Non-fucosylated Anti-Human TNFα (Afelimomab) Therapeutic Antibody (CAT#: BioBet-464ZP) Datasheet

TNF

TNF Gene(Protein Coding)


Tumor Necrosis Factor

This gene encodes a multifunctional proinflammatory cytokine that belongs to the tumor necrosis factor (TNF) superfamily. This cytokine is mainly secreted by macrophages. It can bind to, and thus functions through its receptors TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. This cytokine is involved in the regulation of a wide spectrum of biological processes including cell proliferation, differentiation, apoptosis, lipid metabolism, and coagulation. This cytokine has been implicated in a variety of diseases, including autoimmune diseases, insulin resistance, and cancer. Knockout studies in mice also suggested the neuroprotective function of this cytokine. [provided by RefSeq, Jul 2008]

Afelimomab;156227-98-4;MAK 195F;LU54107;MAK 195F;TNF;tumor necrosis factor;TNFA, tumor necrosis factor (TNF superfamily, member 2);DIF;TNF superfamily;member 2;TNF alpha;TNFSF2;TNF-a;cachectin;APC1 protein;TNF, monocyte-derived;TNF, macrophage-derived;TNF

Plasma membrane, Extracellular region or secreted

Diseases associated with TNF include Asthma and Malaria.

Its related pathways are Apoptosis Modulation and Signaling and Monoamine Transport.

Cytokines that bind to TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. It is mainly secreted by macrophages and can cause cell death in certain tumor cell lines. It is a strong pyrogen that directly acts or stimulates the secretion of interleukin-1 to cause fever. It is related to the induction of cachexia and can stimulate cell proliferation and induce cell differentiation under certain conditions. Dephosphorylation of FOXP3 impairs the function of regulatory T cells (Treg) in individuals with rheumatoid arthritis. Up-regulating the expression of protein phosphatase 1 (PP1), PP1 dephosphorylates the key Ser-418 residue of FOXP3, thereby inactivating FOXP3 and deficient in Treg cell function. In the RT4v6 bladder cancer cell line, bcg-stimulated neutrophils combined with DIABLO/SMAC mimics are key mediators of cell death in the anti-cancer effect. By inhibiting insulin-induced IRS1 tyrosine phosphorylation and insulin-induced glucose uptake, it induces insulin resistance in adipocytes. Induces the degradation of GKAP42 protein in adipocytes, which is partly involved in tnf-induced insulin resistance (similar). The formation of TNF intracellular domain (ICD) can induce dendritic cells to produce IL12.

Cancer antibody; Cell Biology and Cellular Response antibody; Immune System antibody; Metabolism antibody; Signaling Transduction antibody

The soluble form derives from the membrane form by proteolytic processing. The membrane-bound form is further proteolytically processed by SPPL2A or SPPL2B through regulated intramembrane proteolysis producing TNF intracellular domains (ICD1 and ICD2) released in the cytosol and TNF C-domain 1 and C-domain 2 secreted into the extracellular space. The membrane form, but not the soluble form, is phosphorylated on serine residues. Dephosphorylation of the membrane form occurs by binding to soluble TNFRSF1A/TNFR1. O-glycosylated; glycans contain galactose, N-acetylgalactosamine and N-acetylneuraminic acid.

Protein Based Therapies
Monoclonal antibody (mAb)

F(ab')2 - G3 - kappa

Afelimomab

Mouse

Human

ADCC-enhanced Afelimomab is a non-fucosylated anti-TNFα therapeutic biobetter antibody.

Sepsis toxic shock

Sepsis toxic shock