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anti-Human CACNA1H Anticorps:
anti-Mouse (Murine) CACNA1H Anticorps:
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Human Monoclonal CACNA1H Primary Antibody pour ISt, IHC - ABIN1304584
Martinello, Huang, Lujan, Tran, Watanabe, Cooper, Brown, Shah: Cholinergic afferent stimulation induces axonal function plasticity in adult hippocampal granule cells. dans Neuron 2015
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Human Monoclonal CACNA1H Primary Antibody pour 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. dans Neuron 2014
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Our data establish Stac1 (Montrer STAC Anticorps) 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.
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 (Montrer PRDX2 Anticorps)-201 cells.
CaV3.1 (Montrer CACNA1G Anticorps), CaV3.2 and CaV3.3 (Montrer CACNA1I Anticorps) 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 (Montrer CACNA1A Anticorps), 1C, and 1H and antiepileptic drug efficacy in the Chinese Han epileptic population; the TAGAA haplotype of CACNA1A (Montrer CACNA1A Anticorps) 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 important roles of the CaV (Montrer CA5A Anticorps) 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 (Montrer CA2 Anticorps)+) stores and mediating Ca(2 (Montrer CA2 Anticorps)+) influx required for the activation of development.
MTF1 (Montrer MTF1 Anticorps) 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 (Montrer CA2 Anticorps)+) current and association of protein kinase C alpha (PKCalpha (Montrer PKCa Anticorps)) with caveolin-3 (Cav-3 (Montrer CAV3 Anticorps))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 (Montrer RYR3 Anticorps)-BKCa (Montrer KCNMA1 Anticorps) to hyperpolarize and relax arteries.
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