C5105
Anti-Calcium Channel (α2/δ-1 Subunit) antibody produced in rabbit
affinity isolated antibody, lyophilized powder
Synonym(s):
Anti-CACNA2, Anti-CACNL2A, Anti-CCHL2A, Anti-LINC01112, Anti-lncRNA-N3
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About This Item
Recommended Products
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
lyophilized powder
species reactivity
mouse, rat, pig, human
technique(s)
western blot (chemiluminescent): 1:200 using rat brain membranes
UniProt accession no.
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... CACNA2D1(781)
mouse ... Cacna2d1(12293)
rat ... Cacna2d1(25399)
General description
CACNA2D1 (calcium channel, voltage-dependent, α2/δ subunit 1) is a member of a family of GPI-anchored voltage-gated calcium channels (VGCCs)-associated subunits called α2δ. VGCC are composed of three types of subunits- pore-forming α1 and auxiliary β and α2δ subunits.
Immunogen
synthetic peptide corresponding to amino acids 1-15 of α2 subunit (amino acids 27-41 of rabbit α2/δ−1 precursor).
Application
Anti-Calcium Channel (α2/δ-1 Subunit) antibody produced in rabbit has been used in immunoblotting and immunofluorescence.
Biochem/physiol Actions
CACNA2D1 (calcium channel, voltage-dependent, α2/δsubunit 1) is a type of α2δs, which are involved in the synaptic neurotransmitter release as they are concentrated at the synapses. They have a chaperone-like activity in non-neuronal cells. This protein acts as a target for gabapentin, which is a neuropathic analgesic. Mutations in this gene, in humans result in short QT syndrome (SQTS).
Target description
L-type of Voltage-gated Ca2+ Channel.
Physical form
Lyophilized from phosphate buffered saline, pH 7.4, containing 1% bovine serum albumin, and 0.05% sodium azide.
Preparation Note
Reconstitute the 0.05 mL vial with 50 μL deionized water. Reconstitute the 0.2 mL vial with 0.2 mL deionized water. After reconstitution, the antibody concentration is ~0.8 mg/mL.
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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Product No.
Description
Pricing
Storage Class Code
11 - Combustible Solids
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Kjara S Pilch et al.
The Journal of physiology, 600(24), 5333-5351 (2022-11-16)
In the mammalian brain, presynaptic CaV 2 channels play a pivotal role in synaptic transmission by mediating fast neurotransmitter exocytosis via influx of Ca2+ into the active zone of presynaptic terminals. However, the distribution and modulation of CaV 2.2 channels
Macroglia-derived thrombospondin 2 regulates alterations of presynaptic proteins of retinal neurons following elevated hydrostatic pressure
Wang S, et al.
Testing, 12(9), e0185388-e0185388 (2017)
Yuki Domon et al.
The Journal of pharmacology and experimental therapeutics, 365(3), 573-582 (2018-03-23)
Mirogabalin ([(1R,5S,6S)-6-(aminomethyl)-3-ethylbicyclo[3.2.0]hept-3-en-6-yl]acetic acid), a novel ligand for the α2δ subunit of voltage-gated calcium channels, is being developed to treat pain associated with diabetic peripheral neuropathy and postherpetic neuralgia. In the present study, we investigated the in vitro binding characteristics and
Michael B Hoppa et al.
Nature, 486(7401), 122-125 (2012-06-09)
Synaptic neurotransmitter release is driven by Ca(2+) influx through active zone voltage-gated calcium channels (VGCCs). Control of active zone VGCC abundance and function remains poorly understood. Here we show that a trafficking step probably sets synaptic VGCC levels in rats
Meichun Deng et al.
Anesthesiology, 130(5), 804-819 (2019-03-07)
Chronic use of μ-opioid receptor agonists paradoxically causes both hyperalgesia and the loss of analgesic efficacy. Opioid treatment increases presynaptic N-methyl-D-aspartate receptor activity to potentiate nociceptive input to spinal dorsal horn neurons. However, the mechanism responsible for this opioid-induced activation
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