| Target: |
TNF alpha (Tumor necrosis factor alpha (TNF-α)) |
| Binding Specificity: |
C-term |
| Reactivity: |
Human |
| Host: |
Rabbit |
| Clonality: |
Polyclonal |
| Conjugate: |
This TNF alpha antibody is un-conjugated |
| Application: |
ELISA, immunohistochemistry (IHC), western blotting (WB) |
| Cross-Reactivity: |
Human, Mouse, Rat |
| Purification: |
Affinity purification |
| Immunogen: |
C term -peptide of human SFPQ. |
| Isotype: |
IgG |
| Format: |
Liquid |
| Buffer: |
Store at -20°C or -80°C. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3. |
| Precaution of Use: |
This product contains sodium azide: a poisonous and hazardous substance which should be handled by trained staff only. |
| Handling Advice: |
Avoid repeated freeze. |
| Storage: |
- 20°C, - 80°C |
| Storage Comment: |
Upon receipt, store at - 20°C or - 80°C. |
| Alternative Name: |
TNF alpha |
| Synonyms: |
DIF, TNF-alpha, TNFA, TNFSF2, RATTNF, Tnfa, tnf, TNF-a, TNFalpha, Tnfsf1a, TNFa, cTNF, Tnf-alpha, tnfa-like, TNF-ALPHA, dif, tnfa, xtnf, tnfsf2, tnf-alpha, Cachectin, tumor necrosis factor, tumor necrosis factor b (TNF superfamily, member 2), tumor necrosis factor alpha, tumor necrosis factor a (TNF superfamily, member 2), TNF, Tnf, tnf, tnfb, tnf-alpha, LOC103694380, tnfa. |
| Background: |
TNF-α, the prime member of the TNF protein superfamily, exists as a homotrimeric type-II membrane protein. When bound to the membrane, TNF-α undergoes cleavage by the metalloprotease TACE/ADAM17, resulting in the formation of a soluble homotrimer. Both the membrane-bound and soluble forms of TNF-α exhibit biological activity. Various immune cells, such as T cells, B cells, NK cells, and macrophages, contribute to the production of TNF-α. Cellular responses to TNF-α occur through interactions with receptors TNF-R1 and TNF-R2, triggering pathways that promote either cell survival or apoptosis depending on the cell type and context. Activation of kinase pathways like JNK, Erk (p44/42), p38 MAPK, and NF-κB supports cell survival, whereas TNF-α-induced activation of caspase-8 induces programmed cell death. TNF-α serves as a crucial regulator in inflammation and the host's defense against bacterial infections, particularly Mycobacterium tuberculosis. |
