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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.
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In colonic biopsies, the Cav3.2 mRNA level was significantly higher in the irritable bowel syndrome group compared to controls.
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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.
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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
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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.
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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.
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CACNA1H variant is associated with differential antiepileptic drug response in childhood absence epilepsy.
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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.
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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.
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modulation of N-linked glycosylation of hCav3.2 channels may play an important physiological role
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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.
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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.
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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
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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
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Recurrent gain of function mutation in calcium channel CACNA1H causes early-onset hypertension with primary aldosteronism.
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reveal an unexpected role of CaV3.2 channels in regulating NMDA-R-mediated transmission and a novel epileptogenic mechanism for human childhood absence epilepsy
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The I-II loop of the Cav3.2 protein inhibits neuronal Cav3.1 and Cav3.2 channels.
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C456S mutation leads to substantially increased excitability of cultured neurons due to increased spontaneous firing rate.
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N-linked glycosylation of Cav3.2 not only controls surface expression.
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Data indicate that endogenous/exogenous hydrogen sulfide regulates function of T-type Ca(2+) channel Cav3.2 expressed in HEK293 cells
