C1353
Anti-Calcium Channel (α1A Subunit) (P/Q-type of Voltage-gated Ca2+ Channel) antibody produced in rabbit
affinity isolated antibody, lyophilized powder
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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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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
mouse ... Cacna1a(12286)
rat ... Cacna1a(25398)
Related Categories
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)
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.
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
常规特殊物品
含少量动物源组分生物产品
Certificates of Analysis (COA)
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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
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
Lucian Medrihan et al.
Nature communications, 4, 1512-1512 (2013-02-28)
In the central nervous system, most synapses show a fast mode of neurotransmitter release known as synchronous release followed by a phase of asynchronous release, which extends over tens of milliseconds to seconds. Synapsin II (SYN2) is a member of
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
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
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