硝基化α-突触核蛋白
规格：1尘驳/1尘濒
英文名： Alpha-synuclein (nitro-Tyr39)
别名： SYUA_HUMAN; nitrated Alpha-synuclein (nitrated-Tyr39); nitrated Alpha-synuclein (nitro-Tyr39); Alpha-synuclein (nitro-Tyr39); Alpha-synuclein (nitro Tyr39); nitrated Alpha synuclein; nitrated Alpha-Sy
分子量： 15kDa
储存液：0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glyce
克隆类型：笔辞濒测肠濒辞苍补濒
亚型：滨驳骋
纯化方法：affinity purified by Protein A
**原：KLH conjugated Synthesised nitrylpeptide derived from human
交叉反应：Human, Mouse, Rat, Chicken, Dog, Pig, Cow, Horse, Rabbit, Sheep, Guinea Pig,
细胞定位：细胞核 细胞浆 细胞膜
硝基化α-突触核蛋白产物介绍：background: The synuclein family members, including Alpha-synuclein (also designated NACP for non-Beta-Amyloid component) and Beta-synuclein, are predominantly expressed in the brain and are speculated to be involved in synaptic regulation and neuronal plasticity. Alpha-synuclein is localized to neuronal cell bodies and synapses. Alpha-synuclein was first identified as a component of Alzheimer’s disease amyloid plaques. Abnormal platelet function in Alzheimer’s disease has been demonstrated. During megakaryocytic differentiation Alpha-synuclein has been found to be upregulated, while Beta-synuclein is downregulated, indicating that coordinate expression of synucleins may be important during hematopoetic cell differentiation. A mutant form of Alpha-synuclein has been found in patients with early onset Parkinson’s disease. 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. 硝基化α-突触核蛋白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 硝基化α-突触核蛋白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. 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.
硝基化α-突触核蛋白产物应用：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.
研究领域：细胞生物 神经生物学 细胞凋亡
储存条件： Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
来源： Rabbit
外观： Lyophilized or Liquid