Evidence map›Paper›PMID 21994950›Full record

ArticleThe Journal of biological chemistry2011

Phosphorylation of eukaryotic translation initiation factor 4B (EIF4B) by open reading frame 45/p90 ribosomal S6 kinase (ORF45/RSK) signaling axis facilitates protein translation during Kaposi sarcoma-associated herpesvirus (KSHV) lytic replication.

Ersheng Kuang, Bishi Fu, Qiming Liang, Jinjong Myoung, Fanxiu Zhu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

55 citing papers in PubMed, 77 citations in OpenAlex.

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  15. A case of convergent evolution: Several viral and bacterial pathogens hijack RSK kinases through a common linear motif.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  16. Article
  17. Ribosomal Protein S6: A Potential Therapeutic Target against Cancer?International journal of molecular sciences · 2021
    Review
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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

5 authors at 2 institutions in 1 country.

Ersheng KuangDepartment of Biological Science, The Florida State University, Tallahassee, Florida 32306-4370.
Bishi FuDepartment of Biological Science, The Florida State University, Tallahassee, Florida 32306-4370.
Qiming LiangDepartment of Biological Science, The Florida State University, Tallahassee, Florida 32306-4370.
Jinjong MyoungNovartis Institutes for Biomedical Research, Emeryville, California 94608-2916.
Fanxiu ZhuDepartment of Biological Science, The Florida State University, Tallahassee, Florida 32306-4370. Electronic address: fzhu@bio.fsu.edu.
Florida State University · USNovartis (United States) · US

Funding

Role of KSHV ORF45 in Viral Immune Evasion &ReplicationR01DE016680 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI ZHU, FANXIU · 2005 to 2015
$2.5M
NIDCR NIH HHS R01 DE016680NIDCR NIH HHS R01DE016680
6 · The paper itself

Abstract

Open reading frame 45 (ORF45) of Kaposi sarcoma-associated herpesvirus (KSHV) causes sustained activation of p90 ribosomal S6 kinase (RSK), which is crucial for KSHV lytic replication, but the exact functional roles remain to be determined. To characterize the biological consequence of persistent RSK activation by ORF45, we screened known cellular substrates of RSK. We found that ORF45 induced phosphorylation of eukaryotic translation initiation factor 4B (eIF4B), increased its assembly into translation initiation complex, and subsequently facilitated protein translation. The ORF45/RSK-mediated eIF4B phosphorylation was distinguishable from that caused by the canonical AKT/mammalian target of rapamycin/ribosomal S6 kinase and MEK/ERK/RSK pathways because it was resistant to both rapamycin (an mammalian target of rapamycin inhibitor) and U1026 (an MEK inhibitor). The rapamycin and U1026 doubly insensitive eIF4B phosphorylation was induced during KSHV reactivation but was abolished if either ORF45 or RSK1/2 were ablated by siRNA, a pattern that is correlated with reduced lytic gene expression as we observed previously. Ectopic expression of eIF4B but not its phosphorylation-deficient mutant form increased KSHV lytic gene expression and production of progeny viruses. Together, these results indicated that ORF45/RSK axis-induced eIF4B phosphorylation is involved in translational regulation and is required for optimal KSHV lytic replication.

Indexed as

MAP Kinase Signaling SystemProtein BiosynthesisCell Line, TumorEukaryotic Initiation FactorsGene Expression Regulation, ViralHEK293 CellsHerpesvirus 8, HumanHumansImmediate-Early ProteinsImmunosuppressive AgentsMutationPhosphorylationProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 90-kDaSirolimusTOR Serine-Threonine KinaseseIF-4BEukaryotic Initiation FactorsImmediate-Early ProteinsImmunosuppressive AgentsMTOR protein, humanORF45 protein, Kaposi's sarcoma-associated herpesvirusProto-Oncogene Proteins c-aktribosomal protein S6 kinase, 90kDa, polypeptide 3Ribosomal Protein S6 Kinases, 90-kDaRPS6KA1 protein, humanSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID21994950
PMCPMC3308831
OpenAlexW2128765556

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.