Recombinant Human Alpha-synuclein (mutated E46K) protein (ab51188)
Key features and details
- Expression system: Escherichia coli
- Purity: > 95% SDS-PAGE
- Suitable for: SDS-PAGE
製品の詳細
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製品名
Recombinant Human Alpha-synuclein (mutated E46K) protein
Alpha-synuclein タンパク質・ペプチド 製品一覧 -
精製度
> 95 % SDS-PAGE.
Alpha Synuclein E46K was overexpressed in E. coli and purified to apparent homogeneity by using conventional column chromatography techniques. -
発現系
Escherichia coli -
アクセッション番号
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タンパク質長
Full length protein -
Animal free
No -
由来
Recombinant -
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生物種
Human -
配列
MDVFMKGLSK/ AKEGVVAAAE/ KTKQGVAEAA/ GKTKEGVLYV/ GSKTK[K]GVVH/GVATVAEKTK/EQVTNVGGAV/VT GVTAVAQK/TVEGAGSIAA/ ATGFVKKDQL/GKNEEGAPQE/GILEDM PVDP/DNEAYEMPSE/EGYQDYEPEA -
予測される分子量
14 kDa -
領域
1 to 140 -
修飾
mutated E46K
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特性
Our Abpromise guarantee covers the use of ab51188 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
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アプリケーション
SDS-PAGE
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製品の状態
Liquid -
備考
Recent studies have shown that this mutant(E46K) of alpha-synuclein causes Parkinson and Lewy Body dementia(DLB).
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Concentration information loading...
前処理および保存
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保存方法および安定性
Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
pH: 7.50
Constituents: 0.316% Tris HCl, 0.58% Sodium chloride
関連情報
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別名
- Alpha synuclein
- Alpha-synuclein
- Alpha-synuclein, isoform NACP140
see all -
機能
May be involved in the regulation of dopamine release and transport. Induces fibrillization of microtubule-associated protein tau. Reduces neuronal responsiveness to various apoptotic stimuli, leading to a decreased caspase-3 activation. -
組織特異性
Expressed principally in brain but is also expressed in low concentrations in all tissues examined except in liver. Concentrated in presynaptic nerve terminals. -
関連疾患
Genetic alterations of SNCA resulting in aberrant polymerization into fibrils, are associated with several neurodegenerative diseases (synucleinopathies). SNCA fibrillar aggregates represent the major non A-beta component of Alzheimer disease amyloid plaque, and a major component of Lewy body inclusions. They are also found within Lewy body (LB)-like intraneuronal inclusions, glial inclusions and axonal spheroids in neurodegeneration with brain iron accumulation type 1.
Parkinson disease 1
Parkinson disease 4
Dementia Lewy body -
配列類似性
Belongs to the synuclein family. -
ドメイン
The 'non A-beta component of Alzheimer disease amyloid plaque' domain (NAC domain) is involved in fibrils formation. The middle hydrophobic region forms the core of the filaments. The C-terminus may regulate aggregation and determine the diameter of the filaments. -
翻訳後修飾
Phosphorylated, predominantly on serine residues. Phosphorylation by CK1 appears to occur on residues distinct from the residue phosphorylated by other kinases. Phosphorylation of Ser-129 is selective and extensive in synucleinopathy lesions. In vitro, phosphorylation at Ser-129 promoted insoluble fibril formation. Phosphorylated on Tyr-125 by a PTK2B-dependent pathway upon osmotic stress.
Hallmark lesions of neurodegenerative synucleinopathies contain alpha-synuclein that is modified by nitration of tyrosine residues and possibly by dityrosine cross-linking to generated stable oligomers.
Ubiquitinated. The predominant conjugate is the diubiquitinated form.
Acetylation at Met-1 seems to be important for proper folding and native oligomeric structure. -
細胞内局在
Cytoplasm, cytosol. Membrane. Nucleus. Cell junction, synapse. Secreted. Membrane-bound in dopaminergic neurons. - Information by UniProt
プロトコール
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
データシートおよび資料
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Datasheet download
参考文献 (2)
ab51188 は 2 報の論文で使用されています。
- Van Aelst B et al. Psoralen and Ultraviolet A Light Treatment Directly Affects Phosphatidylinositol 3-Kinase Signal Transduction by Altering Plasma Membrane Packing. J Biol Chem 291:24364-24376 (2016). PubMed: 27687726
- Sampson TR et al. Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson's Disease. Cell 167:1469-1480.e12 (2016). PubMed: 27912057