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磷酸化核突觸蛋白α抗體
  • 產(chǎn)品貨號(hào)：
    BN41151R
  • 中文名稱：
    磷酸化核突觸蛋白α抗體
  • 英文名稱：
    Rabbit anti-phospho-Alpha synuclein (Ser129) Polyclonal antibody
  • 品牌：
    Biorigin

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  • BN41151R-100ul

    100ul

    ￥2470.00

    交叉反應(yīng)：Human,Mouse,Rat(predicted:Dog,Pig,Cow,Horse,Rabbit,Sheep) 推薦應(yīng)用：WB,IHC-P,IHC-F,IF,Flow-Cyt,ELISA

產(chǎn)品描述

英文名稱phospho-Alpha synuclein (Ser129)
中文名稱磷酸化核突觸蛋白α抗體
別    名SNCA(phospho S129); alpha Synuclein (phospho S129) ;alpha-Synuclein (Phospho-Ser129); Synuclein alpha(Phospho-Ser129); SNCA; SYUA_HUMAN; Alpha synuclein; Alpha-synuclein, isoform NACP140; alpha SYN; MGC105443; MGC110988; MGC127560; MGC64356; NACP; Non A beta component of AD amyloid; Non A4 component of amyloid precursor; Non-A-beta component of alzheimers disease amyloid , precursor of; Non-A beta component of AD amyloid; Non-A4 component of amyloid precursor; PARK 1; PARK 4; PARK1; PARK4; Parkinson disease (autosomal dominant, Lewy body) 4; Parkinson disease familial 1; Syn; Snca synuclein, alpha (non A4 component of amyloid precursor); Synuclein alpha; Synuclein, alpha (non A4 component of amyloid precursor); Synuclein-α; Synuclein α.  
產(chǎn)品類型磷酸化抗體 
研究領(lǐng)域免疫學(xué)  神經(jīng)生物學(xué)  信號(hào)轉(zhuǎn)導(dǎo)  細(xì)胞凋亡  轉(zhuǎn)錄調(diào)節(jié)因子  細(xì)胞骨架  
抗體來源Rabbit
克隆類型Polyclonal
交叉反應(yīng)Human, Mouse, Rat,  (predicted: Dog, Pig, Cow, Horse, Rabbit, Sheep, )
產(chǎn)品應(yīng)用WB=1:500-2000 ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=1ug/Test IF=1:100-500 （石蠟切片需做抗原修復(fù)）
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量15kDa
細(xì)胞定位細(xì)胞核 細(xì)胞漿 細(xì)胞膜 
性    狀Liquid
濃    度1mg/ml
免 疫 原KLH conjugated Synthesised phosphopeptide derived from human SNCA around the phosphorylation site of Ser129:MP(p-S)EE 
亞    型IgG
純化方法affinity purified by Protein A
儲(chǔ) 存 液0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
PubMedPubMed
產(chǎn)品介紹Alpha-synuclein is a member of the synuclein family, which also includes beta- and gamma-synuclein. Synucleins are abundantly expressed in the brain and alpha- and beta-synuclein inhibit phospholipase D2 selectively. SNCA may serve to integrate presynaptic signaling and membrane trafficking. Defects in SNCA have been implicated in the pathogenesis of Parkinson disease. SNCA peptides are a major component of amyloid plaques in the brains of patients with Alzheimer's disease. Alternatively spliced transcripts encoding different isoforms have been identified for this gene. [provided by RefSeq, Feb 2016]..

Function:
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.

Subunit:
Soluble monomer which can form filamentous aggregates. Interacts with UCHL1. Interacts with phospholipase D and histones.

Subcellular Location:
Cytoplasm. Membrane. Nucleus. Cell junction, synapse. Note=Membrane-bound in dopaminergic neurons.

Tissue Specificity:
Expressed principally in brain but is also expressed in low concentrations in all tissues examined except in liver. Concentrated in presynaptic nerve terminals.

Post-translational modifications:
Note=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.

Defects in SNCA are the cause of Parkinson disease type 1 (PARK1) [MIM:168601]. A complex neurodegenerative disorder characterized by bradykinesia, resting tremor, muscular rigidity and postural instability. Additional features are characteristic postural abnormalities, dysautonomia, dystonic cramps, and dementia. The pathology of Parkinson disease 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. The disease is progressive and usually manifests after the age of 50 years, although early-onset cases (before 50 years) are known. The majority of the cases are sporadic suggesting a multifactorial etiology based on environmental and genetic factors. However, some patients present with a positive family history for the disease. Familial forms of the disease usually begin at earlier ages and are associated with atypical clinical features.

Defects in SNCA are the cause of Parkinson disease type 4 (PARK4) [MIM:605543]. A complex neurodegenerative disorder with manifestations ranging from typical Parkinson disease to dementia with Lewy bodies. Clinical features include parkinsonian symptoms (tremor, rigidity, postural instability and bradykinesia), dementia, diffuse Lewy body pathology, autonomic dysfunction, hallucinations and paranoia.

Defects in SNCA are the cause of dementia Lewy body (DLB) [MIM:127750]. A neurodegenerative disorder clinically characterized by mental impairment leading to dementia, parkinsonism, often with fluctuating cognitive function, visual hallucinations, falls, syncopal episodes, and sensitivity to neuroleptic medication. Brainstem or cortical intraneuronal accumulations of aggregated proteins (Lewy bodies) are the only essential pathologic features. Patients may also have hippocampal and neocortical senile plaques, sometimes in sufficient number to fulfill the diagnostic criteria for Alzheimer disease.

DISEASE:
Note=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.

Defects in SNCA are the cause of Parkinson disease type 1 (PARK1) [MIM:168601]. A complex neurodegenerative disorder characterized by bradykinesia, resting tremor, muscular rigidity and postural instability. Additional features are characteristic postural abnormalities, dysautonomia, dystonic cramps, and dementia. The pathology of Parkinson disease 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. The disease is progressive and usually manifests after the age of 50 years, although early-onset cases (before 50 years) are known. The majority of the cases are sporadic suggesting a multifactorial etiology based on environmental and genetic factors. However, some patients present with a positive family history for the disease. Familial forms of the disease usually begin at earlier ages and are associated with atypical clinical features.

Defects in SNCA are the cause of Parkinson disease type 4 (PARK4) [MIM:605543]. A complex neurodegenerative disorder with manifestations ranging from typical Parkinson disease to dementia with Lewy bodies. Clinical features include parkinsonian symptoms (tremor, rigidity, postural instability and bradykinesia), dementia, diffuse Lewy body pathology, autonomic dysfunction, hallucinations and paranoia.

Defects in SNCA are the cause of dementia Lewy body (DLB) [MIM:127750]. A neurodegenerative disorder clinically characterized by mental impairment leading to dementia, parkinsonism, often with fluctuating cognitive function, visual hallucinations, falls, syncopal episodes, and sensitivity to neuroleptic medication. Brainstem or cortical intraneuronal accumulations of aggregated proteins (Lewy bodies) are the only essential pathologic features. Patients may also have hippocampal and neocortical senile plaques, sometimes in sufficient number to fulfill the diagnostic criteria for Alzheimer disease.

Similarity:
Belongs to the synuclein family.

SWISS:
P37840

Gene ID:
6622

Database links:

Entrez Gene: 6622 Human

Entrez Gene: 20617 Mouse

Entrez Gene: 29219 Rat

Omim: 163890 Human

SwissProt: P37840 Human

SwissProt: O55042 Mouse

SwissProt: P37377 Rat

Unigene: 21374 Human

Unigene: 17484 Mouse

Unigene: 1827 Rat



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

Synuclein 包括α-Synuclein，β-Synuclein 和γ-Synuclein 是神經(jīng)細(xì)胞中富含的前突觸蛋白。α-Synuclein，Alzheimer’(AD)病淀粉樣蛋白沉積的成份之一，集中分布在神經(jīng)細(xì)胞的包體和突觸。在帕金森病人中發(fā)現(xiàn)有α-Synuclein的變異型，而γ-Synuclein與軸突病理學(xué)有關(guān)。此抗體將為L(zhǎng)ewy小體癡呆癥、Parkinson癥、AD和其它一些神經(jīng)性疾病提供有用的病理診斷。












































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