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Kwon, J.-W., Kwon, H.-K., Shin, H.-J., & Choi, Y.-M. (2015). Activating transcription factor 3 represses inflammatory responses by binding to the p65 subunit of NF-κB. Scientific Reports, 5(1), 14470. Added by: Dr. Enrique Feoli (26/03/2024, 14:53) Last edited by: Dr. Enrique Feoli (26/03/2024, 14:59) |
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| Resource type: Journal Article DOI: 10.1038/srep14470 ID no. (ISBN etc.): 2045-2322 BibTeX citation key: Kwon2015 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: Cell plasticity Keywords: , , Creators: Choi, Kwon, Kwon, Shin Collection: Scientific Reports |
Views: 1/92
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| Abstract |
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Activating transcription factor 3 (ATF3) is induced by inflammatory responses, cell death, cytokines and oxidative stress conditions. ATF3 is a negative regulator in the Toll-like receptor 4 signalling pathway. The principal molecule in this pathway is nuclear factor κB (NF-κB) that translocates into the nucleus to initiate the transcription of inflammatory mediators. However, scarce data are available regarding the interaction of ATF3 and p65, a part of the NF-κB dimer. Therefore, we studied the mechanism of regulation of p65 by ATF3 in RAW 264.7 cells. First, LPS-mediated NF-κB activation was confirmed and then the direct interaction of ATF3 and p65 was observed through immunoprecipitation (IP). The presence of histone deacetylase 1 (HDAC1) was also detected in the complex. In ATF3 deficient cells, NF-κB activity was up-regulated and HDAC1 was not detected by IP. These observations suggest that p65 is attenuated by ATF3 such that ATF3 recruits HDAC1 to the ATF3/p65 complex and facilitates the deacetylation of p65. Likewise, inflammatory response genes were induced by translocated NF-κB in ATF3-deficient cells. Cumulatively, we uncovered a novel mechanism for the negative regulation of NF-κB by ATF3 via direct interaction with p65.
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Publisher: Nature Publishing Group
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