plasma membrane.

6. CACNA1H variant is associated with differential antiepileptic drug response in childhood absence epilepsy.

7. There is a direct link between CACNA1H(M1549V) mutation and an increased aldosterone production. This suggests that calcium channel blockers may be beneficial in the treatment of a subset of patients with primary aldosteronism.

8. CACNA1H might be a susceptibility gene predisposing to PA with different phenotypic presentations, opening new perspectives for genetic diagnosis and management of patients with PA.

9. heterozygous mutations identified in a pediatric patient with chronic pain and absence seizures result in loss of channel function, with significantly smaller current densities across a wide range of voltages when co-expressed in tsA (show PRDX2 Antibodies)-201 cells.

10. CaV3.1 (show CACNA1G Antibodies), CaV3.2 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.

Mouse (Murine) Calcium Channel, Voltage-Dependent, T Type, alpha 1H Subunit (CACNA1H) interaction partners

1. identify interleukin-1 beta (show IL1B Antibodies) as an upstream trigger for the upregulation of interactions between USP5 (show USP5 Antibodies) and Cav3.2 channels in the pain pathway

2. Findings provided morphological evidence that T-type Cav3.2 channel, at least partially, mediates the pain facilitation of insulin-like growth factor-1/insulin-like growth factor-1 (show IGF1 Antibodies) receptor (show IGF1R Antibodies) signaling in chronic inflammatory pain condition.

3. This study found that expressions of Cav3.2 and IGF-1R (show IGF1R Antibodies), and their colocalization were not increased in DRGs of mice following axotomy. In addition, Cav3.2 or IGF-1R (show IGF1R Antibodies) subpopulation neurons did not acquire significant switch in expression phenotype after sciatic nerve axotomy.

4. Sensitization was relieved by pharmacological block of TRPV1 (show TRPV1 Antibodies) afferents, but not of myelinated neurons. In spinal cord slice recordings, we could optogenetically trigger an activity-dependent potentiation of presynaptic neurotransmission in the spinal dorsal horn that relied on Cav3.2 channel activity. This neuronal-activity-induced USP5 (show USP5 Antibodies) upregulation may underlie a protective, transient sensitization of the pain pathway.

5. The important roles of the CaV (show CA5A Antibodies) 3.2 T-type calcium channels in myogenic tone.

6. findings show that 2 Amyotrophic lateral sclerosis (ALS)-associated missense mutations produce alterations on the channel activity, consistent with a loss of channel function; findings implicate CACNA1H as a susceptibility gene in one form of ALS

7. findings suggest that chronic intermittent hypoxia leads to an augmented calcium influx via reactive oxygen species -dependent facilitation of CaV3.2 protein trafficking to the plasma membrane.

8. these data show that CaV3.2 T-type channels have prev8iously unrecognized roles in supporting the meiotic-maturation-associated increase in ER Ca(2 (show CA2 Antibodies)+) stores and mediating Ca(2 (show CA2 Antibodies)+) influx required for the activation of development.

9. MTF1 (show MTF1 Antibodies) mediates the increase of CaV3.2 mRNA and a rise in intracellular Zn(2+) which is associated with status epilepticus.

10. both suramin and gossypetin produced dose-dependent and long-lasting mechanical anti-hyperalgesia that was abolished or greatly attenuated in Cav3.2 null mice