C5863
Anti-Calcium Channel (β4 Subunit) (Voltage Gated Ca2+ Channel) antibody produced in rabbit
~1 mg/mL, fractionated antiserum, buffered aqueous solution
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About This Item
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
fractionated antiserum
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
species reactivity
human, rat, mouse
concentration
~1 mg/mL
technique(s)
western blot: 5-10 μg/mL using brain tissue lysate
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... CACNB4(785)
mouse ... Cacnb4(12298)
rat ... Cacnb4(58942)
General description
The gene CACNB4 (Calcium channel voltage-dependent subunit beta 4) is mapped to human chromosome 2q22-23. It is present at the membrane as well as the nucleus.
Specificity
Specifically recognizes a splice variant of β4 (55 kDa).
Immunogen
synthetic peptide derived from the rat β4 calcium channel subunit conjugated to KLH.
Application
Anti-Calcium Channel (β-4 subunit) antibody produced in rabbit is suitable for western blot at a concentration of 5-10μg/mL using brain tissue lysate.
The antibody has been used for:
The antibody has been used for:
- western blotting of proteins extracted from different brain regions of the mouse
- western blotting of proteins isolated from primary culture of mouse cerebral cortical neurons
Biochem/physiol Actions
The CACNB4 (Calcium channel voltage-dependent subunit β 4) is an intracellular regulatory subunit of voltage-activated calcium channels that has significant impact on membrane expression and electrophysical characteristics of the channel. Calcium channel β subunits regulate voltage-dependent calcium currents through direct interaction with α1 subunits. Mutations in CACNB4 are associated with idiopathic generalized epilepsy and episodic ataxia. CACNB4 interacts with heterochromatin protein 1γ (HP1γ). The interaction attenuates the gene silencing activity by HP1.
Physical form
Solution in phosphate buffered saline containing 0.08% 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
10 - Combustible liquids
Certificates of Analysis (COA)
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Masashi Katsura et al.
Journal of pharmacological sciences, 102(2), 221-230 (2006-10-13)
Previous reports revealed up-regulation of L-type high voltage-gated calcium channels (HVCCs) in mouse brains with ethanol physical dependence. We investigated mechanisms of enhancement of L-type HVCC function using mouse cerebrocortical neurons exposed to 50 mM ethanol for 3 days and
Xingfu Xu et al.
The Journal of biological chemistry, 286(11), 9677-9687 (2011-01-12)
The β subunits of voltage-gated Ca(2+) channels are best known for their roles in regulating surface expression and gating of voltage-gated Ca(2+) channel α(1) subunits. Recent evidence, however, indicates that these proteins have a variety of Ca(2+) channel-independent functions. For
A Escayg et al.
American journal of human genetics, 66(5), 1531-1539 (2000-04-14)
Inactivation of the beta4 subunit of the calcium channel in the mouse neurological mutant lethargic results in a complex neurological disorder that includes absence epilepsy and ataxia. To determine the role of the calcium-channel beta4-subunit gene CACNB4 on chromosome 2q22-23
Solmaz Etemad et al.
Channels (Austin, Tex.), 8(4), 334-343 (2014-05-31)
Voltage-gated calcium channels regulate gene expression by controlling calcium entry through the plasma membrane and by direct interactions of channel fragments and auxiliary β subunits with promoters and the epigenetic machinery in the nucleus. Mutations of the calcium channel β(4)
Masahiro Shibasaki et al.
Journal of pharmacological sciences, 105(2), 177-183 (2007-10-06)
As functional changes in L-type high voltage-gated calcium channels (HVCCs) are recognized to be one of the major neurochemical modifications occurring in brains of animals with morphine physical dependence, this study attempts to examine whether regional difference in the expressions
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