Voltage-Dependent P/Q-Type Calcium Channel Subunit Alpha-1A (CACNA1A), ELISA Ki

For Research Use Only. Not for use in diagnostic procedures.

Store all reagents at 2-8 degree C

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Small volumes of CACNA1A elisa kit vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

MBS9351970 is a ready-to-use microwell, strip plate ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the Voltage-Dependent P/Q-Type Calcium Channel Subunit Alpha-1A (CACNA1A) ELISA Kit target analytes in biological samples. The concentration gradients of the kit standards or positive controls render a theoretical kit detection range in biological research samples containing CACNA1A. The ELISA analytical biochemical technique of the MBS9351970 kit is based on CACNA1A antibody-CACNA1A antigen interactions (immunosorbency) and an HRP colorimetric detection system to detect CACNA1A antigen targets in samples. The ELISA Kit is designed to detect native, not recombinant, CACNA1A. Appropriate sample types may include undiluted body fluids and/or tissue homogenates, secretions. Quality control assays assessing reproducibility identified the intra-assay CV (%) and inter-assay CV(%).

282,564 Da

calcium voltage-gated channel subunit alpha1 A

voltage-dependent P/Q-type calcium channel subunit alpha-1A

Voltage-dependent P/Q-type calcium channel subunit alpha-1A

CACH4; CACN3; CACNL1A4; BI  [Similar Products]

CAC1A_HUMAN

Voltage-dependent calcium channels mediate the entry of calcium ions into excitable cells, and are also involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, and gene expression. Calcium channels are multisubunit complexes composed of alpha-1, beta, alpha-2/delta, and gamma subunits. The channel activity is directed by the pore-forming alpha-1 subunit, whereas, the others act as auxiliary subunits regulating this activity. The distinctive properties of the calcium channel types are related primarily to the expression of a variety of alpha-1 isoforms, alpha-1A, B, C, D, E, and S. This gene encodes the alpha-1A subunit, which is predominantly expressed in neuronal tissue. Mutations in this gene are associated with 2 neurologic disorders, familial hemiplegic migraine and episodic ataxia 2. This gene also exhibits polymorphic variation due to (CAG)n-repeats. Multiple transcript variants encoding different isoforms have been found for this gene. In one set of transcript variants, the (CAG)n-repeats occur in the 3' UTR, and are not associated with any disease. But in another set of variants, an insertion extends the coding region to include the (CAG)n-repeats which encode a polyglutamine tract. Expansion of the (CAG)n-repeats from the normal 4-16 to 21-28 in the coding region is associated with spinocerebellar ataxia 6. [provided by RefSeq, Mar 2010]

CACNA1A: Voltage-sensitive calcium channels (VSCC) mediate the entry of calcium ions into excitable cells and are also involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division and cell death. The isoform alpha-1A gives rise to P and/or Q-type calcium currents. P/Q-type calcium channels belong to the 'high-voltage activated' (HVA) group and are blocked by the funnel toxin (Ftx) and by the omega-agatoxin- IVA (omega-Aga-IVA). They are however insensitive to dihydropyridines (DHP), and omega-conotoxin-GVIA (omega-CTx-GVIA). Defects in CACNA1A are the cause of spinocerebellar ataxia type 6 (SCA6). Spinocerebellar ataxia is a clinically and genetically heterogeneous group of cerebellar disorders. Patients show progressive incoordination of gait and often poor coordination of hands, speech and eye movements, due to degeneration of the cerebellum with variable involvement of the brainstem and spinal cord. SCA6 is mainly caused by expansion of a CAG repeat in the coding region of CACNA1A. There seems to be a correlation between the repeat number and earlier onset of the disorder. Defects in CACNA1A are the cause of familial hemiplegic migraine type 1 (FHM1); also known as migraine familial hemiplegic 1 (MHP1). FHM1, a rare autosomal dominant subtype of migraine with aura, is associated with ictal hemiparesis and, in some families, progressive cerebellar atrophy. Defects in CACNA1A are the cause of episodic ataxia type 2 (EA2); also known as acetazolamide-responsive hereditary paroxysmal cerebellar ataxia (APCA). EA2 is an autosomal dominant disorder characterized by acetozolamide- responsive attacks of ataxia, migraine-like symptoms, interictal nystagmus, and cerebellar atrophy. Belongs to the calcium channel alpha-1 subunit (TC 1.A.1.11) family. CACNA1A subfamily. 7 isoforms of the human protein are produced by alternative splicing.

Protein type: Membrane protein, integral; Channel, calcium; Membrane protein, multi-pass

Chromosomal Location of Human Ortholog: 19p13

Cellular Component: cell projection; cell soma; cytoplasm; cytosol; dendrite; integral to membrane; nucleus; plasma membrane; voltage-gated calcium channel complex

Molecular Function: high voltage-gated calcium channel activity; metal ion binding; protein binding; syntaxin binding; voltage-gated calcium channel activity

Biological Process: ***** walking behavior; behavioral response to pain; calcium ion-dependent exocytosis of neurotransmitter; cell death; cell growth; cellular chloride ion homeostasis; cerebellar molecular layer development; cerebellar Purkinje cell differentiation; cerebellum maturation; dendrite morphogenesis; elevation of cytosolic calcium ion concentration; energy reserve metabolic process; gamma-aminobutyric acid secretion; gamma-aminobutyric acid signaling pathway; glucose metabolic process; hormone metabolic process; membrane depolarization; musculoskeletal movement, spinal reflex action; negative regulation of hormone biosynthetic process; negative regulation of neuron apoptosis; neuromuscular process controlling balance; neuromuscular synaptic transmission; neurotransmitter metabolic process; receptor clustering; regulation of acetylcholine secretion; regulation of axonogenesis; regulation of calcium ion-dependent exocytosis; regulation of insulin secretion; rhythmic synaptic transmission; spinal cord motor neuron differentiation; sulfur amino acid metabolic process; synaptic transmission; synaptic transmission, glutamatergic; synaptogenesis; transmission of nerve impulse; vestibular nucleus development

Disease: Episodic Ataxia, Type 2; Migraine, Familial Hemiplegic, 1; Spinocerebellar Ataxia 6

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