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Description
CACNA1B Recombinant Rabbit mAb (S-2992-33)Product Specification Host Rabbit Antigen CACNA1B Synonyms Voltage dependent N type calcium channel subunit alpha 1B; Brain calcium channel III (BIII); Calcium channel; L type; alpha 1 polypeptide isoform 5; Voltage gated calcium channel subunit alpha Cav2. 2; CACH5; CACNL1A5 Immunogen Synthetic Peptide Location Membrane Accession Q00975 Clone Number S 2992 33 Antibody Type Recombinant mAb Isotype IgG Application WB Reactivity Hu, Ms, Rt Positive
Product Specification
| Host | Rabbit |
| Antigen | CACNA1B |
| Synonyms | Voltage-dependent N-type calcium channel subunit alpha-1B; Brain calcium channel III (BIII); Calcium channel; L type; alpha-1 polypeptide isoform 5; Voltage-gated calcium channel subunit alpha Cav2.2; CACH5; CACNL1A5 |
| Immunogen | Synthetic Peptide |
| Location | Membrane |
| Accession | Q00975 |
| Clone Number | S-2992-33 |
| Antibody Type | Recombinant mAb |
| Isotype | IgG |
| Application | WB |
| Reactivity | Hu, Ms, Rt |
| Positive Sample | mouse brain, rat brain, mouse cerebellum, rat cerebellum |
| Purification | Protein A |
| Concentration | 0.5 mg/ml |
| Conjugation | Unconjugated |
| Physical Appearance | Liquid |
| Storage Buffer | PBS, 40% Glycerol, 0.05% BSA, 0.03% Proclin 300 |
| Stability & Storage | 12 months from date of receipt / reconstitution, -20 °C as supplied |
Dilution
| application | dilution | species |
| WB | 1:1000 | Hu, Ms, Rt |
Background
CACNA1B protein, encoded by the CACNA1B gene on chromosome 9q34.3, is the pore-forming α1B subunit of the neuronal N-type (Cav2.2) high-voltage-activated calcium channel; it assembles with auxiliary α2δ, β and δ subunits to form channels that open in response to strong membrane depolarization, allowing Ca²⁺ influx concentrated at presynaptic active zones where it couples action potentials to asynchronous neurotransmitter release, regulates synaptic plasticity, nociception and neuronal survival, and whose expression is highest in early postnatal life; pathogenic CACNA1B variants producing loss-of-function or altered gating are linked to developmental and epileptic encephalopathy, dystonia, migraine and altered opioid responsiveness, while whole-gene deletion in mice causes memory deficits and abnormal locomotion, illustrating its essential role in central synaptic transmission and neuronal excitability.
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