AP-1 transcription factor

Reduction and Fixation of Sacroiliac joint Dislocation by the Combined Use of S1 Pedicle Screws and an Iliac Rod

Published in Kai-Uwe Lewandrowski, Donald L. Wise, Debra J. Trantolo, Michael J. Yaszemski, Augustus A. White, Advances in Spinal Fusion, 2003

Kai-Uwe Lewandrowski, Donald L. Wise, Debra J. Trantolo, Michael J. Yaszemski, Augustus A. White

Nuclear crosstalk of the ERK/Smad pathway is also possible given the number of common nuclear targets. One such target is fos of the AP-1 transcription factor. Fos is phosphorylated by ERK on sites that have been identified as transcriptional inhibitors [32,33], but it is also a functional target of the Smad 3 MH2 domain, which ultimately potentiates transcription of genes

Inhibitory effect of particulate matter on toll-like receptor 9 stimulated dendritic cells by downregulating mitogen-activated protein kinase and NF-κB pathway

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Journal Information

Published in Journal of Toxicology and Environmental Health, Part A, 2020

Madeeha Arooj, Irshad Ali, Hee Kyoung Kang, Jin Won Hyun, Young-Sang Koh

MAPKs activation upregulates AP-1 transcription factor, which leads to induction of AP-1 dependent genes including cytokines (Akira and Takeda 2004; Blasius and Beutler 2010; Huang and Yang 2010). To investigate, the influence of PM2.5 on AP-1 transcriptional activity, luciferase assay was performed on HEK293 T cells transfected with empty pcDNA3 or pcDNA3-mTLR9. HEK293 T cells transfected with empty pcDNA3 showed no induction of AP-1 dependent luciferase activity upon CpG-DNA stimulation. However, pcDNA3-mTLR9 exhibited a rise in AP-1 dependent luciferase activity. In contrast, PM2.5 treatment induced marked concentration-dependent inhibition on AP-1 dependent luciferase activity in HEK293 T cells transfected with pcDNA3-mTLR9 (Figure 5a).

AP-1 transcription factor

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Reduction and Fixation of Sacroiliac joint Dislocation by the Combined Use of S1 Pedicle Screws and an Iliac Rod

Inhibitory effect of particulate matter on toll-like receptor 9 stimulated dendritic cells by downregulating mitogen-activated protein kinase and NF-κB pathway