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C1353

Sigma-Aldrich

Anti-Calcium Channel (α1A Subunit) (P/Q-type of Voltage-gated Ca2+ Channel) antibody produced in rabbit

affinity isolated antibody, lyophilized powder

Synonym(s):

Anti-APCA, Anti-BI, Anti-CACNL1A4, Anti-CAV2.1, Anti-DEE42, Anti-EA2, Anti-EIEE42, Anti-FHM, Anti-HPCA, Anti-MHP1, Anti-SCA6

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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

mol wt

antigen (major) 190 kDa
antigen (minor) 210 kDa

species reactivity

rat, mouse

technique(s)

immunohistochemistry: 1:100
western blot: 1:200

UniProt accession no.

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

Immunogen

synthetic peptide corresponding to amino acids 865-881 of the α1A subunit of rat brain voltage-gated calcium channel (VGCC, CNA1) (with additional N-terminal lysine and tyrosine) conjugated to KLH.

Application

Anti-Calcium Channel (α1A Subunit) (P/Q-type of Voltage-gated Ca2+ Channel) antibody produced in rabbit is suitable for immunohistochemistry at a dilution of 1:100 and western blotting at a dilution of 1:200.
Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Immunoprecipitation (1 paper)

Biochem/physiol Actions

The Cav2.1 P/Q voltage-dependent calcium channel is encoded by the CACNA1A gene in humans. It is a pore-forming essential subunit embedded in the plasma membrane. Mutation in this gene causes a number of human neurologic diseases including familial hemiplegic migraine. CACNA1A is associated with both hemiplegic migraine and migraine with aura in patients. Mutation in this gene is the cause of Type 2 episodic ataxia (EA2) the most common subtype among a group of rare hereditary syndromes characterized by recurrent attacks of ataxia.

Physical form

Lyophilized from phosphate buffered saline, pH 7.4, containing 1% bovine serum albumin 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 2

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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Steven B Condliffe et al.
The Journal of biological chemistry, 288(47), 33873-33883 (2013-10-11)
Mutations in the CACNA1A gene, which encodes the pore-forming α1A subunit of the CaV2.1 voltage-gated calcium channel, cause a number of human neurologic diseases including familial hemiplegic migraine. We have analyzed the functional impact of the E1015K amino acid substitution
Xue Liu et al.
The Journal of physiology, 591(13), 3309-3324 (2013-04-25)
Horizontal cells send inhibitory feedback to photoreceptors, helping form antagonistic receptive fields in the retina, but the neurotransmitter and the mechanisms underlying this signalling are not known. Since the proteins responsible for conventional Ca(2+)-dependent release of GABAergic synaptic vesicles are
Yafang Hu et al.
PloS one, 8(2), e56362-e56362 (2013-02-27)
Type 2 episodic ataxia (EA2) is the most common subtype among a group of rare hereditary syndromes characterized by recurrent attacks of ataxia. More than 60 mutations and several gene rearrangements due to large deletions in CACNA1A gene have been
Wei Chun Chen et al.
Hearing research, 278(1-2), 52-68 (2011-02-02)
As with other elements of the peripheral auditory system, spiral ganglion neurons display specializations that vary as a function of location along the tonotopic axis. Previous work has shown that voltage-gated K(+) channels and synaptic proteins show graded changes in
Shangru Lyu et al.
Neuroscience, 505, 78-90 (2022-10-17)
Genetic analyses have linked BTBD9 to restless legs syndrome (RLS) and sleep regulation. Btbd9 knockout mice show RLS-like motor restlessness. Previously, we found hyperactivity of cerebellar Purkinje cells (PCs) in Btbd9 knockout mice, which may contribute to the motor restlessness

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