Amino Acid Residues Required for Physical and Cooperative Transcriptional Interaction of STAT3 and AP-1 Proteins c-Jun and c-Fos

Ginsberg, Michael D.; Czeko, Elmar; Müller, Patrick; Ren, Zhiyong; Chen, Xiaomin; Darnell, James

doi:10.1128/mcb.00613-07

Cited by 38 publications

(30 citation statements)

References 32 publications

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“…The c-fos antiserum recognizes a single band of the predicted protein size of 60 kDa MW in Western blots (manufacturer's website and datasheet) and has been described extensively in the literature (e.g., Ginsberg et al, 2007). The nuclear staining pattern in brain is consistent with the well-documented activity-dependent upregulation of c-fos (Friemel et al, 2010).…”

Section: Primary Antisera Characterizationmentioning

confidence: 72%

Molecular fingerprint of neuropeptide s‐producing neurons in the mouse brain

Liu

Zeng

Zhou

et al. 2011

J of Comparative Neurology

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Neuropeptide S (NPS) has been associated with a number of complex brain functions, including anxiety-like behaviors, arousal, sleep-wakefulness regulation, drug-seeking behaviors, and learning and memory. In order to better understand how NPS influences these functions in a neuronal network context, it is critical to identify transmitter systems that control NPS release and transmitters that are co-released with NPS. For this purpose, we generated several lines of transgenic mice that express enhanced green-fluorescent protein (EGFP) under control of the endogenous NPS precursor promoter. NPS/EGFP-transgenic mice show anatomically correct and overlapping expression of both NPS and EGFP. A total number of ∼500 NPS/EGFP-positive neurons are present in the mouse brain, located in the pericoerulear region and the Kölliker-Fuse nucleus. NPS and transgene expression is first detectable around E14, indicating a potential role for NPS in brain development. EGFP-positive cells were harvested by laser-capture microdissection, and mRNA was extracted for expression profiling by using microarray analysis. NPS was found co-localized with galanin in the Kölliker-Fuse nucleus of the lateral parabrachial area. A dense network of orexin/hypocretin neuronal projections contacting pericoerulear NPS-producing neurons was observed by immunostaining. Expression of a distinct repertoire of metabotropic and ionotropic receptor genes was identified in both NPS neuronal clusters that will allow for detailed investigations of incoming neurotransmission, controlling neuronal activity of NPS-producing neurons. Stress-induced functional activation of NPS-producing neurons was detected by staining for the immediate-early gene c-fos, thus supporting earlier findings that NPS might be part of the brain stress response network.

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Section: Primary Antisera Characterizationmentioning

confidence: 72%

Molecular fingerprint of neuropeptide s‐producing neurons in the mouse brain

Liu

Zeng

Zhou

et al. 2011

J of Comparative Neurology

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“…JUN also frequently interacts with members of the ETS transcription factor family, which usually requires very close spacing for interaction to occur (Basuyaux et al, 1997;Kim et al, 2006). A small distance between sites has also been reported for JUN-STAT3 interaction (Schaefer et al, 1995;Ginsberg et al, 2007). It appears that such close spacing is not required for the functional interaction of TCF4 with JUN on the JUN promoter (Nateri et al, 2005).…”

Section: Discussionmentioning

confidence: 98%

Cooperation between GLI and JUN enhances transcription of JUN and selected GLI target genes

et al. 2009

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Sustained Hedgehog (HH) signaling is implicated in basal cell carcinoma of the skin and other types of cancer. Here we show that GLI1 and GLI2, the main transcriptional activators of the HH pathway, directly regulate expression of the activator protein 1 (AP-1) family member JUN, a transcription factor controlling keratinocyte proliferation and skin homeostasis. Activation of the JUN promoter by GLI is dependent on a GLI-binding site and the AP-1 sites known to be involved in self-activation of JUN. Transcription of JUN is greatly enhanced in the presence of GLI and requires activated JUN protein.GLI2act is a more potent activator than GLI1 in these experiments and physical interaction with phosphorylated JUN was only detected for GLI2act. The synergistic effect of GLI and JUN extends to the activation of further GLI target genes as shown by shRNA-mediated knockdown of JUN in human keratinocytes. Some of these cooperatively activated genes are involved in cell-cycle progression, which is consistent with a significant reduction of the proliferative potential of GLI in the absence of JUN. These results suggest a novel connection between HH/GLI pathway activity and JUN, which may contribute to the oncogenic activity of HH/GLI signaling in skin.

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“…It is possible that the activated STAT3 and AP-1 may cooperatively promote hBD-3 gene transcription by their direct interaction and/or the additive effects of the interaction between individual transcription factors (AP-1 and STAT3) and general transcriptional apparatuses such as TATA-binding proteins [36]. It is also reported that the coiled-coil domain of STAT3 interacts with B-zip domains of c-Jun and c-Fos [34], and that STAT3 and AP-1 cooperatively induce the expression of the a2-macroglobulin or heme oxygenase-1 genes [36,37].…”

Section: Discussionmentioning

confidence: 99%

“…The tyrosine phosphorylation of STAT3 may potentiate its DNA binding and nuclear translocation, while its serine phosphorylation may promote its transactivation potential [39]. The serine phosphorylation of STAT3 may potentiate its interaction with general transcriptional apparatuses such as TFII-I, transcriptional coactivators such as CBP/p300, or other transcription factors such as c-Jun on the hBD-3 promoter; moreover, it may also alter chromatin structure, leading to enhanced gene expression [34,36,39]. The tyrosine and serine phosphorylation were mediated by JAK2 and ERK, respectively (Fig.…”

Section: Discussionmentioning

confidence: 99%