C1478
Anti-Calcium Channel (α1B Subunit) (N-type of Voltage-gated Ca2+ Channel) antibody produced in rabbit
affinity isolated antibody, lyophilized powder
Product Name
Anti-Calcium Channel (α1B Subunit) (N-type of Voltage-gated Ca2+ Channel) antibody produced in rabbit, affinity isolated antibody, lyophilized powder
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
lyophilized powder
mol wt
antigen 210 kDa (low)
antigen 240 kDa (high)
species reactivity
rat, mouse
technique(s)
immunocytochemistry: suitable using rat brain sections
immunoprecipitation (IP): suitable
western blot: 1:100-1:200 using rat brain membranes
UniProt accession no.
storage temp.
−20°C
target post-translational modification
unmodified
Quality Level
Gene Information
mouse ... Cacna1b(12287)
rat ... Cacna1b(257648)
Application
Anti-Calcium Channel (α1B Subunit) (N-type of Voltage-gated Ca2+ Channel) antibody produced in rabbit is suitable for the following applications:
- immunocytochemistry using rat brain sections
- immunoprecipitation
- western blotting at a dilution of 1:100-1:200 using rat brain membranes
Anti-Calcium Channel (α1B Subunit) (N-type of Voltage-gated Ca2+ Channel) antibody produced in rabbit has been used in immunofluorescence analysis.
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
Calcium channel, voltage-dependent, N type, α1B subunit (CACNA1B) plays a vital role in regulation of trafficking and biophysical properties of voltage-gated calcium channels. Members of voltage-gated calcium channel family act as key transducers of cell surface membrane potential changes to local intracellular calcium transients that initiate various physiological events. The N-type voltage-gated calcium channels (VGCCs) expressed mainly in the neurons, facilitate neurotransmitter release at the sympathetic nerve terminals. CACNA1B is expressed on presynaptic nerve terminals of nociceptors control neurotransmitter release.
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.
General description
The calcium channel, voltage-dependent, N type, α1B subunit (CACNA1B) or Cav2.2 gene consists of 47 exons and 46 introns, spanning 244kb. The gene is mapped to human chromosome 9q34. The encoded protein is a member of the voltage-gated calcium channel family.
Immunogen
synthetic peptide corresponding to amino acids 851-867 of the α1B subunit of rat brain voltage-gated calcium channel (VGCC, CNB1), with additional N-terminal lysine and tyrosine, conjugated to KLH.1
Physical form
Lyophilized from phosphate buffered saline, pH 7.4, containing 1% bovine serum albumin and 0.05% sodium azide.
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Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Regulatory Information
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Benjamin Dombert et al.
Frontiers in molecular neuroscience, 10, 346-346 (2017-11-23)
Spontaneous Ca2+ transients and actin dynamics in primary motoneurons correspond to cellular differentiation such as axon elongation and growth cone formation. Brain-derived neurotrophic factor (BDNF) and its receptor trkB support both motoneuron survival and synaptic differentiation. However, in motoneurons effects
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
Daniele Ferrante et al.
Cell reports, 35(11), 109248-109248 (2021-06-17)
Loss-of-function mutations in proline-rich transmembrane protein-2 (PRRT2) cause paroxysmal disorders associated with defective Ca2+ dependence of glutamatergic transmission. We find that either acute or constitutive PRRT2 deletion induces a significant decrease in the amplitude of evoked excitatory postsynaptic currents (eEPSCs)
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