CACNA1H Membrane Protein Introduction

Introduction of CACNA1H

CACNA1H, calcium channel, voltage-dependent, T type, alpha 1H subunit, also known as CACNA1H, is a protein which in humans is encoded by the CACNA1H gene. The protein encoded by this gene is also called Ca_v3.2, which is a T-type member of the α1 subunit family, and also a functional protein of the voltage-dependent calcium channel complex. Calcium channels mediate the influx of calcium ions into the cell upon membrane polarization and consist of a complex of α1, α2δ, β, and γ subunits in a 1:1:1:1 ratio.

Function of CACNA1H Membrane Protein

CACNA1H is voltage-sensitive calcium channel that gives rise to T-type calcium currents. T-type calcium channels are members of the "low-voltage activated (LVA)" group. One of the major characteristics is an opening status at quite negative potentials of this type of channel, and another feature is voltage-dependent inactivation. T-type channels show pacemaking functions in central neurons, as well as cardiac nodal cells and support the calcium signaling pathway in secretory cells and vascular smooth muscle. Scientists have reported that they may be involved in the regulation of firing patterns of neurons. In the adrenal zona glomerulosa, CACNA1H has been identified as a participant in the calcium signaling pathway which leads to aldosterone production in response to either AGT/angiotensin II or hyperkalemia.

Fig.1 Schematic representations of hCa_v3.2. (Proft, 2017)

Application of CACNA1H Membrane Protein in Literature

1. Becker F. Functional variants in HCN4 and CACNA1H may contribute to genetic generalized epilepsy. Epilepsia Open. 2017, 2(3): 334-342. PubMed ID: 29588962
   
   

   This article reveals that voltage-clamp analysis of CACNA1H (p.G1158S) verifies a small but significant gain-of-function, including increased current density and a depolarizing shift of steady-state inactivation. HCN4 p.P1117L and p.G153E both can cause a hyperpolarizing shift in activation and reduced current amplitudes, resulting in a loss-of-function.

2. Cain S.M., et al. Ca_v3.2 drives sustained burst-firing, which is critical for absence seizure propagation in reticular thalamic neurons. Epilepsia. 2018, 59(4): 778-791. PubMed ID: 29468672
   
   

   This article indicates that TRN Ca_v3.2 T-type channels play roles in propagating thalamocortical network seizures and setting the pacemaking frequency of SWDs.

3. Falcón D., et al. Dexamethasone-induced upregulation of Ca_v3.2 T-type Ca²⁺ channels in rat cardiac myocytes. J Steroid Biochem Mol Biol. 2018, 178: 193-202. PubMed ID: 29262379
   
   

   This study revealed that dexamethasone induces the upregulation of Ca_v3.2 mRNA in neonatal rat ventricular myocytes, whereas Ca_v3.1 mRNA is only slightly affected.

4. Ozaki T., et al. Zinc deficiency promotes cystitis-related bladder pain by enhancing function and expression of Ca_v3.2 in mice. Toxicology. 2018, 393: 102-112. PubMed ID: 29129814
   
   

   This article shows that zinc deficiency promotes bladder pain accompanying CPA-induced cystitis by enhancing function and expression of Ca_v3.2 in nociceptors, suggesting a novel therapeutic avenue for the treatment of bladder pain, such as zinc supplementation.

5. Proft J., et al. The Cacna1h mutation in the GAERS model of absence epilepsy enhances T-type Ca²⁺ currents by altering calnexin-dependent trafficking of Ca_v3.2 channels. Sci Rep. 2017, 7(1): 11513. PubMed ID: 28912545
   
   

   This article reveals a novel mechanism that controls the expression of T-type channels - Ca_v3.2 and provides a molecular explanation for the enhancement of T-type calcium conductance in GAERS.

CACNA1H Preparation Options

We provide custom membrane protein preparation services for worldwide customers. Leveraging by our advanced Magic™ membrane protein production platform, we are able to present target membrane protein in multiple active formats. Our professional scientists are happy to help you find an ideal method and make your project a success. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-CACNA1H antibody development services.

• Magic™ Membrane Protein Production Platform
• Magic™ Anti-Membrane Protein Antibody Discovery Platform

Creative Biolabs provides high-quality membrane protein preparation service to facilitate the development of worldwide customer’s research. During the past years, we have successfully established a powerful Magic™ membrane protein platform which enables us to provide a series of membrane protein preparation services. For more detailed information, please feel free to contact us.

Reference

1. Proft J, et al. (2017). The Cacna1h mutation in the GAERS model of absence epilepsy enhances T-type Ca²⁺ currents by altering calnexin-dependent trafficking of Ca_v3.2 channels. Sci Rep. 7(1): 11513.

All listed services and products are For Research Use Only. Do Not use in any diagnostic or therapeutic applications.