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C1241

Sigma-Aldrich

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

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

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.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

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 Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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
William A Catterall et al.
Pharmacological reviews, 57(4), 411-425 (2005-12-31)
The family of voltage-gated calcium channels serves as the key transducers of cell surface membrane potential changes into local intracellular calcium transients that initiate many different physiological events. There are 10 members of the voltage-gated calcium channel family that have
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
Nina Daschil et al.
Journal of Alzheimer's disease : JAD, 37(2), 439-451 (2013-08-21)
Increased activity of L-type Ca2+ channels has been implicated in the pathogenesis of dementia and Alzheimer's disease (AD). Previously we detected CaV1.2 α1-subunit-positive expression in reactive astrocytes surrounding the plaques of 12 month-old transgenic mice overexpressing hAβPP751 with the London

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