Tumor Necrosis Factors (TNF) are proteins present mostly at immune cells surface. They are homotrimeric transmembrane proteins of type II. They can be further secreted as homotrimeric soluble cytokines upon cleavage by metalloproteases. For example TNF alpha is cleaved by TNF alpha converting enzyme (TACE, or ADAM17). TNF Family members can be found in about all metazoans.
At the origin, Tumor Necrosis Factors were named after their ability to trigger cell death. They now have been found to regulate many cells functions such as embryogenesis, proliferation, differentiation, inflammation, immune response and apoptosis. They also can send survival signal and some of them are especially responsible for T and B lymphocytes subsistence. Concerning inflammation, TNF have been identified as having a role in initiation, progression and termination. In most of their functions TNF have antagonist effect; they both promote and block inflammation or cell death for example.
The signaling cascade induced by these proteins goes through the binding on Tumor Necrosis Factor Receptors (TNFR). All cell types produce TNFR proteins and many of them produce also TNF. TNF to TNFR association mechanisms vary greatly in the family. TNF cascade are often induced by the up-regulation of the ligand. Receptors may also be regulated, although less frequently, to enable the corresponding pathways. The first studied TNF family members were TNF alpha and beta. TNFR1 and TNFR2 are the receptors that are activated upon TNF alpha or TNF beta binding.
Antibodies targeting TNF or TNFR might be studied for various purposes including drug development. Indeed mutations on the TNFRs have been associated with autoimmune diseases and blocking their pathways is expected to be leading to treatments of cancers, autoimmunity and infectious diseases.
ProteoGenix involves itself in your research in the field of tumor necrosis factor signaling by providing both proteins and antibodies that target this superfamily.
