NDLI: Identification and functional characterization of a novel binding site on TNF-promoter

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Identification and functional characterization of a novel binding site on TNF-promoter

Content Provider	Semantic Scholar
Author	Tang, Xiaoren Amar, Salomon
Copyright Year	2003
Abstract	Transcription of the tumor necrosis factor (TNF) gene is rapidly and transiently induced by lipopolysaccharide in cells of monocyte macrophage lineage. Previous studies have suggested that in the mouse, multiple NFB Rel-binding sites contribute to the TNF transcriptional response to LPS. But the role of these regulatory elements in transcriptional activation of the TNFgene in human monocytes remains unclear. Previously, a transcription factor, termed lipopolysaccharideinduced TNFfactor (LITAF), was found to regulate TNFgene expression. However, the specific protein domain(s) of human (h)LITAF that interact with the hTNFpromoter had not been identified. In this study, we identify by footprinting a sequence motif, CTCCC ( 515 to 511), within the TNFpromoter that binds to hLITAF. We also identify the region of hLITAF (amino acids 165–180) that was named peptide B and specifically mediates binding to the hTNFpromoter. When THP-1 cells were stimulated with this peptide B, it was sufficient to induce TNFsecretion. Induction of TNFtranscription by LPS or peptide B depended on the presence of the 515 to 511 promoter region, which was found to be essential for hLITAF binding. Together, these findings help to clarify the mechanism of hLITAF hTNFinteraction and the manner by which hLITAF contributes to hTNFregulation in an attempt to design new pharmacological interventions to address TNF-related diseases.
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://www.pnas.org/content/100/7/4096.full.pdf
Language	English
Access Restriction	Open
Subject Keyword	Amino Acid Metabolism, Inborn Errors Amino Acids Binding Sites DNA binding site F Factor Footprinting LITAF gene Lightweight Portable Security Lineage (evolution) Lipopolysaccharides Medical transcription Monocytes Name Neoplasms Neurofeedback Pharmacology Promoter Regions, Genetic Protein Domain REL gene Sequence motif TRANSCRIPTION FACTOR Transcription (software) Transcription, Genetic Transcriptional Activation Tumor Necrosis Factor-alpha
Content Type	Text
Resource Type	Article

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