本公司经销phospho-Alpha synuclein（Tyr133），磷酸化核突触蛋白α抗体，克隆类型为polyclonal，宿主来源是Rabbit，phospho-Alpha synuclein（Tyr133）磷酸化核突触蛋白α抗体可应用于WB、elisa、IP、IF、IHC等实验，欢迎垂询订购！
货号：BY-5625R
英文名称：Anti-phospho-Alpha synuclein（Tyr133）
中文名称：磷酸化核突触蛋白α抗体
其他名称：名SNCA（phospho Y133）; alpha-Synuclein （Phospho-Tyr133）; Synuclein alpha（Phospho-Tyr133）; synuclein; Alpha-synuclein, isoform NACP140; Alpha synuclein; alphaSYN; 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; PARK 1; PARK 4; PARK1; PARK4; Parkinson disease familial 1; PD 1; PD1; SNCA; Snca synuclein, alpha （non A4 component of amyloid precursor）; Synuclein alpha; Synuclein, alpha （non A4 component of amyloid precursor）; SYUA_HUMAN.
抗体来源：Rabbit
克隆类型：polyclonal
蛋白分子量：predicted molecular weight: 15kDa
纯化方法：affinity purified by Protein A
交叉反应：hu, mo, rat, cow, pig, shp, hrs, dog, Rb
产品介绍：The synucleins, including Alpha-synuclein （also designated NACP for nonamyloid component precursor）,Beta-synuclein （also designated PNP 14 for phospho-neuroprotein 14）and Gamma-synuclein （also designated persyn or BCSG1 for breast cancer-specific gene 1）are presynaptic protein abundant in neurons. Alpha-synuclein, a component of Alzheimer’s disease amyloid plaques, is localized to neuronal cell bodies ａnd synapses. Coordinate expression of Alpha-synucleinand Beta-synuclein may be important during hematopoetic cell differentiation. In patients with Parkinson’s disease, a mutant form of Alpha-synuclein has been found ａnd Gamma-synuclein is associated with axonal pathology.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.Synuclein 包括α-Synuclein，β-Synuclein 和γ-Synuclein 是神经细胞中富含的前突触蛋白。α-Synuclein，Alzheimer’（AD）病淀粉样蛋白沉积的成份之一，集中分布在神经细胞的包体和突触。在帕金森病人中发现有α-Synuclein的变异型，而γ-Synuclein与轴突病理学有关。此抗体将为Lewy小体痴呆症、Parkinson症、AD和其它一些神经性疾病提供有用的病理诊断。
