重组大鼠TNF - α

肿瘤坏死因子α

产品号 #(选择产品)

产品号 #78124_C

肿瘤坏死因子α

总览

肿瘤坏死因子-α (TNF-α)是一种促炎细胞因子,可激活NF-κB、MAPK和PI3K/AKT通路。炎症和感染条件下,活化的T细胞和巨噬细胞是TNF-α的主要产生者。许多其他类型的细胞已被证明产生TNF-α,其中包括B细胞、NK细胞、肥大细胞、中性粒细胞、树突状细胞、小胶质细胞、内皮细胞、平滑肌细胞、心肌细胞和成纤维细胞。TNF-α对癌细胞具有细胞毒作用,其机制是通过激发抗肿瘤的免疫抑制反应。TNF-α刺激E-和p -选择素的表达,从而促进中性粒细胞、单核细胞和记忆T细胞粘附于活化的血小板和内皮细胞(zelov<e:1> & Hošek)。TNF-α的其他作用包括血管扩张和水肿形成。体外研究表明,在成年大鼠的神经前体细胞(NPCs)中,TNF-α可抑制源自齿状回的NPCs的神经发生,并促进源自脑室下区的NPCs向星形胶质细胞形成(Borsini等人)。

亚型
细胞因子
 
别名
Cachectin;细胞毒素;分化诱导因子;DIF;坏死因子;TNFA;TNFSF2;肿瘤坏死因子
 
细胞类型
粒细胞及其亚群,单核细胞,T 细胞
 
种属
大鼠
 
研究领域
免疫
 
分子量
17.4 千道尔顿
 
纯度
≥ 95 %
 

Data Figures

(A) The biological activity of Rat Recombinant TNF-alpha was tested by its ability to inhibit cell growth of mouse L929 cells. Cell viability was measured using a fluorometric assay method. The EC50 is defined as the effective concentration of the growth factor at which cell proliferation is at 50% of maximum. The EC50 in the above example is less than 0.05 ng/mL. (B) 2 μg of Rat Recombinant TNF-alpha was resolved with SDS-PAGE under reducing (+) and non-reducing (-) conditions and visualized by Coomassie Blue staining.

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
78124.1
Lot #
All
Language
English
Document Type
Safety Data Sheet
Catalog #
78124.1
Lot #
All
Language
English

Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Resources and Publications

Educational Materials (1)

更多信息

更多信息
Molecular Weight 17.4 kDa
Species Rat
Alternative Names Cachectin, Cytotoxin, Differentiation-inducing factor, DIF, Necrosin, TNFA, TNFSF2, Tumor necrosis factor
Purity ≥ 95%
PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED.
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