Cell Signaling Technology

Product Pathways - NF-kB Signaling

TNF-α (D5G9) Rabbit mAb #6945

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H Endogenous 18, 25 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

TNF-α (D5G9) Rabbit mAb recognizes endogenous levels of total full length and secreted TNF-α protein. It can detect up to 10 pg of recombinant TNF-α by western blot.

Source / Purification

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

Western Blotting

Western Blotting

Western blot analysis of recombinant human TNF-α #8902 using TNF-α (D5G9) Rabbit mAb (left) or TNF-α Antibody #3707 (right).

Western Blotting

Western Blotting

Western blot analysis of extracts from the media of THP-1 cells differentiated with TPA #4174 (80 nM; overnight), with or without LPS (1 μg/ml; overnight), using TNF-α (D5G9) Rabbit mAb.

Western Blotting

Western Blotting

Western blot analysis of extracts from THP-1 cells differentiated with TPA #4174 (80 nM; overnight), with or without LPS (1 μg/ml; various time points), using TNF-α (D5G9) Rabbit mAb.


Background

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, Erk1/2, 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).

  1. Aggarwal, B.B. (2003) Nat Rev Immunol 3, 745-56.
  2. Hehlgans, T. and Pfeffer, K. (2005) Immunology 115, 1-20.
  3. Lin, P.L. et al. (2007) J Investig Dermatol Symp Proc 12, 22-5.

Application References

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Companion Products


For Research Use Only. Not For Use In Diagnostic Procedures.

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