Evidence map›Paper›PMID 17438267›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

The dynein light chain 8 binding motif of rabies virus phosphoprotein promotes efficient viral transcription.

Gene S Tan, Mirjam A R Preuss, John C Williams, Matthias J Schnell

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.6field-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

62 citing papers in PubMed, 129 citations in OpenAlex.

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  14. Ebolaviruses: New roles for old proteins.PLoS neglected tropical diseases · 2018
    Review
  15. Article
  16. Ebola virus proteins NP, VP35, and VP24 are essential and sufficient to mediate nucleocapsid transport.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
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  18. Article
  19. Review
  20. Review

2 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

4 authors at 1 institution in 1 country.

Gene S TanDepartment of Microbiology and Immunology, Jefferson Medical College, Thomas Jefferson University, 233 South 10th Street, Philadelphia, PA 19107-5541, USA.
Mirjam A R Preuss
John C Williams
Matthias J Schnell
Thomas Jefferson University · US

Funding

CENTER FOR NEUROANATOMY WITH NEUROTROPIC VIRUSES: COMPARATIVE MEDICINEP40RR018604 · NCRR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STRICK, PETER · 2004 to 2011
$6.5M
TRAINING PROGRAM IN DEVELOPMENTAL IMMUNOLOGYT32AI007492 · NIAID · THOMAS JEFFERSON UNIVERSITY · PI MANSER, TIMOTHY L · 1996 to 2005
$1.3M
NCRR NIH HHS P40 RR 018604NCRR NIH HHS P40 RR018604NIAID NIH HHS T32 AI 007492NIAID NIH HHS T32 AI007492
6 · The paper itself

Abstract

Recent studies indicate that the interaction between rabies virus (RV) phosphoprotein and the dynein light chain 8 (LC8) is essential for RV pathogenesis. Through its association with the dynein motor complex, LC8 has been suggested as a molecular factor that links the viral ribonucleoprotein to the host cell transport system. Recent structural investigations, however, dispute this model. To understand the role of LC8 in RV pathogenesis, we generated recombinant RVs with or without the LC8 binding domain (LC8-BD) deleted from the RV phosphoprotein. Peripheral infection of adult mice showed that removal of the LC8-BD did not inhibit entry into the CNS, although it prevented onset of RV-induced CNS disease. However, deletion of the LC8-BD significantly attenuated viral transcription and replication in the CNS. Studies in RAG2 knockout (KO) mice infected with the same recombinant RVs confirmed this finding and indicated that the adaptive immune system is not a factor in the attenuation of viral replication early in the infection. In cell culture, the deletion of the LC8-BD greatly attenuated growth on neuronal cells whereas the growth pattern on nonneuronal cells remained unchanged. However, deletion of the LC8-BD did not affect production of RV virions. We provide evidence that removal of the LC8-BD decreases primary transcription. In this study, we propose that LC8 does not play a role in the retrograde axonal transport of RV and that the deletion of the LC8-BD impairs the infectivity of the virions by reducing early transcription and replication in neurons.

Indexed as

Transcription, GeneticAmino Acid MotifsAnimalsCell LineCentral Nervous SystemDyneinsGlycoproteinsMiceNeuronsPhosphoproteinsProtein BindingProtein Structure, TertiaryRabiesRabies virusRNA, ViralSequence DeletionDyneinsGlycoproteinsPhosphoproteinsRNA, ViralViral Proteins

Identifiers

PMID17438267
PMCPMC1855364
OpenAlexW2150832705

What OpenQuestion holds

Textmetadata
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.