Browse our anti-CACNA1H (CACNA1H) Antibodies

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

1. these findings demonstrated that the SNPs in the CACNA 1A, CACNA 1C, and CACNA 1H genes were involved in the pathophysiology of DPN. In addition, polymorphisms in the CACNA 1A, CACNA 1C, and CACNA 1H genes and their interactions also had effects on diabetic peripheral neuropathy (DPN) .

2. 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.

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

4. 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.

5. 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

6. 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.

7. Our data establish Stac1 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.

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

9. 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.

10. 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.

11. modulation of N-linked glycosylation of hCav3.2 channels may play an important physiological role

12. 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-201 cells.

13. 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.

14. Study revealed no association between the 15 tagSNPs of CACNA1A, 1C, and 1H and antiepileptic drug efficacy in the Chinese Han epileptic population; the TAGAA haplotype of CACNA1A may be a risk factor for drug resistance

15. Cav3.2 channels are highly phosphorylated in the mammalian brain and establish phosphorylation as an important mechanism involved in the dynamic regulation of Cav3.2 channel gating properties

16. Recurrent gain of function mutation in calcium channel CACNA1H causes early-onset hypertension with primary aldosteronism.

17. reveal an unexpected role of CaV3.2 channels in regulating NMDA-R-mediated transmission and a novel epileptogenic mechanism for human childhood absence epilepsy

18. The I-II loop of the Cav3.2 protein inhibits neuronal Cav3.1 and Cav3.2 channels.

19. C456S mutation leads to substantially increased excitability of cultured neurons due to increased spontaneous firing rate.

20. N-linked glycosylation of Cav3.2 not only controls surface expression.

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

1. Caveolae play a critical role in protein targeting and preserving the close structural relationship between CaV3.2 and RyR needed to drive BKCa-mediated feedback control in resistance arteries.

2. Study shows that the T-type Ca(2+) channel Cav3.2 regulates differentiation of neural progenitor cells during cortical development via caspase-3.

3. these findings reveal ENaC as an interactor and potential regulator of Cav3.2 calcium channels expressed in neuronal tissues.

4. The purinergic channel pannexin1, the ATP-gated purinergic receptor P2 x 7R and the low voltage transiently opened T-type calcium channel CaV3.2-1 all reside in close proximity to beta3 integrin attachment foci on osteocyte processes, suggesting a specialized mechanotransduction complex at these sites.

5. In Cav3.2-/- mice NO levels increased significantly with age. Cav3.2-deficient mice develop less age-dependent endothelial dysfunction.

6. USP5 mediated dysregulation of Cav3.2 channel activity does not exhibit sex differences, and potential therapeutics targeting this interaction should be effective in both male and female subjects.

7. The identification of TRPM7 and CaV3.2 as key mediators of Ca(2+) influx following fertilization.

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

9. T-channels contribute to the development and maintenance of the referred hyperalgesia.

10. 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 receptor signaling in chronic inflammatory pain condition.

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

12. Sensitization was relieved by pharmacological block of TRPV1 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 upregulation may underlie a protective, transient sensitization of the pain pathway.

13. The important roles of the CaV 3.2 T-type calcium channels in myogenic tone.

14. 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

15. 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.

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

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

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

19. Data show increased expression of T-type Ca(2+) current and association of protein kinase C alpha (PKCalpha) with caveolin-3 (Cav-3)was disrupted in the hypertrophic ventricular myocyte.

20. the asymmetric effects of the Cav3.2 and its partial reversal by behavior training on the hippocampal transcriptome