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Alpha-synuclein (nitro-Tyr39) Rabbit pAb (bs-9587R)  
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產(chǎn)品編號 bs-9587R
英文名稱 Alpha-synuclein (nitro-Tyr39) Rabbit pAb
中文名稱 硝基化α-突觸核蛋白/n-syn抗體
別    名 SYUA_HUMAN; nitrated alpha-synuclein(nitrated-Tyr39); alpha-synuclein 3-nitrotyrosines(Tyr39); alpha-synuclein 3-nitrotyrosines Tyr39; alpha synuclein 3-nitrotyrosines Tyr39; nitrated alpha-synuclein(nitro-Tyr39); alpha-synuclein(nitro-Tyr39); alpha-synuclein(nitro Tyr39); 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.  α Synuclein; α-Synuclein; nitrated α-synuclein; n-syn.
研究領(lǐng)域 細胞生物  神經(jīng)生物學(xué)  細胞凋亡  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) Human,Mouse,Rat (predicted: Rabbit,Pig,Sheep,Cow,Chicken,Dog,GuineaPig,Horse)
產(chǎn)品應(yīng)用 IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500,Flow-Cyt=1ug/Test
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
理論分子量 15 kDa
檢測分子量
細胞定位 細胞核 細胞漿 細胞膜 
性    狀 Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated Synthesised nitrylpeptide derived from human SNCA around the nitrosation site of Tyr39: VL(nitrated-Y)VG 
亞    型 IgG
純化方法 affinity purified by Protein A
緩 沖 液 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
保存條件 Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.
注意事項 This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed PubMed
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:
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.

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



產(chǎn)品圖片
Paraformaldehyde-fixed, paraffin embedded (Rat brain); Antigen retrieval by boiling in sodium citrate buffer (pH6.0) for 15min; Block endogenous peroxidase by 3% hydrogen peroxide for 20 minutes; Blocking buffer (normal goat serum) at 37°C for 30min; Anti
Paraformaldehyde-fixed, paraffin embedded (Mouse brain); Antigen retrieval by boiling in sodium citrate buffer (pH6.0) for 15min; Block endogenous peroxidase by 3% hydrogen peroxide for 20 minutes; Blocking buffer (normal goat serum) at 37°C for 30min; An
Paraformaldehyde-fixed, paraffin embedded (rat kidney tissue); Antigen retrieval by boiling in sodium citrate buffer (pH6.0) for 15min; Block endogenous peroxidase by 3% hydrogen peroxide for 20 minutes; Blocking buffer (normal goat serum) at 37°C for 30m
Blank control (Black line): HUVEC (Black). Primary Antibody (green line): Rabbit Anti-Alpha-synuclein (nitro-Tyr39) antibody (bs-9587R) Dilution: 1μg /10^6 cells; Isotype Control Antibody (orange line): Rabbit IgG . Secondary Antibody (white blue li
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