推薦產品
product name
Monoclonal Anti-OLIG2 antibody produced in mouse, clone 1G11, ascites fluid
生物源
mouse
品質等級
共軛
unconjugated
抗體表格
ascites fluid
抗體產品種類
primary antibodies
無性繁殖
1G11, monoclonal
分子量
32 kDa
物種活性
human
技術
direct ELISA: 1:10,000
immunohistochemistry: 1:200-1:1,000
indirect immunofluorescence: 1:200-1:1,000
western blot: 1:500-1:2,000
同型
IgG1
NCBI登錄號
UniProt登錄號
運輸包裝
wet ice
儲存溫度
−20°C
目標翻譯後修改
unmodified
基因資訊
human ... OLIG2(10215)
免疫原
Purified recombinant fragment of human OLIG2 expressed in E.coli.
Mouse monoclonal antibody raised against OLIG2
Mouse monoclonal antibody raised against OLIG2
外觀
Ascitic fluid containing 0.03% sodium azide.
免責聲明
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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儲存類別代碼
10 - Combustible liquids
水污染物質分類（WGK）
WGK 3
閃點（°F）
Not applicable
閃點（°C）
Not applicable
分析證明 (COA)
輸入產品批次/批號來搜索 分析證明 (COA)。在產品’s標籤上找到批次和批號，寫有 ‘Lot’或‘Batch’.。
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Tumor hypoxia is associated with poor patient survival and is a characteristic of glioblastoma. Notch signaling is implicated in maintaining glioma stem-like cells (GSCs) within the hypoxic niche, although the molecular mechanisms linking hypoxia to Notch activation have not been
Benjamin Ettle et al.
Molecular and cellular neurosciences, 62, 68-78 (2014-07-16)
Myelin loss is a widespread neuropathological hallmark of the atypical parkinsonian disorder multiple system atrophy (MSA). On a cellular level, MSA is characterized by alpha-synuclein (aSyn)-positive glial cytoplasmic inclusions (GCIs) within mature oligodendrocytes leading to demyelination as well as axonal
Vanja Tepavčević et al.
Annals of neurology, 76(2), 252-268 (2014-06-20)
Chronically demyelinated multiple sclerosis (MS) lesions are frequently characterized by scarce undifferentiated oligodendrocyte progenitor cells (OPCs), suggesting the exhaustion of a local OPC pool followed by failure of recruitment and differentiation. Stimulating prompt OPC recruitment following demyelination could improve myelin
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