TNFα (Tumor Necrosis Factor α) is a pleiotropic cytokine that conveys either beneficial (prevention of cancers and infection, activation of inflammatory responses) or detrimental (mediation of septic shock, inflammation, and apoptosis) effects to the host. It is produced and secreted primarily by monocytes and macrophages in response to stimulation with lipopolysaccharide (LPS), a principle endotoxic component. LPS-induced TNFα factor (LITAF) is a nuclear factor that was purified as a result of its ability to bind to a DNA fragment from the TNFα promoter region. LITAF expression is dependent on LPS induction and PMA differentiation in THP-1 cells and is observed at high levels in spleen, lymph node, and peripheral blood leukocytes. Antisense inhibition of LITAF causes a reduction in TNFα expression in THP-1 cells. In addition, p53 induces the expression of a transcript called PIG7, which has 98% homology with LITAF. Thus, LITAF is thought to link p53 pathways with the induction of TNFα gene expression in response to LPS stimulation and to function, possibly as a transcription factor, to regulate the expression of this highly potent cytokine. This antibody was generated to the LITAF aa 1-212 sequence (Genbank accession # U77396). Recent reports indicate that the nucleotide coding sequence for LITAF may differ and instead, encode for a protein designated as SIMPLE. Under the sequence for SIMPLE, the LITAF aa 1-212 sequence used to generate this antibody corresponds to the aa 1-126 region of SIMPLE.
This antibody is routinely tested by western blot analysis. Other applications were tested at BD Biosciences Pharmingen during antibody development only or reported in the literature.