Involvement of common and cell type-specific pathways in c-fos gene control: Stable induction by cAMP in macrophages

Bravo, Rodrigo; Neuberg, Manfred; Burckhardt, Johann Jakob; Almendral, José M.; Wallich, Reinhard; Müller, Rolf

doi:10.1016/0092-8674(87)90428-4

Cited by 210 publications

(93 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The alterations in signal transduction pathways caused by measles virus may be a general phenomenon, since alteration in the cAMP-dependent signalling pathway has also been reported for measles-virus infected rat glioma cells [26]. The increase in c-fos protooncogene expression may or may not correlate with the increase in PKC activity, since at least one more pathway involving adenylate cyclase was reported [9]. The c-fos protein product is a nuclear DNA-binding phosphoprotein which binds to the regulatory sequences of the responsive genes [24,25].…”

Section: Discussionmentioning

confidence: 99%

“…Thus, the c-fos protein product is among the early inducible regulatory proteins synthesized in response to cell differentiation agents [7]. Studies on the molecular mechanism leading to the expression of c-fos suggest that the inductive signals are delivered to the DNA transcription machinery by different transduction pathways [8,9], such as phosphatidylinositol (PI)/protein kinase C (PKC) which is the major transducing pathway in neuronal cells [10]. Activation of PKC by serum growth factors or phorbol esters results in rapid expression of the c-fos gene [11,12].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of persistent measles virus infection on protein kinase C activity and c‐fos protooncogene expression in neuroblastoma cells

et al. 1989

View full text Add to dashboard Cite

The effect of persistent measles virus infection on c‐fos protooncogene and protein kinase C (PKC‐I) gene expression in a murine neuroblastoma cell line was studied. Overexpression of c‐fos protooncogene by infected NS20Y/MS cells was detected when compared with uninfected NS20Y cells. The level of PKC‐I‐specific mRNA was increased in infected NS20Y/MS cells. In addition, the level of total PKC activity in these cells was also enhanced. We conclude that persistent measles virus infection can alter both protooncogene expression and signal transduction in cells of neuronal origin.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of persistent measles virus infection on protein kinase C activity and c‐fos protooncogene expression in neuroblastoma cells

et al. 1989

View full text Add to dashboard Cite

show abstract

“…The gel mobility shift assay was performed essentially as described previously (13,14,40 2 ,ug of poly)(dI-dC) poly(dI-dC) and 50 ng of various competitor DNA fragments, as indicated in the figure legends. In the gel shift assay to detect the direct-repeat binding factor, 3 ,ug of poly(dI-dC)-poly(dIdC) and 50 ng of competitor DNA fragment were used.…”

mentioning

confidence: 99%

c-fos sequence necessary for basal expression and induction by epidermal growth factor, 12-O-tetradecanoyl phorbol-13-acetate and the calcium ionophore.

Fisch¹,

Prywes²,

Roeder³

1987

Mol. Cell. Biol.

270

181

View full text Add to dashboard Cite

We have investigated the sequence requirements for induction of the human c-fos gene by epidermal growth factor (EGF), 12-0-tetradecanoyl phorbol-13-acetate (TPA), and the calcium ionophore A23187 by transfecting c-fos promoter mutants into HeLa and A431 cells. Induction by both EGF and TPA in HeLa cells required the presence of the c-fos enhancer located at -317 to -298 relative to the mRNA cap site. A23187, however, did not induce expression of the transfected gene, even though it strongly induced expression of the endogenous gene, suggesting that it has different requirements for induction than do EGF and TPA. We have also investigated the role of promoter sequences downstream of the enhancer in general expression and induction of c-fos. A sequence between -97 and -76, which includes an 8-base-pair perfect direct repeat, was needed for efficient general expression but not for induction of the gene. A factor in nuclear extracts that bound specifically to this sequence was detected by a gel mobility shift assay. A 7-base-pair sequence, located between -63 and -57 relative to the mRNA cap site and previously shown to be important for general expression of mouse c-fos, was also important for general expression of the human gene. In addition, this element was important for inducibility by EGF and TPA, since induction was significantly reduced when internal deletion mutants that retained the enhancer but lacked the -63 to -57 sequence element were analyzed in transfection assays.

show abstract

“…cAMP regulates the expression of a number of genes through a conserved promoter element, the CRE (Roesler et al, 1988). Moreover, cAMP induced stable transcription of specific genes such as the c-fos gene in macrophages, and this induction is qualitatively different from the response to cAMP of other cell types (Bravo et al, 1987). These data underline the specific responses of macrophages to cAMP.…”

Section: Discussionmentioning

confidence: 56%

Cyclic AMP-mediated inhibition of vesicular stomatitis virus and herpes simplex virus replication in mouse macrophage-like cells

Borghi

Marzio

Varano

et al. 1992

Journal of General Virology

View full text Add to dashboard Cite

In this study, we have analysed the effects of cAMP inducers on the multiplication of vesicular stomatis virus (VSV) and herpes simplex virus type 1 (HSV-1) in mouse macrophage-like cells. The addition ofdibutyryl cAMP (dB-cAMP) or cholera toxin to resting peritoneal macrophages aged in vitro or P388D1 cells resulted in a 10-to 100-fold reduction of VSV yield compared to control cultures. In contrast, no cAMP-dependent inhibition was found in VSV-infected L929 cells. In macrophage-like cells, the dB-cAMP-induced antiviral state was not inhibited by antibodies to interferon (IFN)-~//] and did not correlate with any increase in the intracellular levels of 2-5 oligo(A) synthetase. Dibutyryl cAMP did not inhibit virus yields in mouse macrophages infected with encephalomyocarditis virus. In P388D~ cells, the addition of dB-cAMP resulted in an approximately 10-fold inhibition of HSV-1 replication with respect to control cultures, as evaluated both by TCIDso and plaque assays on Vero cells. Dibutyryl cAMP did not affect VSV binding or entry into mouse macrophages and the cAMPmediated anti-VSV state was significantly reduced by inhibitors of protein kinase C (i.e. staurosporine and H7). These data suggest that macrophages may acquire resistance to infection by VSV and HSV-1 after treatment with cAMP inducers. This cAMP-mediated antiviral activity does not depend on the modulation of the endogenous IFN system, suggesting that macrophages exhibit multiple resistance mechanisms (i.e. IFN-dependent and IFN-independent) to maintain their intrinsic antiviral activity.

show abstract

Involvement of common and cell type-specific pathways in c-fos gene control: Stable induction by cAMP in macrophages

Cited by 210 publications

References 46 publications

Effect of persistent measles virus infection on protein kinase C activity and c‐fos protooncogene expression in neuroblastoma cells

Effect of persistent measles virus infection on protein kinase C activity and c‐fos protooncogene expression in neuroblastoma cells

c-fos sequence necessary for basal expression and induction by epidermal growth factor, 12-O-tetradecanoyl phorbol-13-acetate and the calcium ionophore.

Cyclic AMP-mediated inhibition of vesicular stomatitis virus and herpes simplex virus replication in mouse macrophage-like cells

Contact Info

Product

Resources

About