Role of the Cyclic AMP Response Element Binding Complex and Activation of Mitogen-Activated Protein Kinases in Synergistic Activation of the Glycoprotein Hormone α Subunit Gene by Epidermal Growth Factor and Forskolin

Roberson, Mark S.; Ban, Makiko; Zhang, Tong; Mulvaney, Jennifer M.

doi:10.1128/.20.10.3331-3344.2000

Cited by 5 publications

(6 citation statements)

References 33 publications

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“…Furthermore, cAMP may interfere with the perhaps most important signaling cascade of the EGF receptor, the activation of ERK1 and ERK2 (12,28,60). However, in some cell systems cAMP-elevating agents do not interfere with EGF-induced activation of ERK1 and ERK2 (4,32) or they can even enhance EGF-dependent activation of these mitogen-activated protein kinases (48,61). As discussed above, recent studies that show that isoforms with different domain composition may even have an opposite response to certain stimulus illustrate how the cross talk between signaling systems can be cell type specific.…”

Section: Discussionmentioning

confidence: 99%

Effects of epidermal growth factor on epinephrine-stimulated heart function in rodents

Lorita

Escalona

Faraudo

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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Epidermal growth factor (EGF) interferes with beta-adrenergic receptor (beta-AR) signaling in adipocytes and hepatocytes, which leads to decreased lipolytic and glycogenolytic responses, respectively. We studied the effect of EGF on the heart. EGF interfered with the cAMP signal generated by beta-AR agonists in cardiac myocytes. In perfused hearts, EGF decreased inotropic and chronotropic responses to epinephrine but not to 8-(4-chlorophenylthio)adenosine 3',5'-cyclic monophosphate. Sustained epinephrine infusion induced heart contracture, which resulted in altered heart function as demonstrated by decreased inotropy and increased heart rate variability. EGF prevented all these alterations. In the whole animal (anesthetized mice), EGF administration reduced the rise in heart rate induced by a single epinephrine dose and the occurrence of Bezold-Jarisch reflex episodes induced by repeated doses. Sialoadenectomy enhanced the response to epinephrine, and EGF administration restored normal response. All these results suggest that, by interfering with beta-AR signaling, EGF protects the heart against the harmful effects of epinephrine.

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Section: Discussionmentioning

confidence: 99%

Effects of epidermal growth factor on epinephrine-stimulated heart function in rodents

Lorita

Escalona

Faraudo

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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“…4d, lane 3), suggesting that c‐Jun may be a member of the specific complex that binds to this site, in keeping with a similar result with the DYNCRE3 element (equivalent AP1/CRE site in prodynorphin gene promoter), which was also supershifted with a p‐c‐Jun antibody (Messersmith et al . 1996), and previous reports that c‐Jun can bind to both canonical AP1 and CRE consensus elements (Hai and Curran 1991; Roberson et al . 2000).…”

Section: Resultsmentioning

confidence: 82%

Regulation of the preprotachykinin‐I gene promoter through a protein kinase A‐dependent, cyclic AMP response element‐binding protein‐independent mechanism

Calin‐Jageman¹,

Wang²,

Bannon³

2006

Journal of Neurochemistry

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Preprotachykinin-I (PPT) gene expression is regulated by a number of stimuli that signal through cyclic AMP (cAMP)-mediated pathways. In the present study, forskolin, an adenylyl cyclase stimulator, significantly increased PPT mRNA levels in PPT-expressing RINm5F cells, an effect paralleled by an increase in PPT promoter-luciferase reporter construct activity. The forskolin-induced stimulation of PPT transcription was protein kinase A dependent (PKA), as shown by blockade with the PKA inhibitor N-[2-(p-bromocinnamylamino) ethyl]-5-isoquinolinesulfonamide. We found that the activation protein 1/cAMP response element (AP1/CRE) site centered at ) 196 relative to the transcription start site was important for basal and forskolin-induced PPT promoter activity. Because of the involvement of PKA and the similarity of the AP1/CRE element to consensus CRE sequences, we investigated the role of CREbinding protein (CREB) in the regulation of the PPT promoter. Surprisingly, overexpression of a dominant-negative CREB (i.e. CREB-A) did not affect basal or forskolin-induced PPT promoter activity. Furthermore, binding of CREB to the PPT promoter AP1/CRE site was not demonstrable in electrophoretic mobility shift assays. Rather, our experiments suggested that c-Jun is a member of the complex that binds to this site. We conclude that, at least in RINm5F cells, cAMP-mediated up-regulation of PPT gene expression does not involve CREB or CREB-related transcription factor recruitment to the AP1/CRE site.

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“…In both cases, the CRE is located in proximity to a functional TATA box, which is a critical feature needed to confer a full response to cAMP agonists (22). In addition, both genes are similarly regulated by EGF, which acts synergistically with cAMP agonists through activation of a composite transcription factor module, consisting of CRE-binding protein, cJun, and cfos, which are activated and recruited to the CRE in a single complex (9,12).…”

Section: Discussionmentioning

confidence: 99%

“…In addition to the CRE-TATA unit, there are other important determinants of placental expression in the ␣CG promoter, such as CCAAT boxes, GATA elements, and upstream regulatory elements (12).…”

mentioning

confidence: 99%

CCAAT/Enhancer-Binding Proteins Are Key Regulators of Human Type Two Deiodinase Expression in a Placenta Cell Line

et al. 2012

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An appropriate concentration of intracellular T(3) is a critical determinant of placenta development and function and is mainly controlled by the activity of type II deiodinase (D2). The levels of this enzyme are finely regulated in different tissues by coordinated transcriptional mechanisms, which rely on dedicated promoter sequences (e.g. cAMP response element and TATA elements) that impart inducibility and tissue specificity to Dio2 mRNA expression. Here we show that CCAAT enhancer-binding proteins α and β (C/EBPα and C/EBPβ) promote Dio2 expression in the trophoblastic cell line JEG3 through a conserved CCAAT element, which is a novel key component of the Dio2 promoter code that confers tissue-specific expression of D2 in these cells. Increased C/EBPs levels potently induce Dio2 transcription, whereas their ablation results in loss of Dio2 mRNA. By measuring the activity of several deletion and point mutant promoter constructs, we have identified the functional CCAAT element responsible for this effect, which is located in close proximity to the most 5' TATA box. Notably, this newly identified sequence is highly conserved throughout the species and binds in vivo and in vitro C/EBP, indicating the relevance of this regulatory mechanism. Together, our results unveil a novel mechanism of regulation of D2 expression in a trophoblastic cell line, which may play a relevant role during placenta development.

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Role of the Cyclic AMP Response Element Binding Complex and Activation of Mitogen-Activated Protein Kinases in Synergistic Activation of the Glycoprotein Hormone α Subunit Gene by Epidermal Growth Factor and Forskolin

Cited by 5 publications

References 33 publications

Effects of epidermal growth factor on epinephrine-stimulated heart function in rodents

Effects of epidermal growth factor on epinephrine-stimulated heart function in rodents

Regulation of the preprotachykinin‐I gene promoter through a protein kinase A‐dependent, cyclic AMP response element‐binding protein‐independent mechanism

CCAAT/Enhancer-Binding Proteins Are Key Regulators of Human Type Two Deiodinase Expression in a Placenta Cell Line

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