Multiple sequence elements in the c-fos promoter mediate induction by cAMP.

Fisch, T M; Prywes, Ron; Simon, Michel; Roeder, R G

doi:10.1101/gad.3.2.198

Cited by 221 publications

(146 citation statements)

References 43 publications

(44 reference statements)

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“…The FAP1 site in the c-fos enhancer was previously found to mediate cAMP induction of reporter constructs redundantly with other elements in the cfos promoter such as the CRE site at 760 (Berkowitz et al, 1989;Fisch et al, 1989). However, the role of the FAP1 site in serum or growth factor induction has been less clear.…”

Section: Discussionmentioning

confidence: 99%

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Activation of the c-fos enhancer by the Erk MAP kinase pathway through two sequence elements: the c-fos AP-1 and p62TCF sites

2000

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The c-fos enhancer can be activated by many signaling pathways through distinct elements of the enhancer. The enhancer contains at its core the serum response element (SRE) that binds serum response factor (SRF). On the 5' side of the SRE is a site for p62 TCF which binds only when SRF is bound as well. p62 TCF is encoded by three ets-related genes, Elk-1, SAP1 and SAP2. Each of these factors contain a transcriptional activation domain that is activated by phosphorylation by MAP kinases. On the 3' side of the SRE is the`c-fos AP1 site' (FAP1) whose role has been less clear. We ®nd here that the FAP1 site contributes strongly to phorbol ester (TPA) and Erk MAP kinase activation of the c-fos enhancer and that both the p62 TCF and FAP1 sites are required for e ective activation of the enhancer. We further ®nd that the FAP1 site binds ATF1 and CREB from HeLa nuclear extracts and that the phosphorylation of these factors is induced by TPA. ATF1 and CREB can be phosphorylated by Rsk2 which is a protein kinase directly activated by Erk MAP kinases. These results suggest a signaling pathway in which Erk MAP kinase activates the c-fos enhancer by direct phosphorylation of p62 TCF and by activation of Rsk related kinases that phosphorylate ATF1 and CREB.

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Section: Discussionmentioning

confidence: 99%

“…The CRE can mediate cAMP and calcium induction in certain cell types but may also contribute to growth factor induction (Berkowitz et al, 1989;Fisch et al, 1989;Sassone-Corsi et al, 1988;Sheng et al, 1990). The CRE is bound by CREB and the related transcription factor ATF1 (Ginty et al, 1994;Montminy, 1997;Sassone-Corsi et al, 1988).…”

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confidence: 99%

Activation of the c-fos enhancer by the Erk MAP kinase pathway through two sequence elements: the c-fos AP-1 and p62TCF sites

2000

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“…We chose the c-fos promoter because it is highly responsive to cAMP Berkowitz et al, 1989;Fisch et al, 1989; Metz and Zi, 1991) and because c-fos is ubiquitously expressed and unlikely to be dominantly repressed in MMSP cells. The c-fos promoter is also of signi®cance to MMSP because it is a possible target for EWS/ ATF1 (Brown et al, 1995) and is activated by a variety of mitogenic agents (Janknecht and Nordheim, 1996;Bannister et al, 1995;Nakajima et al, 1996;Ginty et al, 1994;Sheng et al, 1990;Dash et al, 1991;Bhattacharya et al, 1996).…”

Section: Activity Of the C-fos Promoter In Mmsp Cellsmentioning

confidence: 99%

MMSP tumor cells expressing the EWS/ATF1 oncogene do not support cAMP-inducible transcription

Lee

1998

Oncogene

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Malignant Melanoma of Soft Parts (MMSP) is associated with the EWS/ATF1 fusion protein that arises due to chromosomal fusion of the Ewings Sarcoma oncogene (EWS) and the cellular transcription factor ATF1. EWS/ATF1 can activate several cAMP-inducible promoters, suggesting that cellular transformation in MMSP might involve constitutive activation of cAMPinducible promoters. To assess this possibility we have examined the status of the cAMP-signaling pathway in the available MMSP-derived cell lines (DTC1 and Succs-1) and ®nd that both cell lines share several features. First, in contrast to previous eects observed in transient assays, three chromosomal promoters containing ATF binding sites are not constitutively activated by endogenous EWS/ATF1 in MMSP cells. Second, all the components that are known to be required for cAMP-inducible transcription are present. Third, phosphorylation of the cAMP-response-element-binding protein (CREB) can be eciently induced by cAMP. Fourth, cAMP is unable to activate transcription, as assessed by a GAL4/ATF1 reporter assay and analysis of the c-fos and adenovirus early promoters. Thus, cell lines derived from MMSP have a block to cAMPsignaling that lies downstream of CREB phosphorylation. In light of the cAMP-responsiveness of almost all mammalian cell types, our ®ndings suggest that the inability to respond to cAMP might be an important feature of MMSP cells.

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“…Among those CRElike sequences, some have effects on basal or on cAMP-stimulated transcription or on both. These CRE-like motifs play either positive or negative roles in basal transcription (26,27) and display redundant roles in the response to cAMP (24,28). In the present study we have shown that dCRE, a motif conserved between rats, mice and humans, is a negative cis regulator of ACE gene basal expression.…”

Section: Discussionmentioning

confidence: 59%

“…CRE-like motifs in these promoters are usually multimers or single elements closely associated with other motifs and located in separated domains (24,25). Among those CRElike sequences, some have effects on basal or on cAMP-stimulated transcription or on both.…”

Section: Discussionmentioning

confidence: 99%

Control of the rat angiotensin I converting enzyme gene by CRE-like sequences

Xavier‐Neto

Pereira

Oliveira

et al. 2004

Braz J Med Biol Res

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We characterized the role of potential cAMP-responsive elements (CRE) in basal and in induced angiotensin converting enzyme (ACE) gene promoter activity in order to shed light on the regulation of somatic ACE expression. We identified stimulators and repressors of basal expression between 122 and 288 bp and between 415 and 1303 bp upstream from the transcription start site, respectively, using a rabbit endothelial cell (REC) line. These regions also contained elements associated with the response to 8BrcAMP. When screening for CRE motifs we found pCRE, a proximal sequence between 209 and 222 bp. dCRE, a distal tandem of two CRE-like sequences conserved between rats, mice and humans, was detected between 834 and 846 bp. Gel retardation analysis of nuclear extracts of REC indicated that pCRE and dCRE bind to the same protein complexes as bound by a canonical CRE. Mutation of pCRE and dCRE in REC established the former as a positive element and the latter as a negative element. In 293 cells, a renal cell line, pCRE and dCRE are negative regulators. Co-transfection of ATF-2 or ATF-2 plus c-Jun repressed ACE promoter activity, suggesting that the ACE gene is controlled by cellular stress. Although mapping of cAMP responsiveness was consistent with roles for pCRE and dCRE, mutation analysis indicated that they were not required for cAMP responsiveness. We conclude that the basal activity of the somatic ACE promoter is controlled by proximal and distal CREs that can act as enhancers or repressors depending on the cell context. Correspondence

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Multiple sequence elements in the c-fos promoter mediate induction by cAMP.

Cited by 221 publications

References 43 publications

Activation of the c-fos enhancer by the Erk MAP kinase pathway through two sequence elements: the c-fos AP-1 and p62TCF sites

Activation of the c-fos enhancer by the Erk MAP kinase pathway through two sequence elements: the c-fos AP-1 and p62TCF sites

MMSP tumor cells expressing the EWS/ATF1 oncogene do not support cAMP-inducible transcription

Control of the rat angiotensin I converting enzyme gene by CRE-like sequences

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