phospho-Alpha synuclein(Ser129)抗体特异性结合抗原：抗体本身不能直接溶解或杀伤带有特异抗原的靶细胞，通常需要补体或吞噬细胞等共同发挥效应以**病原微生物或导致病理损伤。然而，抗体可通过与病毒或**的特异性结合，直接发挥中和病毒的作用。
产品编号xy- 5628R
英文名称phospho-Alpha synuclein(Ser129)
中文名称磷酸化核突触蛋白α抗体
别 名SNCA(phospho S129); alpha Synuclein (phospho S129) ;alpha-Synuclein (Phospho-Ser129); Synuclein alpha(Phospho-Ser129); Alpha synuclein; 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; PD 1; PD1; Syn; SNCA; Snca synuclein, alpha (non A4 component of amyloid precursor); SYUA_HUMAN; Synuclein alpha; Synuclein, alpha (non A4 component of amyloid precursor); α Synuclein; α-Synuclein.
说 明 书100ul
产品类型磷酸化抗体
研究领域**学 神经生物学 信号转导 细胞凋亡 转录调节因子 细胞骨架
抗体来源Rabbit
克隆类型Polyclonal
phospho-Alpha synuclein(Ser129)抗体交叉反应 Human, Mouse, Rat, Dog, Pig, Cow, Horse, Rabbit, Sheep,
产品应用WB=1:500-2000 ELISA=1:500-1000 IHC-P=1:400-800 IHC-F=1:400-800 Flow-Cyt=1ug/Test IF=1:100-500 （石蜡切片需做抗原修复）
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量15kDa
细胞定位细胞核 细胞浆 细胞膜
性 状Lyophilized or Liquid
浓 度1mg/ml
免 疫 原KLH conjugated Synthesised phosphopeptide derived from human SNCA around the phosphorylation site of Ser129 [MP(p-S)EE]:MP(p-S)EE
亚 型IgG
纯化方法affinity purified by Protein A
储 存 液0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
phospho-Alpha synuclein(Ser129)抗体保存条件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.
PubMedPubMed
产品介绍background:
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
phospho-Alpha synuclein(Ser129)抗体（antibody,
Ab）是由效应B细胞（效应**B细胞）分泌，机体用于抵御外来物质，如病毒，**等抗原，结构呈“Y”字型的球状蛋白质，仅仅存在于脊椎动物的血液和B**细胞膜表面。凡是能够跟抗体结合的物质，均被称作抗原，因此对于抗抗体（能够结合抗体的抗体）来说，抗体本身也是一种抗原物质。
phospho-Alpha synuclein(Ser129)抗体普通抗体重链和轻链的结构
重链结构：普通的**球蛋白具有2条重链（H链），分子量约为50kD,有μ、δ、γ、ε和α五种重链亚型，对应的**球蛋白名称分别为IgM、IgG、IgA、IgD和IgE。
轻链结构： 普通**球蛋白具有2条轻链（L链），分子质量约25kDa，有κ链和λ链两种亚型，这两种轻链决定了Ig的亚型类别（IgG1，IgG2，IgG3，IgG4）。一个天然的Ig分子两条轻链总是相同的，但在同一个体内可存在分别带有κ或λ链的抗体分子。不同种属生物体内两型轻链的比例不同，正常人血清**球蛋白κ链：λ链约为2：1，而在小鼠的比例为20：1。
2.2抗体Fab段和Fc段
IgG经木瓜蛋白酶酶切后裂解为2个完全相同的Fab段和1个Fc段,每个Fab段都为单价,可与抗原结合但不会再发生凝集反应；经胃蛋白酶酶切后裂解为1个完整F(ab)2片段和碎片化的Fc片段,F(ab’)2片段为双价,可同时结合两个抗原表位。Fab段为抗原结合片段（fragment of antigen binding，Fab），相当于抗体分子的两个臂，由一个完整的轻链和重链的VH和CH1结构域组成。Fc段为可结晶段（fragment crystallizable，Fc）相当于Ig的CH2和CH3结构域，是Ig与效应分子或者细胞相互作用的部位。Fab段包含完整的可变区，以及恒定区的CH1区域。Fc段仅指Ig恒定区CH2和CH3的区域，相当于Y字结构下面那一部分。
合格 合格 TGF alpha 转移生长因子α抗体
合格 NGFB 神经生长因子β抗体
合格 NFkB Inducing Kinase NIK NFkB诱导激酶抗体
合格 beta-Amyloid 1-42 (CT) β淀粉样肽1-42(C端)/β-Amyloid 1-42 (CT)抗体
合格 合格 beta-Amyloid 1-42(CT) β淀粉样肽/Aβ42抗体
合格 合格 CD19 CD19抗体
合格 CD20 CD20抗体
合格 合格 合格 Caspase-3 活化半胱胺酸蛋白酶蛋白-3抗体
合格 Caspase-6 subunit p18 半胱胺酸蛋白酶蛋白-6抗体
合格 合格 合格 TGF beta 1 转化生长因子β1/TGF β1/TGF-β1抗体
合格 合格 caspase-3 p12 subunit 活化半胱胺酸蛋白酶蛋白3抗体
合格 Secretin 分泌素抗体
合格 Caspase-10 半胱胺酸蛋白酶-10抗体
合格 Calponin 1 钙调节蛋白-1抗体
合格 alpha 1 Antitrypsin α-1抗胰蛋白酶抗体
合格 ALK 间变型**瘤激酶抗体
合格 TGF beta 3 propeptide 转移生长因子β3抗体（TGFβ3）
合格 PKM2 丙酮酸激酶-M2抗体
合格 PKM2 小鼠抗丙酮酸激酶-M2抗体
合格 beta Amyloid 1-40 β淀粉样肽（1-40）抗体
合格 合格 beta Amyloid 1-42 β淀粉样肽（1-42）抗体
合格 合格 合格 Leptin receptor 瘦素受体抗体
合格 合格 FE65 铁蛋白Fe65抗体
合格 Amyloid Precursor Protein APP/ABPP淀粉样肽前体蛋白抗体
合格 Aromatase 芳香化酶抗体
合格 合格 AKT1 蛋白激酶B抗体
合格 合格 AKT1 蛋白激酶B抗体
合格 Estrogen receptor beta 雌**受体β 抗体
合格 TGF beta Receptor II 转移生长因子β受体2抗体
合格 Androgen receptor 雄**受体抗体
合格 FLIP 凋亡调节基因之一抗体
合格 SYAP1 突触素抗体/突触相关蛋白-1