TNF-α (D1G2) Rabbit mAb (IF/Flow Preferred)Product information
|100 µl (400 assays)||-||Unavailable in your region|
Product Pathways - Growth Factors/Cytokines
TNF-α (D1G2) Rabbit mAb (IF/Flow Preferred) #8184
|8184S||100 µl (400 assays)||---||In Stock||---|
|8184||carrier free and custom formulation / quantity||email request|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation, IF-IC=Immunofluorescence (Immunocytochemistry), F=Flow Cytometry
Specificity / Sensitivity
TNF-α (D1G2) Rabbit mAb (IF/Flow Preferred) recognizes endogenous levels of total TNF-α protein. TNF-α (D5G9) Rabbit mAb #6945 is more sensitive by western blot.
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant human TNF-α protein.
Western blot analysis of extracts from THP-1 cells, differentiated with TPA #4174 (80 nM, overnight) and then untreated (-) or treated with LPS (1 μg/ml, 1 hr; +), using TNF-α (D1G2) Rabbit mAb (IF/Flow Preferred) (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower).
Confocal immunofluorescent analysis of THP-1 cells, treated with TPA #4174 (80 nM, 16 hr) (left) or treated with TPA followed by LPS (1 μg/ml, 1 hr) (right), using TNF-α (D1G2) Rabbit mAb (IF/Flow Preferred) (green). Actin filaments were labeled with DY-554 phalloidin (red). Blue pseudocolor = DRAQ5® #4084 (fluorescent DNA dye).
Flow cytometric analysis of human peripheral blood lymphocytes, untreated (left) or treated with TPA #4174 (40 nM, 4 hr), Ionomycin #9995 (2 μM, 4 hr), and Brefeldin A #9972 (1 μg/ml, last 3 hr of treatment) (right), using a CD3 antibody and TNF-α (D1G2) Rabbit mAb (IF/Flow Preferred).
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).
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