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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 Cav3.2, 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.

Basic Information of CACNA1H
Protein Name Voltage-dependent T-type calcium channel subunit alpha-1H
Gene Name CACNA1H
Aliases Low-voltage-activated calcium channel alpha1 3.2 subunit, Voltage-gated calcium channel subunit alpha Cav3.2
Organism Homo sapiens (Human)
UniProt ID O95180
Transmembrane Times 24
Length (aa) 2353
Sequence MTEGARAADEVRVPLGAPPPGPAALVGASPESPGAPGREAERGSELGVSPSESPAAERGAELGADEEQRVPYPALAATVFFCLGQTTRPRSWCLRLVCNPWFEHVSMLVIMLNCVTLGMFRPCEDVECGSERCNILEAFDAFIFAFFAVEMVIKMVALGLFGQKCYLGDTWNRLDFFIVVAGMMEYSLDGHNVSLSAIRTVRVLRPLRAINRVPSMRILVTLLLDTLPMLGNVLLLCFFVFFIFGIVGVQLWAGLLRNRCFLDSAFVRNNNLTFLRPYYQTEEGEENPFICSSRRDNGMQKCSHIPGRRELRMPCTLGWEAYTQPQAEGVGAARNACINWNQYYNVCRSGDSNPHNGAINFDNIGYAWIAIFQVITLEGWVDIMYYVMDAHSFYNFIYFILLIIVGSFFMINLCLVVIATQFSETKQRESQLMREQRARHLSNDSTLASFSEPGSCYEELLKYVGHIFRKVKRRSLRLYARWQSRWRKKVDPSAVQGQGPGHRQRRAGRHTASVHHLVYHHHHHHHHHYHFSHGSPRRPGPEPGACDTRLVRAGAPPSPPSPGRGPPDAESVHSIYHADCHIEGPQERARVAHAAATAAASLRLATGLGTMNYPTILPSGVGSGKGSTSPGPKGKWAGGPPGTGGHGPLSLNSPDPYEKIPHVVGEHGLGQAPGHLSGLSVPCPLPSPPAGTLTCELKSCPYCTRALEDPEGELSGSESGDSDGRGVYEFTQDVRHGDRWDPTRPPRATDTPGPGPGSPQRRAQQRAAPGEPGWMGRLWVTFSGKLRRIVDSKYFSRGIMMAILVNTLSMGVEYHEQPEELTNALEISNIVFTSMFALEMLLKLLACGPLGYIRNPYNIFDGIIVVISVWEIVGQADGGLSVLRTFRLLRVLKLVRFLPALRRQLVVLVKTMDNVATFCTLLMLFIFIFSILGMHLFGCKFSLKTDTGDTVPDRKNFDSLLWAIVTVFQILTQEDWNVVLYNGMASTSSWAALYFVALMTFGNYVLFNLLVAILVEGFQAEGDANRSDTDEDKTSVHFEEDFHKLRELQTTELKMCSLAVTPNGHLEGRGSLSPPLIMCTAATPMPTPKSSPFLDAAPSLPDSRRGSSSSGDPPLGDQKPPASLRSSPCAPWGPSGAWSSRRSSWSSLGRAPSLKRRGQCGERESLLSGEGKGSTDDEAEDGRAAPGPRATPLRRAESLDPRPLRPAALPPTKCRDRDGQVVALPSDFFLRIDSHREDAAELDDDSEDSCCLRLHKVLEPYKPQWCRSREAWALYLFSPQNRFRVSCQKVITHKMFDHVVLVFIFLNCVTIALERPDIDPGSTERVFLSVSNYIFTAIFVAEMMVKVVALGLLSGEHAYLQSSWNLLDGLLVLVSLVDIVVAMASAGGAKILGVLRVLRLLRTLRPLRVISRAPGLKLVVETLISSLRPIGNIVLICCAFFIIFGILGVQLFKGKFYYCEGPDTRNISTKAQCRAAHYRWVRRKYNFDNLGQALMSLFVLSSKDGWVNIMYDGLDAVGVDQQPVQNHNPWMLLYFISFLLIVSFFVLNMFVGVVVENFHKCRQHQEAEEARRREEKRLRRLERRRRSTFPSPEAQRRPYYADYSPTRRSIHSLCTSHYLDLFITFIICVNVITMSMEHYNQPKSLDEALKYCNYVFTIVFVFEAALKLVAFGFRRFFKDRWNQLDLAIVLLSLMGITLEEIEMSAALPINPTIIRIMRVLRIARVLKLLKMATGMRALLDTVVQALPQVGNLGLLFMLLFFIYAALGVELFGRLECSEDNPCEGLSRHATFSNFGMAFLTLFRVSTGDNWNGIMKDTLRECSREDKHCLSYLPALSPVYFVTFVLVAQFVLVNVVVAVLMKHLEESNKEAREDAELDAEIELEMAQGPGSARRVDADRPPLPQESPGARDAPNLVARKVSVSRMLSLPNDSYMFRPVVPASAPHPRPLQEVEMETYGAGTPLGSVASVHSPPAESCASLQIPLAVSSPARSGEPLHALSPRGTARSPSLSRLLCRQEAVHTDSLEGKIDSPRDTLDPAEPGEKTPVRPVTQGGSLQSPPRSPRPASVRTRKHTFGQRCVSSRPAAPGGEEAEASDPADEEVSHITSSACPWQPTAEPHGPEASPVAGGERDLRRLYSVDAQGFLDKPGRADEQWRPSAELGSGEPGEAKAWGPEAEPALGARRKKKMSPPCISVEPPAEDEGSARPSAAEGGSTTLRRRTPSCEATPHRDSLEPTEGSGAGGDPAAKGERWGQASCRAEHLTVPSFAFEPLDLGVPSGDPFLDGSHSVTPESRASSSGAIVPLEPPESEPPMPVGDPPEKRRGLYLTVPQCPLEKPGSPSATPAPGGGADDPV

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.

Schematic representations of hCa<sub>v</sub>3.2. Fig.1 Schematic representations of hCav3.2. (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. Cav3.2 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 Cav3.2 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 Cav3.2 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 Cav3.2 mRNA in neonatal rat ventricular myocytes, whereas Cav3.1 mRNA is only slightly affected.

  4. Ozaki T., et al. Zinc deficiency promotes cystitis-related bladder pain by enhancing function and expression of Cav3.2 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 Cav3.2 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 Cav3.2 channels. Sci Rep. 2017, 7(1): 11513. PubMed ID: 28912545

    This article reveals a novel mechanism that controls the expression of T-type channels - Cav3.2 and provides a molecular explanation for the enhancement of T-type calcium conductance in GAERS.

CACNA1H Preparation Options

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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 Cav3.2 channels. Sci Rep. 7(1): 11513.

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