LITAF Human

Lipopolysaccharide-Induced TNF Factor (LITAF) is a DNA-binding protein that plays a crucial role in the regulation of tumor necrosis factor-alpha (TNF-α) expression. TNF-α is a key proinflammatory cytokine involved in various immune responses and inflammatory processes. The recombinant form of LITAF, derived from human sources, is used extensively in research to study its functions and implications in various biological pathways.

LITAF is encoded by the LITAF gene, which is induced by the tumor suppressor protein p53. This induction is part of the p53-mediated apoptotic pathway, highlighting LITAF’s role in cell death and survival mechanisms . The protein mediates TNF-α expression by directly binding to the promoter region of the TNF-α gene, thereby influencing its transcription.

The transcription of the TNF-α gene is rapidly and transiently induced by lipopolysaccharide (LPS), a component of the outer membrane of Gram-negative bacteria . LPS triggers a cascade of inflammatory responses, with TNF-α being one of the primary cytokines produced. LITAF’s role in this process involves binding to specific sites on the TNF-α promoter, facilitating the recruitment of transcription factors such as NF-κB/Rel . This interaction is crucial for the full transcriptional response to LPS.

LITAF and TNF-α are central to the body’s response to bacterial infections, particularly those caused by Gram-negative bacteria. The rapid production of TNF-α in response to LPS is a critical component of the immune response, helping to control and eliminate bacterial pathogens . However, excessive or uncontrolled TNF-α production can lead to severe inflammatory conditions, such as septic shock.

Recombinant LITAF is used in various research applications to study its role in inflammation, immune response, and cell death. By understanding how LITAF regulates TNF-α expression, researchers can develop targeted therapies for inflammatory diseases and conditions associated with dysregulated TNF-α production .