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核突觸蛋白α+β抗體規(guī)格 英文名稱  Anti-alpha + beta Synuclein

中文名稱  核突觸蛋白α+β抗體規(guī)格 

別    名 Alpha synuclein; Beta synuclein; NACP; Non A beta component of AD amyloid; Non A4 component of amyloid precursor; PARK1; PARK4; Parkinson disease familial 1; PD1; SNCA; SYUA_HUMAN; SNCB; SNCB protein; Synuclein alpha; Synuclein beta; SYUB_HUMAN.

產(chǎn)品屬性：

濃    度  1mg/1ml

規(guī) 格  0.1ml/100μg 0.2ml/200μg

抗體來源  Rabbit

克隆類型   polyclonal

交叉反應(yīng)   Human, Mouse, Rat, Chicken, Dog, Pig, Cow, Rabbit, zebrafinch

產(chǎn)品類型   一抗  

研究領(lǐng)域    細胞生物 神經(jīng)生物學(xué) Alzheimer's

蛋白分子量  predicted molecular weight: 14kDa 

性    狀   Lyophilized or Liquid

免 疫 原  KLH conjugated synthetic peptide derived from human alpha + beta Synuclein

亞    型  IgG

純化方法   affinity purified by Protein A

儲 存 液   Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.01M PBS, pH 7.4

核突觸蛋白α+β抗體規(guī)格 產(chǎn)品應(yīng)用   WB=1:100-500 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 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.  

保存條件  Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. 

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

產(chǎn)品介紹 Synucleins are small soluble proteins expressed primarily in neural tissues and in certain tumors. The family includes 3 known proteins, alpha synuclein, beta synuclein and gamma synuclein. All synucleins have in common a highly conserved alpha helical lipid binding motif with similarity to the class A2 lipid binding domains of the exchangeable apolipoproteins. The alpha and beta synuclein proteins are found primarily in brain tissue, where they are seen mainly in pre synaptic terminals. Alpha synuclein is believed to be a major component of Lewy bodies in Parkinson’s disease. Mutations in alpha synuclein are associated with rare familial cases of early onset Parkinson’s disease, Alzheimer’s disease and several other neurodegenerative illnesses.

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 (By similarity). Interacts with phospholipase D and histones.

Subcellular Location : Cytoplasmic. Membrane bound in dopaminergic neurons. Also found in the nucleus.

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 (By similarity).

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.

Database links : UniProtKB/Swiss-Prot: P37840.1 UniProtKB/Swiss-Prot: Q16143.1

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