antibody

CACNA1A Antibody (Center)

MBS9216411

0.05 mL

165 USD

polyclonal

rabbit

nonconjugated

western blot, ELISA

Antibody

CACNA1A Antibody (Center)

[CACNA1A]

[Purified Rabbit Polyclonal Antibody (Pab); Voltage-dependent P/Q-type calcium channel subunit alpha-1A; Brain calcium channel I; BI; Calcium channel; L type; alpha-1 polypeptide isoform 4; Voltage-gated calcium channel subunit alpha Cav21; CACNA1A; CACH4; CACN3; CACNL1A4]

[voltage-dependent P/Q-type calcium channel subunit alpha-1A isoform 1; Voltage-dependent P/Q-type calcium channel subunit alpha-1A; voltage-dependent P/Q-type calcium channel subunit alpha-1A; calcium channel, voltage-dependent, P/Q type, alpha 1A subunit; Brain calcium channel I; BI; Calcium channel, L type, alpha-1 polypeptide isoform 4; Voltage-gated calcium channel subunit alpha Cav2.1]

[CACNA1A]

[CACNA1A; CACNA1A; BI; EA2; FHM; MHP; APCA; HPCA; MHP1; SCA6; CAV2.1; CACNL1A4; CACH4; CACN3; CACNL1A4; BI]

CAC1A_HUMAN

Polyclonal

Ig

Rabbit

Human

2266

This CACNA1A antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between 898-932 amino acids from the Central region of human CACNA1A.

Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.

Maintain refrigerated at 2-8 degree C for up to 2 weeks. For long term storage store at -20 degree C in small aliquots to prevent freeze-thaw cycles.

Western Blot (WB); ELISA

WB ~~ 1:2000

Western Blot (WB)

Antigen Source: Human

Cellular Location: Cell membrane; Multi-pass membrane protein. Tissue Location: Brain specific; mainly found in cerebellum, cerebral cortex, thalamus and hypothalamus. Expressed in the small cell lung carcinoma cell line SCC-9. No expression in heart, kidney, liver or muscle. Purkinje cells contain predominantly P- type VSCC, the Q-type being a prominent calcium current in cerebellar granule cells.

Cancer; Metabolism; Neuroscience

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).

Hans M.,et al.Biophys. J. 76:1384-1400(1999). Ophoff R.A.,et al.Cell 87:543-552(1996). Zhuchenko O.,et al.Nat. Genet. 15:62-69(1997). Toru S.,et al.J. Biol. Chem. 275:10893-10898(2000). Grimwood J.,et al.Nature 428:529-535(2004).

148536844

NP_000059.3

NM_000068.3

O00555

282564

Calcium Regulation In The Cardiac Cell Pathway (198906); Calcium Signaling Pathway (83050); Calcium Signaling Pathway (459); Cholinergic Synapse Pathway (217716); Depolarization Of The Presynaptic Terminal Triggers The Opening Of Calcium Channels Pathway (1268767); Dopaminergic Synapse Pathway (469199); Dopaminergic Synapse Pathway (469185); GABAergic Synapse Pathway (377263); GABAergic Synapse Pathway (377129); Glutamatergic Synapse Pathway (213818)

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, multi-pass; Channel, calcium; Membrane protein, integral. Chromosomal Location of Human Ortholog: 19p13. Cellular Component: cell projection; cell soma; dendrite; cytoplasm; integral to membrane; plasma membrane; voltage-gated calcium channel complex; nucleus; cytosol. Molecular Function: voltage-gated calcium channel activity; protein binding; syntaxin binding; metal ion binding; high voltage-gated calcium channel activity. Biological Process: cell death; vestibular nucleus development; musculoskeletal movement, spinal reflex action; gamma-aminobutyric acid secretion; regulation of axonogenesis; adult walking behavior; cellular chloride ion homeostasis; receptor clustering; synaptic transmission; elevation of cytosolic calcium ion concentration; behavioral response to pain; synaptogenesis; neurotransmitter metabolic process; calcium ion transport; negative regulation of neuron apoptosis; cell growth; neuromuscular process controlling balance; cerebellum maturation; synaptic transmission, glutamatergic; rhythmic synaptic transmission; dendrite morphogenesis; regulation of acetylcholine secretion; calcium ion-dependent exocytosis of neurotransmitter; glucose metabolic process; transmission of nerve impulse; spinal cord motor neuron differentiation; regulation of calcium ion-dependent exocytosis; cerebellar molecular layer development; calcium ion-dependent exocytosis; membrane depolarization; sulfur amino acid metabolic process; cerebellar Purkinje cell differentiation; energy reserve metabolic process; neuromuscular synaptic transmission; hormone metabolic process; regulation of insulin secretion; gamma-aminobutyric acid signaling pathway; negative regulation of hormone biosynthetic process. Disease: Spinocerebellar Ataxia 6; Migraine, Familial Hemiplegic, 1; Episodic Ataxia, Type 2

0.05 mL

165 USD

0.2 mL

370