2006
DOI: 10.1128/jvi.80.9.4422-4430.2006
|View full text |Cite
|
Sign up to set email alerts
|

Negative Regulation of the Alpha Interferon-Induced Antiviral Response by the Ras/Raf/MEK Pathway

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
3
1
1

Citation Types

7
70
1

Year Published

2006
2006
2021
2021

Publication Types

Select...
7
3

Relationship

0
10

Authors

Journals

citations
Cited by 81 publications
(78 citation statements)
references
References 62 publications
7
70
1
Order By: Relevance
“…Therefore, although Ras mutations and consequent reduction of STAT1 expression do not eliminate the responsiveness of cells to IFNg, they are likely to alter the biological response to IFN significantly. Consistent with our data, it has been recently shown that the antiviral activity of IFN is abrogated in cells that carry oncogenic Ras mutation (Battcock et al, 2006).…”
Section: Discussionsupporting
confidence: 81%
“…Therefore, although Ras mutations and consequent reduction of STAT1 expression do not eliminate the responsiveness of cells to IFNg, they are likely to alter the biological response to IFN significantly. Consistent with our data, it has been recently shown that the antiviral activity of IFN is abrogated in cells that carry oncogenic Ras mutation (Battcock et al, 2006).…”
Section: Discussionsupporting
confidence: 81%
“…EBOV's persistence in a form that continually produces RNA but suppresses the translation of that RNA until the Ras/MAPK pathway is activated is a novel mechanism of viral reactivation from persistence. This mechanism relies on the IFN response through PKR and eIF2␣ signaling and is supported by previous studies showing suppression of IFN signaling by oncogenic transformation (33)(34)(35)(36), as well as by exogenous stimulation of these pathways (45). This is not the first evidence indicating that EBOV is capable of causing prolonged infection in cells, animal models, or even human patients.…”
Section: Discussionsupporting
confidence: 59%
“…Although MEK1 and MEK2 activities are rarely distinguished in the literature, growing evidence indicates that MEK1 and MEK2 may be differentially regulated and exert non-redundant functions [42][43][44][45][46][47][48][49][50][51]. That MEK1 and MEK2 play different roles in the regulation of several cellular processes implies that either substrate other than ERK1/2 might be differentially phosphorylated by MEK1 and MEK2, or MEK1/2 functions that do not directly require kinase activity, or both [29,52].…”
Section: Discussionmentioning
confidence: 99%