黑色素(醇溶) 號：8005-02-5  
英文名稱：Nigrosine alcohol soluble；Nigrosin spirit soluble；Nigrosin B spirit soluble；Oil soluble black；C.I. 50415    
其他名稱：酒精元；油溶黑5；醇溶尼格洛辛；精元；胺黑；醇溶黑；醇黑；醇溶苯胺黑；油溶苯胺黑；醇溶黑色素   
號：8005-02-5   
級別：BS   
生物染色試驗：合格   
性狀(以下信息僅供參考)：灰黑色到藍黑色粉末或塊狀。系由苯胺、鹽酸苯胺、硝基苯和鐵或銅灼燒至180～200℃而得，或為硝基*(硝基甲酚)、苯胺、鹽酸苯胺和鐵灼熱而成的各種組分。易溶于油酸和硬脂酸，溶于丙同，溶于汽油呈紅紫色，溶于苯呈藍紫色，溶于乙醇和油脂呈深藍色。不溶于水。Z大吸收波長565nm。   
用途：本品僅供科研，不得用于其它用途。(以下用途僅供參考)生物染色   
保存：RT 黑色素(醇溶) 號：8005-02-5儲存條件：
避光、干燥陰涼處封閉貯存,嚴禁與有毒、有害物品混放、混運。本品為非危險 產品可按一般化學品運輸,輕搬動輕放,防止日曬、雨淋！受熱、受潮、受光后易喪失活力,保存期短,因此貯存和運輸條件比較苛刻。
運輸：汽車運輸、EMS郵政快遞，申通快遞等， 款到上海3天內發(fā)貨；
售后：如您對我們的產品服務及技術指標有特殊要求，請及時通知我方。
存儲：應貯存在干燥清潔避光的環(huán)境中，嚴禁與有毒物質混放，以免污染（保質期為兩年）。
黑色素(醇溶) 號：8005-02-5主要優(yōu)級純、分級純和化學純3種：
（1）優(yōu)級純（GR：Guaranteed reagent），又稱一級品或保證試劑，99.8%，這種試劑純度Z高，雜質含量Z低，適合于重要精密的分析工作和科學研究工作，使用綠色瓶簽。
（2）分析純（AR），又稱二級試劑，純度很高，99.7%，略次于優(yōu)級純，適合于重要分析及一般研究工作，使用紅色瓶簽。
（3）化學純（CP），又稱三級試劑，≥ 99.5%，純度與分析純相差較大，適用于工礦、學校一般分析工作。使用藍色（深藍色）標簽。
（4）實驗試劑（LR：Laboratory reagent），又稱四級試劑。
服務承諾：
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產品應用   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）
 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.
產品介紹 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 plaet 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, 黑色素(醇溶) 號：8005-02-5tissues 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.