| ID | Sequence | Length | GC content |
|---|---|---|---|
| AGACCUCCCGGCUCGACAGGCGGCGCGGGCGGCGGUAAAAUGUCGGUUC… | 2440 nt | 0.4643 | |
| CCUUUUCUCGGGGCGCCCGAGAGGCCAGCUCAGACCUCCCGGCUCGACA… | 2577 nt | 0.4715 | |
| CCUCUUACUGCUGAUGGCACCCAGCUCUGGGCCCAGACGCCGCUCACCG… | 2472 nt | 0.4656 |
Lipopolysaccharide is a potent stimulator of monocytes and macrophages, causing secretion of tumor necrosis factor-alpha (TNF-alpha) and other inflammatory mediators. This gene encodes lipopolysaccharide-induced TNF-alpha factor, which is a DNA-binding protein and can mediate the TNF-alpha expression by direct binding to the promoter region of the TNF-alpha gene. The transcription of this gene is induced by tumor suppressor p53 and has been implicated in the p53-induced apoptotic pathway. Mutations in this gene cause Charcot-Marie-Tooth disease type 1C (CMT1C) and may be involved in the carcinogenesis of extramammary Paget's disease (EMPD). Multiple alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Dec 2014]
A study in mice demonstrated that the LITAF was upregulated in common in white blood cells at day 1 post-injury following both burn and trauma-hemorrhage, where it was identified as a gene expression marker associated with cell-to-cell signaling pathways [Lederer et al. DOI:10.1152/physiolgenomics.00086.2007]. A study in mice demonstrated that the LITAF (LITAF) gene was upregulated in common in spleen leukocytes across all three injury models of trauma/hemorrhage, burn, and lipopolysaccharide (LPS) infusion at a 2-hour post-injury time point, as part of a common early transcriptional response to systemic inflammation [Brownstein et al. DOI:10.1152/physiolgenomics.00213.2005].