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Human Monoclonal CACNA1H Primary Antibody für ISt, IHC - ABIN1304584
Martinello, Huang, Lujan, Tran, Watanabe, Cooper, Brown, Shah: Cholinergic afferent stimulation induces axonal function plasticity in adult hippocampal granule cells. in Neuron 2015
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Human Monoclonal CACNA1H Primary Antibody für ICC, IHC (fro) - ABIN447362
García-Caballero, Gadotti, Stemkowski, Weiss, Souza, Hodgkinson, Bladen, Chen, Hamid, Pizzoccaro, Deage, François, Bourinet, Zamponi: The deubiquitinating enzyme USP5 modulates neuropathic and inflammatory pain by enhancing Cav3.2 channel activity. in Neuron 2014
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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.
In colonic biopsies, the Cav3.2 mRNA level was significantly higher in the irritable bowel syndrome group compared to controls.
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.
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
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.
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.
CACNA1H variant is associated with differential antiepileptic drug response in childhood absence epilepsy.
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.
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.
modulation of N-linked glycosylation of hCav3.2 channels may play an important physiological role
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.
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.
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
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
Recurrent gain of function mutation in calcium channel CACNA1H causes early-onset hypertension with primary aldosteronism.
reveal an unexpected role of CaV3.2 channels in regulating NMDA-R-mediated transmission and a novel epileptogenic mechanism for human childhood absence epilepsy
The I-II loop of the Cav3.2 protein inhibits neuronal Cav3.1 and Cav3.2 channels.
C456S mutation leads to substantially increased excitability of cultured neurons due to increased spontaneous firing rate.
N-linked glycosylation of Cav3.2 not only controls surface expression.
Data indicate that endogenous/exogenous hydrogen sulfide regulates function of T-type Ca(2+) channel Cav3.2 expressed in HEK293 cells
In Cav3.2-/- mice NO levels increased significantly with age. Cav3.2-deficient mice develop less age-dependent endothelial dysfunction.
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.
The identification of TRPM7 and CaV3.2 as key mediators of Ca(2+) influx following fertilization.
identify interleukin-1 beta as an upstream trigger for the upregulation of interactions between USP5 and Cav3.2 channels in the pain pathway
T-channels contribute to the development and maintenance of the referred hyperalgesia.
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.
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.
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.
The important roles of the CaV 3.2 T-type calcium channels in myogenic tone.
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
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.
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.
MTF1 mediates the increase of CaV3.2 mRNA and a rise in intracellular Zn(2+) which is associated with status epilepticus.
both suramin and gossypetin produced dose-dependent and long-lasting mechanical anti-hyperalgesia that was abolished or greatly attenuated in Cav3.2 null mice
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.
the asymmetric effects of the Cav3.2 and its partial reversal by behavior training on the hippocampal transcriptome
This study demonstrated that CaV3.2 KO mice have altered retinal waves but normal direction selectivity.
Suggest a negative feedback mechanism of the myogenic response in which CaV3.2 channel modulates downstream ryanodine receptor-BKCa to hyperpolarize and relax arteries.
our results indicate that inhibition of Cav3 currents by 5,6-epoxyeicosatrienoic acid is an important mechanism controlling the vascular tone.
NMP-7 inhibits chronic inflammatory and neuropathic pain via block of Cav3.2 T-type calcium channels and activation of CB2 receptors
This gene encodes a T-type member of the alpha-1 subunit family, a protein in 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 alpha-1, alpha-2/delta, beta, and gamma subunits in a 1:1:1:1 ratio. The alpha-1 subunit has 24 transmembrane segments and forms the pore through which ions pass into the cell. There are multiple isoforms of each of the proteins in the complex, either encoded by different genes or the result of alternative splicing of transcripts. Alternate transcriptional splice variants, encoding different isoforms, have been characterized for the gene described here. Studies suggest certain mutations in this gene lead to childhood absence epilepsy (CAE).
calcium channel, voltage-dependent, T type, alpha 1Hb subunit
, low-voltage-activated calcium channel alpha1 3.2 subunit
, low-voltage-activated calcium channel alpha13.2 subunit
, voltage dependent t-type calcium channel alpha-1H subunit
, voltage-dependent T-type calcium channel subunit alpha-1H
, voltage-gated calcium channel alpha subunit Cav3.2
, voltage-gated calcium channel alpha subunit CavT.2
, voltage-gated calcium channel subunit alpha Cav3.2
, T-type Cav3.2
, calcium channel alpha13.2 subunit