Cell
Volume 55, Issue 3, 4 November 1988, Pages 395-397
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Fos and jun: The AP-1 connection

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    The three main MAPK families are p38, the extracellular signal-regulated protein kinase (ERK), and the c-Jun amino-terminal kinase (JNK), which differentially control various physiological processes including inflammation [6]. The MAPK signaling pathways stimulate the activator protein-1 (AP-1)-DNA binding activity by inducing the formation of the c-Jun and c-Fos heterodimer, which results in binding to promoters related to inflammation [7]. Similar to NF-κB and MAPK/AP-1, the Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway mediate inflammatory processes in macrophages exposed to LPS.

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    Consistent with our previous IF analyses, c-fos was found among the most significant differentially expressed genes (p = 7.91 ∗ 10−22) (Figures 2A and 2B). In addition to c-fos, other members of the AP-1 transcription factor complex—Fosb, Fosl2, and Junb (Curran and Franza, 1988; Su et al., 2017)—and of the nuclear receptor subfamily 4 group A—Nr4a1 and Nr4a3 (Volakakis et al., 2010)—together with early growth response transcription factors Egr1, Egr2, Egr3, and Egr4 (Duclot and Kabbaj, 2017; Gao et al., 2017), were induced in the WT, but not in the ChI-D2RKO DMS (Figures 2A and 2B). Gene Ontology analyses performed using the Database for Annotation, Visualization, and Integrated Discovery (DAVID) indicated that differentially expressed genes with significant fold changes found in cocaine-treated mice (Figure 2B, red), were heavily involved in the regulation of transcription.

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