CACNA1H

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CACNA1H

A gene on chromosome 16p13.3 that encodes the alpha-1H subunit of a voltage-dependent calcium channel, which mediates the entry of calcium ions into excitable cells. These channels are also involved in various calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division and apoptosis. CACNA1H gives rise to T-type calcium channels that belong to the low-voltage activated (LVA) group, which are remarkable for opening at very negative potentials and for voltage-dependent inactivation. T-type channels are pacemakers for both central neurons and cardiac nodal cells, and support calcium signalling in secretory cells and vascular smooth muscle. They may be involved in modulating firing patterns of neurons, which is key to information processing as well as cell growth.
References in periodicals archive ?
C inhibits the Cav3.2 isoform of T-type calcium channels involved in neuropathic pain (37).
In the current study, we detected the mRNA of the three isoforms of the T-type calcium channel CACNA1G (T-type [Ca.sup.2+] channel, Cav3.1), CACNA1H (T-type [Ca.sup.2+] channel, Cav3.2), and CACNA1I (T-type [Ca.sup.2+] channel, Cav3.3).
Cacna1d ([Ca.sub.v]1.3), Cacna1h (Cav3.2), and Cacng4 ([Cav.sub.[gamma]]4) were downregulated in GK compared to control SAN.
For example, Gja5 (Cx40) and Gjd3 (Cx31.9) were downregulated in GK and unaltered in STZ SAN; Trpc6 (TRPC6) was downregulated in GK and upregulated in STZ SAN; Ryr2 (RYR2) was upregulated in GK and unaltered in STZ SAN; Hcn1 (HCN1) and Hcn4 (HCN4) were downregulated in GK and unaltered in STZ SAN; Cacna1d ([Ca.sub.v]1.3), Cacna1h (Cav3.2), and Cacng4 ([Cav.sub.[gamma]]4) were downregulated in GK SAN; however, in the STZ study, Cacna1d was unaltered, Cacna1h was upregulated, and Cacng4 was downregulated; Kcna5 ([K.sub.v]1.5) and Kcnk1 (TWIK1) were downregulated in GK SAN and unaltered in STZ SAN; Nppb (BNP) was upregulated in GK and in STZ SAN.
Opthof et al., "Cav3.2 subunit underlies the functional T-type [Ca.sup.2+] channel in murine hearts during the embryonic period," American Journal of Physiology-Heart and Circulatory Physiology, vol.
Monteil et al., "Silencing of the Cav3.2 T-type calcium channel gene in sensory neurons demonstrates its major role in nociception," EMBO Journal, vol.
Monteilet al., "Silencing of the Cav3.2 T-type calcium channel gene in sensory neurons demonstrates its major role in nociception," The EMBO Journal, vol.
Kim et al., "Attenuated pain responses in mice lacking CaV3.2 T-type channels," Genes, Brain and Behavior, vol.
Jagodic et al., "In vivo silencing of the CaV3.2 T-type calcium channels in sensory neurons alleviates hyperalgesia in rats with streptozocin-induced diabetic neuropathy," Pain, vol.
Sekiguchi et al., "Hyperalgesia inducedby spinal and peripheral hydrogen sulfide: evidence for involvement of Cav3.2 T-type calcium channels," Pain, vol.
Okubo et al., "Upregulation of Cav3.2 T-type calcium channels targeted by endogenous hydrogen sulfide contributes to maintenance of neuropathic pain," Pain, vol.