LITAF activators, short for Lipopolysaccharide-Induced Tumor Necrosis Factor Alpha Factor activators, constitute a fascinating group of compounds within the realm of biochemistry and molecular biology. LITAF, also known as Simplexin or PIG7, is a critical transcription factor responsible for regulating the expression of various genes involved in immune response and inflammation. LITAF itself plays a pivotal role in the innate immune system's defense against bacterial infections, particularly in response to lipopolysaccharides (LPS), which are found on the cell membranes of gram-negative bacteria. LITAF activators, therefore, are chemical agents or molecules that modulate the activity of this transcription factor.
The primary function of LITAF activators is to enhance the transcriptional activity of LITAF, leading to the upregulation of target genes associated with immune responses. These activators can exert their effects through various mechanisms, including post-translational modifications of LITAF, such as phosphorylation or acetylation, or by directly interacting with LITAF to increase its binding affinity to specific gene promoters. As a result, LITAF activators can amplify the production of key immune mediators like tumor necrosis factor alpha (TNF-α), which plays a central role in inflammation and host defense.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Arachidonic Acid (20:4, n-6) | 506-32-1 | sc-200770 sc-200770A sc-200770B | 100 mg 1 g 25 g | $92.00 $240.00 $4328.00 | 9 | |
Arachidonic acid is a polyunsaturated fatty acid that can activate LITAF by serving as a signaling molecule. It is released from cell membranes in response to various stimuli and can trigger intracellular pathways that lead to LITAF activation and the production of pro-inflammatory cytokines. | ||||||
Lipopolysaccharide, E. coli O55:B5 | 93572-42-0 | sc-221855 sc-221855A sc-221855B sc-221855C | 10 mg 25 mg 100 mg 500 mg | $98.00 $171.00 $425.00 $1560.00 | 12 | |
LPS, found in the outer membrane of Gram-negative bacteria, can activate LITAF by binding to Toll-like receptor 4 (TLR4) on immune cells. This binding initiates a signaling cascade that ultimately leads to LITAF activation and the release of pro-inflammatory molecules. | ||||||