Cell Signaling Technology

Product Pathways - NF-kB Signaling

Mouse TNF-α Neutralizing (D2H4) Rabbit mAb #11969

Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
N 1:1 Mouse, Rabbit IgG

Species cross-reactivity is determined by western blot.

Applications Key: N=Neutralizing,

Specificity / Sensitivity

Mouse TNF-α Neutralizing (D2H4) Rabbit mAb binds to mouse TNF-α and neutralizes its cytotoxic effects. This antibody does not cross-react with human TNF-α or human LTA.

小鼠TNF-α Neutralizing (D2H4) Rabbit mAb(中和抗体)能够结合鼠源TNF-α并且中和它的细胞毒活性。这种抗体不能够与人源TNF-α或人源LTA发生交叉反应。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a recombinant mouse TNF-α protein.



Neutralizing antibodies can be used to inhibit normal biological function through their binding to biological molecules. These reagents can be used to determine the effects that a particular molecule has in biological systems. Mouse TNF-α Neutralizing (D2H4) Rabbit mAb has been shown to neutralize the cytotoxic effects of TNF-α in L-929 cells in vitro with an ND50 in the range of 1-6 ng/ml.

此中和抗体能够通过结合生物分子抑制其正常生物学功能。这些试剂可以用来确定一个特定大分子在生物系统中的影响。小鼠TNF-α Neutralizing (D2H4) Rabbit mAb能够中和体外L-929细胞中的TNF-α的细胞毒活性,ND50的范围在1-6 ng/ml。



The viability of L-929 cells treated with increasing amounts of mTNF-α #5178 in the presence of 1 µg/ml actinomycin D was determined. After a 24 hr treatment, cells were incubated with a tetrazolium salt and the OD450 was determined.使用含有1 µg/ml 放线菌素D的浓度递增的mTNF-α #5178处理L-929细胞,并检查生存活性。处理24小时后,细胞中加入四唑盐,在OD450处检测。



The ability of Mouse TNF-α Neutralizing (D2H4) Rabbit mAb to inhibit mTNF-α-induced L-929 cell cytotoxicity was assessed. Cells were incubated with increasing concentrations of antibody in the presence of mTNF-α #5178 (250 pg/ml) and 1 µg/ml actinomycin D. After 24 hr, viable cells were detected by incubation with a tetrazolium salt and the OD450 was determined.Mouse TNF-α Neutralizing (D2H4) Rabbit mAb具有抑制mTNF-α诱导的L-929细胞毒性的能力已被评估。细胞与浓度递增的抗体(含有mTNF-α #5178 (250 pg/ml) 和1 µg/ml actinomycin D)共同孵育。24小时后,活细胞通过四唑盐的处理,在OD450进行检测。


TNF-α, the prototypical member of the TNF protein superfamily, is a homotrimeric type-II membrane protein (1,2). Membrane-bound TNF-α is cleaved by the metalloprotease TACE/ADAM17 to generate a soluble homotrimer (2). Both membrane and soluble forms of TNF-α are biologically active. TNF-α is produced by a variety of immune cells including T cells, B cells, NK cells, and macrophages (1). Cellular response to TNF-α is mediated through interaction with receptors TNF-R1 and TNF-R2, and results in activation of pathways that favor both cell survival and apoptosis depending on the cell type and biological context. Activation of kinase pathways (including JNK, Erk (p44/42), p38 MAPK, and NF-κB) promotes the survival of cells, while TNF-α-mediated activation of caspase-8 leads to programmed cell death (1,2). TNF-α plays a key regulatory role in inflammation and host defense against bacterial infection, notably Mycobacterium tuberculosis (3). The role of TNF-α in autoimmunity is underscored by research studies that show that blocking TNF-α action may be used to treat rheumatoid arthritis and Crohn’s disease (1,2,4).

TNF-α是TNF家族典型成员, 是II型的同源三聚体膜蛋白(1,2)。细胞膜锚定的TNF-α通过金属蛋白酶 TACE/ADAM17的剪切,形成可溶性的同型三聚体(2)。膜锚定和可溶性两种形式都有生物活性。TNF-α可由很多种类的细胞产生包括T细胞、 B细胞、巨噬细胞和NK细胞(1)。TNF-α的细胞内应答是通过与 TNF-R1 和 TNF-R2 两种受体互作而介导的,从而激活细胞存活和细胞凋亡两个截然相反地过程,这两个过程的发生主要决定于细胞的类型和生物学环境。某些激酶激活的通路(包括JNK、Erk (p44/42)、p38 MAPK 和 NF-κB) 可促进细胞的存活,然而TNF-α介导的对caspase-8的活化导致了程序性的细胞死亡(1,2)。TNF-α在炎症反应和宿主抵抗细菌入侵的过程特别是针对结核分枝杆菌感染发挥了重要的调控作用(3)。一些研究发现,通过抑制TNF-α可能来治疗类风湿性关节炎和Crohn’s 病,提示TNF-α在自免疫中的作用可能被低估(1,2,4)。

Application References

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