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Recombinant Mouse Voltage-dependent P/Q-type calcium channel subunit alpha-1A (Cacna1a), partial

  • 中文名稱:
    Recombinant Mouse Voltage-dependent P/Q-type calcium channel subunit alpha-1A(Cacna1a) ,partial,Yeast
  • 貨號:
    CSB-YP004397MO
  • 規(guī)格:
  • 來源:
    Yeast
  • 其他:
  • 中文名稱:
    Recombinant Mouse Voltage-dependent P/Q-type calcium channel subunit alpha-1A(Cacna1a) ,partial,Yeast
  • 貨號:
    CSB-EP004397MO
  • 規(guī)格:
  • 來源:
    E.coli
  • 其他:
  • 中文名稱:
    Recombinant Mouse Voltage-dependent P/Q-type calcium channel subunit alpha-1A(Cacna1a) ,partial,Yeast
  • 貨號:
    CSB-EP004397MO-B
  • 規(guī)格:
  • 來源:
    E.coli
  • 共軛:
    Avi-tag Biotinylated

    E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.

  • 其他:
  • 中文名稱:
    Recombinant Mouse Voltage-dependent P/Q-type calcium channel subunit alpha-1A(Cacna1a) ,partial,Yeast
  • 貨號:
    CSB-BP004397MO
  • 規(guī)格:
  • 來源:
    Baculovirus
  • 其他:
  • 中文名稱:
    Recombinant Mouse Voltage-dependent P/Q-type calcium channel subunit alpha-1A(Cacna1a) ,partial,Yeast
  • 貨號:
    CSB-MP004397MO
  • 規(guī)格:
  • 來源:
    Mammalian cell
  • 其他:

產(chǎn)品詳情

  • 純度:
    >85% (SDS-PAGE)
  • 基因名:
    Cacna1a
  • Uniprot No.:
  • 別名:
    Cacna1a; Caca1a; Cach4; Cacn3; Cacnl1a4; Ccha1a; 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 Cav2.1
  • 種屬:
    Mus musculus (Mouse)
  • 蛋白長度:
    Partial
  • 蛋白標(biāo)簽:
    Tag?type?will?be?determined?during?the?manufacturing?process.
    The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
  • 產(chǎn)品提供形式:
    Lyophilized powder
    Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
  • 復(fù)溶:
    We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
  • 儲存條件:
    Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
  • 保質(zhì)期:
    The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
    Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
  • 貨期:
    Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
    Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
  • 注意事項:
    Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
  • Datasheet :
    Please contact us to get it.

產(chǎn)品評價

靶點詳情

  • 功能:
    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 specifically blocked by the spider omega-agatoxin-IVA (AC P54282). They are however insensitive to dihydropyridines (DHP).
  • 基因功能參考文獻(xiàn):
    1. Study demonstrates that the functional defects in Cav2.1+/R1497X knock-in mice are due to the dominant-negative suppression of Cav2.1 channels and attests to the importance of the Cav2.1+/R1497X mouse model for studies of Episodic Ataxia type 2 pathophysiology as well as the development of therapeutic strategies for this disease. PMID: 28688851
    2. These results identified a region that directly controlled fast synaptic vesicle release and vesicle docking at the active zone independent of CaV2.1 calcium channel abundance. PMID: 28786379
    3. These results demonstrate that a functional deficit in P/Q-type channels does not alter propulsive colonic motility. Myenteric neuron L-type Ca(2+) channel function increases to compensate for loss of functional P/Q-type Ca(2+) channels. PMID: 27586650
    4. Electrophysiological characterization of VDCC currents revealed that the suppressive effect of RIM2alpha on voltage-dependent inactivation (VDI) was stronger than that of RIM1alpha for the CaV2.1 variant containing the region encoded by exons 44 and 47. PMID: 28377503
    5. Cacna1a mutation plays a significant role in protein expression patterns in cerebellum of mutant mice. PMID: 26887908
    6. Our findings that BAG3 is localized at the sarcolemma and t-tubules while modulating myocyte contraction and action potential duration through specific interaction with the beta1-adrenergic receptor and L-type Ca(2+) channel provide novel insight into the role of BAG3 in cardiomyopathies and increased arrhythmia risks in heart failure. PMID: 26796036
    7. Findings demonstrate that the mutant Cav2.1 channel exerts a protective effect against cryogenic brain injury in rolling Nagoya mice PMID: 26616403
    8. results indicate that regulation of CaV2.1 channels by Ca(2+) sensor proteins is essential for normal synaptic plasticity at the neuromuscular junction and for muscle strength, endurance, and motor coordination in mice in vivo PMID: 26755585
    9. regulation of CaV2.1 channels by calcium sensor proteins is required for normal short-term plasticity PMID: 26755594
    10. Thus, GHSR1a differentially inhibits CaV2 channels by Gi/o or Gq protein pathways depending on its mode of activation. PMID: 26283199
    11. Genetic ablation of Cacna1a in layer VI neurons produced Absence Epilepsy. PMID: 26758833
    12. study showed that spontaneous C mutations causing cerebellar pathology are impaired in motor functions during the neonatal period. PMID: 25907855
    13. CACNA1A regulates lysosomal fusion with endosomes and autophagosomes and is required for neuronal homeostasis. PMID: 25811491
    14. CaV2.1 Ca2+ channel mutation leads to developmental abnormalities in Cl- transporter expression and GABAA receptor compositions in hippocampal neurons. PMID: 24947601
    15. Study of interstrain comparisons providing some insight into the role that specific Purkinje cell firing rate alterations play in the Cacna1a mutant phenotype PMID: 25143538
    16. Cacna1a mutations elevate neuronal [Ca(2+)]i and alter synaptic morphology as a mechanism for enhanced cortical spreading depression susceptibility in a mouse model of familial hemiplegic migraine type 1. PMID: 26032020
    17. cav2.1 calcium channels have roles in regulating inhibitory and excitatory synaptic transmission in the lateral superior olive of mice PMID: 25481823
    18. The tottering-6j mouse is a useful model for studying Cav2.1 channel functions and Cacna1a-related diseases, including absence epilepsy. PMID: 26002462
    19. LTP was augmented by twofold in R192Q mice. R192Q mice showed significant spatial memory deficits. PMID: 25716839
    20. This study emonstrated that the high-power low-frequency oscillations in the tg/tg cerebral cortex represent a highly abnormal excitability state that may underlie noncerebellar symptoms that characterize CACNA1A mutations. PMID: 25855180
    21. The data of this study revealed that P/Q-type channel suppression in adult mice supports the episodic status of EA2 disease. PMID: 24768804
    22. Findings suggest that the unaltered inhibitory transmission at multipolar interneuron autapses is due to the expression of specific CaV2.1 channels whose gating is barely affected by the familial hemiplegic migraine type 1 mutation PMID: 24907493
    23. two functional classes of wild type or knock-in neurons were distinguished according to the first spike latency, which suggests that a subgroup of neurons may be indirectly activated PMID: 24583041
    24. Cav2.1-2.3 have unique contributions to the dynamics at the Schaffer collateral synapse that are engaged by the complex patterns of afferent activity seen in vivo PMID: 24523520
    25. Despite pronounced consequences of migraine gene mutations at the neurobiological level, changes in cortical RNA expression in FHM1 migraine mice compared to wild-type are modest. PMID: 23985897
    26. Cortical inhibitory interneurons are affected by loss of CaV2.1 channel function, which contributes to the onset of generalized epilepsy. PMID: 23595603
    27. This study demonistrated that Synaptic gain-of-function effects of mutant Cav2.1 channels in a mouse model of familial hemiplegic migraine are due to increased basal. PMID: 24849341
    28. Calcium {Ca(2+)} entry through beta-adrenergic-stimulated LTCC underlies hypoxia-induced [Ca(2+)]i overload and the ensuing loss of mitochondrial function in intact heart. PMID: 24041537
    29. These findings identify an interaction between ankyrin-B and both Cav2.1 and Cav2.2 at the amino acid level that is necessary for proper Cav2.1 and Cav2.2 targeting in vivo. PMID: 24394417
    30. The results of this study reveal a mechanism by which a Ca(v)2.1 gating modifier can ameliorate defects associated with a disease-causing mutation in Ca(v)2.1. PMID: 24411734
    31. Ths results of this study suggested that Cacna1a transgenic mice can experience migraine-related head pain and can thus serve as unique tools to study the pathogenesis of migraine and test novel antimigraine agents. PMID: 23673147
    32. Data indicate that TNFalpha expression and macrophage occurrence were significantly higher in calcium channel Cav2.1 R192Q KI ganglia with respect to wildtype ganglia. PMID: 23326332
    33. The mutant CaV2.1 channel in rolling Nagoya and leaner mice plays a different protective role in a brain ischemia model. PMID: 23545255
    34. Developmental alteration of patterned input confined to only one of the main afferent cerebellar excitatory synaptic pathways has a role in generating the neurological phenotype associated with the global genomic loss of P/Q-type channel function. PMID: 23516282
    35. Excitatory postsynaptic currents in neurons with mutant Cav2.1 (R192Q) showed increased amplitudes and faster recovery from synaptic depression. PMID: 22956801
    36. Loss of Cav2.1 calcium channel is associated with an alteration in functional dependency of N-type calcium channel Cav2.2. PMID: 23426690
    37. Two distinct patterns of Cav2.1 distribution--scattered and clustered--are found in Purkinje cells. PMID: 23426693
    38. These results indicate that tottering-6j is a useful model for functional studies of the Ca(v)2.1 channel. PMID: 22952933
    39. Gain in synaptic inhibition shown here would compromise the fidelity of information coding in these neurons and may contribute to impaired cerebellar function resulting from loss-of function mutations in the Ca(V)2.1 channel gene PMID: 20845003
    40. In a mouse model with cell type-specific ablation of Cav2.1 channels, ablation of Cav2.1 channels restricted to Purkinje cells is sufficient to cause cerebellar ataxia. PMID: 21870131
    41. This study demonistrated that cacna1a gene expression in mouse dorsal raphe nucleus PMID: 22534482
    42. Study of episodic ataxia 2 in mutant mice has implications for a haploinsufficiency mechanism at least for some of the Cacna1a mutations leading to a premature stop codon. PMID: 21440913
    43. Calcium channel Cacna1a and ELKS1b protein interact in vitro and colocalize in the cerebellum may play a role at the molecular layer synapses of the cerebellum. PMID: 22107844
    44. Cav2.1 in Purkinje cells (PCs) is essential for competitive synaptic wiring, cell survival, and the establishment of precise boundaries and reciprocity of biochemical compartments in PCs. PMID: 22279216
    45. Data suggest that Ca(v)2.1 P/Q-type Ca(2+) channels in postsynaptic PCs mediate synaptic competition among multiple CFs and trigger synapse elimination in developing cerebellum. PMID: 21628556
    46. Th findings of this study suggested that heterozygous mice show age-related emotional changes due to alterations in the serotonin system associated with mutant-type Ca(v)2.1alpha(1). PMID: 19345443
    47. Ca2+ influx through presynaptic P/Q-type Ca2+ channels with consequent release of glutamate from recurrent cortical pyramidal cell synapses and activation of NMDA receptors are required for initiation and propagation of the CSD involved in migraine PMID: 21150292
    48. Presynaptic VDCCs link the target-derived synapse organizer laminin beta2 to active-zone proteins and function as scaffolding proteins to anchor active-zone proteins to the presynaptic membrane. PMID: 21228161
    49. CACNA1A mutation conferred a novel molecular phenotype to P2X3 receptors of trigeminal ganglion neurons via CaMKII-dependent activation of calcineurin. PMID: 20735819
    50. Suggest that both Cav2.1 P/Q- and Cav3.1 T-type calcium channels are required for the dynamic control of neuronal oscillations in the inferior olive neurons. PMID: 20547676

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  • 相關(guān)疾?。?/div>
    Defects in Cacna1a are the cause of a delayed-onset, recessive neurological disorder seen in tottering (tg) mutants, resulting in ataxia, motor seizures and behavioral absence seizures resembling petit mal epilepsy (or absence epilepsy) in humans. There are two more alleles, leaner (tg(lA)), that is characterized by severe ataxia and frequent death past weaning, but no motor seizures; and rolling Nagoya (tg(rol)), that presents an intermediary phenotype, the ataxia being somewhat more severe that with tg, but without motors seizures. Selective degeneration of cerebellar Purkinje cells has been shown for all these types of mutants. Selective degeneration of cerebellar Purkinje cells has been shown for all these types of mutants.
  • 亞細(xì)胞定位:
    Cell membrane; Multi-pass membrane protein.
  • 蛋白家族:
    Calcium channel alpha-1 subunit (TC 1.A.1.11) family, CACNA1A subfamily
  • 組織特異性:
    Brain specific; mainly found in the cerebellum, olfactory bulb, cerebral cortex, hippocampus, and inferior colliculus. In the hippocampus, expression occurs in pyramidal and granule neurons, as well as in interneurons. Purkinje cells contain predominantly
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