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SNCAIP 抗体 (Internal Region)

This anti-SNCAIP antibody is a 兔 多克隆 antibody detecting SNCAIP in WB 和 IHC. Suitable for 人.
产品编号 ABIN350932
发货至: 中国

Quick Overview for SNCAIP 抗体 (Internal Region) (ABIN350932)

抗原

See all SNCAIP 抗体
SNCAIP (Synuclein, alpha Interacting Protein (SNCAIP))

适用

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宿主

  • 31
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克隆类型

  • 34
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多克隆

标记

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This SNCAIP antibody is un-conjugated

应用范围

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Western Blotting (WB), Immunohistochemistry (IHC)
  • 抗原表位

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    Internal Region

    原理

    Rabbit antibody to Synphilin-1

    特异性

    Specific for Synphilin-1.

    交叉反应

    交叉反应 (详细)

    Other species not yet tested.

    纯化方法

    IgG

    免疫原

    A synthetic peptide from the internal region of human Synphilin-1 (Synphilin 1 alpha synuclein interacting protein) conjugated to an immunogenic carrier protein was used as the antigen.

    亚型

    IgG
  • 应用备注

    IHC WB. A concentration of 10-50,micro,g,ml is recommended. The optimal concentration should be determined by the end user. Not yet tested in other applications.

    限制

    仅限研究用
  • 状态

    Lyophilized

    溶解方式

    Reconstitute in 500 µl of sterile water. Centrifuge to remove any insoluble material.

    注意事项

    Avoid freeze and thaw cycles.

    储存条件

    4 °C,-20 °C

    储存方法

    Maintain the lyophilised/reconstituted antibodies frozen at -20°C for long term storage and refrigerated at 2-8°C for a shorter term. When reconstituting glycerol (1:1) may be added for an additional stability. Avoid freeze and thaw cycles.

    有效期

    12 months
  • 抗原

    SNCAIP (Synuclein, alpha Interacting Protein (SNCAIP))

    别名

    Synphilin-1

    背景

    Tissue specificity: Widely expressed with highest levels in brain heart and placenta. Defects in SNCAIP are a cause of Parkinson disease (PD). PD is a complex multifactorial disorder that typically manifests after the age of 50 years although early-onset cases (before 50 years) are known. PD generally arises as a sporadic condition but is occasionally inherited as a simple mendelian trait. Although sporadic and familial PD are very similar inherited forms of the disease usually begin at earlier ages and are associated with atypical clinical features. PD is characterized by bradykinesia resting tremor muscular rigidity and postural instability as well as by a clinically significant response to treatment with levodopa. The pathology involves the loss of dopaminergic neurons in the substantia nigra and the presence of Lewy bodies (intraneuronal accumulations of aggregated proteins) in surviving neurons in various areas of the brain. Constructs encoding portions of SNCA and SNCAIP co-transfected in mammalian cells promote cytosolic inclusions resembling the Lewy bodies of Parkinson disease. Coexpression of SNCA SNCAIP and PARK2 result in the formation of Lewy body-like ubiquitin-positive cytosolic inclusions. Familial mutations in PARK2 disrupt the ubiquitination of SNCAIP and the formation of the ubiquitin-positive inclusions. These results provide a molecular basis for the ubiquitination of Lewy body-associated proteins and link PARK2 and SNCA in a common pathogenic mechanism through their interaction with SNCAIP.

    UniProt

    Q9Y6H5
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