Evidence map›Paper›PMID 20610653›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

NF-kappa B RelA subunit is crucial for early IFN-beta expression and resistance to RNA virus replication.

Junmei Wang, Suresh H Basagoudanavar, Xingyu Wang, Emily Hopewell, Randy Albrecht, Adolfo García-Sastre, Siddharth Balachandran, Amer A Beg

Open access · greenAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
3.8field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

88 citing papers in PubMed, 137 citations in OpenAlex.

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  7. Transcriptomic Differences Between Immortalized Oral and Skin Keratinocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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28 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Junmei WangDepartment of Immunology, Moffitt Cancer Center, University of South Florida, Tampa, FL 33612, USA.
Suresh H Basagoudanavar
Xingyu Wang
Emily Hopewell
Randy Albrecht
Adolfo García-Sastre
Siddharth Balachandran
Amer A Beg
Moffitt Cancer Center · USFox Chase Cancer Center · USCzech Academy of Sciences, Institute of Microbiology · CZIcahn School of Medicine at Mount Sinai · US

Funding

TRIM mediated host antiviral responses during influenza virus infectionsU19AI083025 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HA, TAEKJIP · 2009 to 2013
$10.0M
Mechanisms of co-stimulatory molecule expression in DCsR01AI059715 · NIAID · H. LEE MOFFITT CANCER CTR & RES INST · PI BEG, AMER AZIZ · 2005 to 2009
$1.7M
NIAID NIH HHS R01 AI059715NIAID NIH HHS U19 AI083025NIAID NIH HHS U19AI083025
6 · The paper itself

Abstract

RNA virus infection results in expression of type 1 IFNs, especially IFN-alpha/beta, which play a crucial role in host antivirus responses. Type 1 IFNs are induced in a cell type-specific manner through TLR and RIG-I-like receptor pathways, both of which activate IFN regulatory factors (IRFs) and NF-kappaB transcription factors. Although NF-kappaB activation and association with the IFN-beta promoter after RNA virus infection is well documented, our previous work showed that, surprisingly, NF-kappaB is not essential for IFN-beta gene expression. Thus, the actual function of NF-kappaB in IFN-beta expression and virus replication is not clear. In this study, we found Newcastle disease virus and vesicular stomatitis virus replication is enhanced in mouse embryonic fibroblasts (MEFs) lacking the NF-kappaB RelA subunit. Increased virus replication was traced to a specific requirement for RelA in early virus-induced IFN-beta expression. At these time points, when IFN-beta expression is ~100-fold less than peak levels, impaired IFN-beta production delayed IFN-induced gene expression, resulting in increased virus replication in RelA(-/-) MEFs. Importantly, our results show that RelA requirement is crucial only when IRF3 activation is low. Thus, high levels of activated IRF3 expression are sufficient for induction of IFN-beta in RelA(-/-) MEFs, transcriptional synergism with the coactivator CREB-binding protein, and rescue of susceptibility to virus. Together, these findings indicate that NF-kappaB RelA is not crucial for regulating overall IFN-beta production, as previously believed; instead, RelA is specifically required only during a key early phase after virus infection, which substantially impacts the host response to virus infection.

Indexed as

AnimalsCell LineCells, CulturedEmbryo, MammalianFibroblastsHumansImmunity, InnateInterferon-betaMiceMice, KnockoutNewcastle disease virusNF-kappa B p50 SubunitTime FactorsTranscription Factor RelAVesicular stomatitis Indiana virusVirus ReplicationInterferon-betaNF-kappa B p50 SubunitRela protein, mouseTranscription Factor RelA

Identifiers

PMID20610653
PMCPMC2910841
OpenAlexW2111724750

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.