C1241
Anti-Calcium Channel CaV1.2 (human) antibody produced in rabbit
affinity isolated antibody, lyophilized powder
Synonym(s):
Anti-Human α1C, L-Type of Voltage-gated Calcium Channel
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About This Item
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biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
lyophilized powder
species reactivity
human, mouse, rat
technique(s)
immunocytochemistry: suitable
western blot: 1:200 using rat heart membranes
UniProt accession no.
Related Categories
Specificity
Recognizes mouse Cav1.2, splice variants P22002-4 and P22002-5 of rat Cav1.2 and splice variant P15381-4 of rabbit Cav1.2.
Immunogen
peptide corresponding to residues 2-15 of human Cav1.2 (exon 1B). The sequence has 14/15 residues identical in mouse and rat.
Biochem/physiol Actions
Calcium channel, voltage-dependent, L type, α1C subunit (Cav1.2) is a protein encoded by the CACNA1C gene in humans and belongs to the family of voltage-gated calcium channels. It serves as the key transducers of cell surface membrane potential changes into local intracellular calcium transients that initiate different physiological events. CACNA1C is a subunit of L-type voltage-dependent calcium channel. It is mapped to chromosome 12p13.3 and is implicated as a susceptibility gene for schizophrenia. CACNA1C is selectively expressed in human TH2 cells and blockage of Cav1.2 channel activation in TH2 cells may represent new strategies to treat allergic diseases in human subjects. Its increased activity is implicated in the pathogenesis of dementia and Alzheimer′s disease (AD).
Target description
Calcium Channel CaV1.2 (CACNA1C ) encodes an alpha-1 subunit of a voltage-dependent calcium channel. Calcium channels mediate the influx of calcium ions into the cell upon membrane polarization.
Physical form
Lyophilized from phosphate buffered saline, pH 7.4, with 1% BSA and 0.05% sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class
11 - Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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Fanfan Zheng et al.
Schizophrenia research, 152(1), 105-110 (2013-12-21)
CACNA1C (12p13.3) has been implicated as a susceptibility gene for schizophrenia by several replicated genome wide association studies. While these results have been consistent among studies in European populations, the findings in East Asian populations have varied. To test whether
Monika A Davare et al.
Proceedings of the National Academy of Sciences of the United States of America, 100(26), 16018-16023 (2003-12-11)
An increase in Ca2+ influx through L-type Ca2+ channels is thought to contribute to neuronal dysfunctions that underlie senile symptoms and Alzheimer's disease. The molecular basis of the age-dependent up-regulation in neuronal L-type Ca2+ channel activity is largely unknown. We
Man Xu et al.
The Journal of biological chemistry, 278(42), 40837-40841 (2003-08-06)
Voltage-gated calcium (Ca2+) channels play a key role in the control of heart contraction and are essential for normal heart development. The Cav1.2 L-type calcium channel is the predominant isoform in cardiomyocytes and is essential for excitation-contraction coupling. Although the
Virginie Robert et al.
The Journal of allergy and clinical immunology, 133(4), 1175-1183 (2013-12-25)
In addition to calcium release-activated calcium channel/ORAI calcium channels, the role of voltage-gated calcium (Cav1) channels in T-cell calcium signaling is emerging. Cav1 channels are formed by α1 (CaV1.1 to CaV1.4) and auxiliary subunits. We previously demonstrated that mouse TH2
Sven Moosmang et al.
The EMBO journal, 22(22), 6027-6034 (2003-11-12)
Blood pressure is regulated by a number of key molecules involving G-protein-coupled receptors, ion channels and monomeric small G-proteins. The relative contribution of these different signaling pathways to blood pressure regulation remains to be determined. Tamoxifen-induced, smooth muscle-specific inactivation of
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