C5738
Anti-Calcium Channel (β2 subunit) (Voltage Gated Ca2+ Channel) antibody produced in rabbit
~1 mg/mL, fractionated antiserum, buffered aqueous solution
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About This Item
Source biologique
rabbit
Niveau de qualité
Conjugué
unconjugated
Forme d'anticorps
fractionated antiserum
Type de produit anticorps
primary antibodies
Clone
polyclonal
Forme
buffered aqueous solution
Espèces réactives
rat, human, mouse
Concentration
~1 mg/mL
Technique(s)
western blot: 5-10 μg/mL using brain tissues lysate
Numéro d'accès UniProt
Température de stockage
−20°C
Modification post-traductionnelle de la cible
unmodified
Informations sur le gène
human ... CACNB2(783)
mouse ... Cacnb2(12296)
rat ... Cacnb2(116600)
Description générale
CACNB2 (Voltage-dependent L-type calcium channel subunit β-2) is particularly expressed in cardiovascular tissue.
Spécificité
Specifically recognizes a splice variant of β2 (68 kDa) from human, mouse and rat.
Immunogène
synthetic peptide derived from the rat β2 calcium channel subunit conjugated to KLH.
Application
Anti-Calcium Channel (β2 subunit) antibody produced in rabbit is suitable for western blot at a concentration of 5-10μg/mL using rat brain tissue lysate.
Actions biochimiques/physiologiques
CACNB2 (Voltage-dependent L-type calcium channel subunit β-2) is a subunit of voltage-activated L-type calcium channelsl. CACNB2 regulates voltage-dependent calcium currents through direct interaction with α1 subunits. Loss of function mutation in CACNB2 is associated with familial cardiac death combined with short QT intervals and ST-segment elevation. It is down-regulated in humans with atrial fibrillation and miR-21 is suggested to be responsible for the down-regulation. Mutations in CACNB2 are linked to autism spectrum disorders.
Forme physique
Solution in phosphate buffered saline containing 0.08% sodium azide.
Clause de non-responsabilité
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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Adriana Barana et al.
Circulation. Arrhythmia and electrophysiology, 7(5), 861-868 (2014-08-12)
Atrial fibrillation is characterized by progressive atrial structural and electrical changes (atrial remodeling) that favor arrhythmia recurrence and maintenance. Reduction of L-type Ca(2+) current (I(Ca,L)) density is a hallmark of the electrical remodeling. Alterations in atrial microRNAs could contribute to
Giuseppe Ronzitti et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 34(32), 10603-10615 (2014-08-08)
α-Synuclein is thought to regulate neurotransmitter release through multiple interactions with presynaptic proteins, cytoskeletal elements, ion channels, and synaptic vesicles membrane. α-Synuclein is abundant in the presynaptic compartment, and its release from neurons and glia has been described as responsible
Alexandra F S Breitenkamp et al.
PloS one, 9(4), e95579-e95579 (2014-04-23)
Autism Spectrum Disorders (ASD) are complex neurodevelopmental diseases clinically defined by dysfunction of social interaction. Dysregulation of cellular calcium homeostasis might be involved in ASD pathogenesis, and genes coding for the L-type calcium channel subunits CaV1.2 (CACNA1C) and CaVβ2 (CACNB2)
Yuxin Niu et al.
Circulation. Cardiovascular genetics, 3(6), 548-555 (2010-12-16)
Single-nucleotide polymorphisms (SNPs) within the regulatory β2 subunit of the voltage-gated calcium channel (CACNB2) may contribute to variable treatment response to antihypertensive drugs and adverse cardiovascular outcomes. SNPs in CACNB2 from 60 ethnically diverse individuals were identified and characterized. Three
Charles Antzelevitch et al.
Circulation, 115(4), 442-449 (2007-01-17)
Cardiac ion channelopathies are responsible for an ever-increasing number and diversity of familial cardiac arrhythmia syndromes. We describe a new clinical entity that consists of an ST-segment elevation in the right precordial ECG leads, a shorter-than-normal QT interval, and a
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