A mutant cell line partially responsive to both IFN-&lt;FONT FACE=Symbol&gt;a&lt;/font&gt; and IFN-&lt;FONT FACE=Symbol&gt;g&lt;/font&gt;

Bonjardim, Cláudio Antônio

doi:10.1590/s0100-879x1997000100007

Cited by 8 publications

(2 citation statements)

References 47 publications

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“…When appropriate, cells were incubated with the specific IPK for 15-60 min prior to and throughout VV infection. EMSA was carried out essentially as described (38). Whole cell extracts were prepared by a modification of the method already described (39).…”

Section: P]dctp or ␥[mentioning

confidence: 99%

A Mitogenic Signal Triggered at an Early Stage of Vaccinia Virus Infection

Magalhães¹,

Andrade²,

Silva³

et al. 2001

Journal of Biological Chemistry

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Vaccinia virus (VV) triggers a mitogenic signal at an early stage of infection. VV-induced proto-oncogene c-fos mRNA with kinetics paralleling that stimulated by serum. The VV virokine, or vaccinia virus growth factor (VGF), was not crucial for c-fos induction because it was observed upon infection with the virokine-minus mutant VV (VGF ؊ ). Furthermore, c-fos expression did not require infectious virus particles, as it occurred even with UV-inactivated VV and was equally induced by the different multiplicities of infection, i.e. 1.0, 5.0, and 25.0. c-fos expression was preceded by VV-induced DNA binding activity and was mediated via the cis-acting elements serum response element (SRE), activating protein-1 (AP-1), and cAMP-response element (CRE). VV activated the protein kinases p42MAPK/ERK2 and p44MAPK/ERK1 and the transcription factor ATF1 in a time-dependent manner with kinetics that paralleled those of VV-stimulated DNAprotein complex formation. The mitogenic signal transmission pathways leading to c-fos activation upon VV infection were apparently mediated by the protein kinases MEK, ERK, and PKA. This assumption was based on the findings that: 1) c-fos transcript was down-regulated; 2) the SRE, AP-1, and CRE binding activities were significantly reduced; and 3) the activation of p42MAPK/ERK2, p44MAPK/ERK1, and ATF1 were drastically affected when the viral infections were carried out in the presence of specific protein kinase inhibitor. Moreover, the mutant VV (VGF ؊ ) was also able to activate ERK1/2. It is noteworthy that virus multiplication was equally affected by the same kinase inhibitors. Taken together, our data provide evidence that the early mitogenic signal triggered upon VV infection relies upon the activation of the protein kinases MEK, ERK, and PKA, which are needed for both signal transduction and virus multiplication.

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Section: P]dctp or ␥[mentioning

confidence: 99%

A Mitogenic Signal Triggered at an Early Stage of Vaccinia Virus Infection

Magalhães¹,

Andrade²,

Silva³

et al. 2001

Journal of Biological Chemistry

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“…A31 cells were cultured and starved as above and then treated with IFN for the indicated times, or were incubated with PD98059 (50µM) for 30 min prior to and throughout IFN treatment. EMSA was carried out essentially as described (42). Nuclear cell extracts were prepared as described elsewhere (43).…”

Section: Electrophoretic Mobility Shift Assay (Emsa)mentioning

confidence: 99%

Characterization of alpha-enolase as an interferon-alpha 2 alpha 1 regulated gene

LirlÃ¢ndia¹

2005

Front Biosci

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Interferons (IFNs) are multifunctional cytokines that after binding to the cell surface receptor induce the expression of a large number of genes, which in turn, mediate many biological processes including host defense, cell growth control, signaling, and metabolism. Here we show that IFN-alpha activates the mitogen-activated protein kinases (MAPK) ERK1/2 and the transcription factor CREB/ATF-1, which lead to the alpha-enolase (alpha-ENO) gene expression in fibroblasts. Alpha-ENO mRNA accumulation was apparent 6 h post-IFN stimulation and required both de novo protein synthesis and active gene transcription, which is typical of a secondary response gene. Alpha-ENO expression does not appear to be restricted to fibroblasts, since it was equally verified in peripheral blood mononuclear cells (PBMC). Furthermore, IFN-alpha stimulates the expression of the primary response genes c-fos and egr-1, which was followed by an increase in DNA binding activity of c-FOS and EGR-1 proteins, as verified by shift assays using the cis-acting elements AP-1 and EGR-1 localized at the alpha-ENO promoter. Finally, we also demonstrated that IFN treatment of PBMC cause an increase in both, alpha-ENO expression on the cell surface and plasmin generation followed addition of exogenous plasminogen.

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