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CACNA1H encodes a T-type member of the alpha-1 subunit family, a protein in the voltage-dependent calcium channel complex. Additionally we are shipping CACNA1H Proteins (8) and CACNA1H Kits (3) and many more products for this protein.
Showing 10 out of 61 products:
Human Monoclonal CACNA1H Primary Antibody for ICC, IF - ABIN361762
Chen, Lu, Pan, Zhang, Wu, Xu, Liu, Jiang, Bao, Yao, Ding, Lo, Qiang, Chan, Shen, Wu: Association between genetic variation of CACNA1H and childhood absence epilepsy. in Annals of neurology 2003
Show all 3 references for ABIN361762
Human Monoclonal CACNA1H Primary Antibody for 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
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 (show PRDX2 Antibodies)-201 cells.
CaV3.1 (show CACNA1G Antibodies), CaV3.2 and CaV3.3 (show CACNA1I Antibodies) 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 (show CACNA1A Antibodies), 1C, and 1H and antiepileptic drug efficacy in the Chinese Han epileptic population; the TAGAA haplotype of CACNA1A (show CACNA1A Antibodies) 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 (show CACNA1G Antibodies) and Cav3.2 channels.
N-linked glycosylation of Cav3.2 not only controls surface expression.
Data indicate that endogenous/exogenous hydrogen sulfide (show SQRDL Antibodies) regulates function of T-type Ca(2 (show CA2 Antibodies)+) channel Cav3.2 expressed in HEK293 cells
Both Asp (show ASIP Antibodies) residues critically control the biophysical properties of Ca(v)3.2, including relative permeability between Ba2+ and Ca2 (show CA2 Antibodies)+, voltage dependency of channel activation, Cd2 (show CD2 Antibodies)+ blocking sensitivity, and pH effects, in distinctive ways.
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 (show CA2 Antibodies)+) stores and mediating Ca(2 (show CA2 Antibodies)+) influx required for the activation of development.
MTF1 (show MTF1 Antibodies) 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 (show CA2 Antibodies)+) current and association of protein kinase C alpha (PKCalpha (show PKCa Antibodies)) with caveolin-3 (Cav-3 (show CAV3 Antibodies))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 (show RYR3 Antibodies)-BKCa (show KCNMA1 Antibodies) to hyperpolarize and relax arteries.
our results indicate that inhibition of Cav3 (show CAV3 Antibodies) 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 (show CNR2 Antibodies) 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