Evidence map›Paper›PMID 17267477›Full record

ArticleJournal of virology2007

Degrons at the C terminus of the pathogenic but not the nonpathogenic hantavirus G1 tail direct proteasomal degradation.

Nandini Sen, Adrish Sen, Erich R Mackow

Erratum issuedAbstract read
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

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  15. Recent advances in hantavirus molecular biology and disease.Advances in applied microbiology · 2011
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

Nandini SenDepartments of Medicine, HSC T17, Rm. 60, SUNY at Stony Brook, Stony Brook, NY 11794, and Northport VA Medical Center, NY 11768, USA.
Adrish Sen
Erich R Mackow
Northport VA Medical Center · USState University of New York · USStony Brook University · US

Funding

Viral Pathogenesis and TherapeuticsU54AI057158 · NIAID · WADSWORTH CENTER · PI LEVY, DAVID E · 2003 to 2014
$100.8M
Virulence Mechanism of Y. pestis and tularensisP01AI055621 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI BENACH, JORGE L. · 2004 to 2010
$20.7M
HANTAVIRUS CELL INTERACTIONSR01AI047873 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI MACKOW, ERICH R. · 2000 to 2003
$1.1M
NIAID NIH HHS P01 AI055621NIAID NIH HHS P01AI055621NIAID NIH HHS R01 AI047873NIAID NIH HHS R01AI47873NIAID NIH HHS U54 AI057158NIAID NIH HHS U54AI57158
6 · The paper itself

Abstract

Pathogenic hantaviruses cause two human diseases: hantavirus pulmonary syndrome (HPS) and hemorrhagic fever with renal syndrome (HFRS). The hantavirus G1 protein contains a long, 142-amino-acid cytoplasmic tail, which in NY-1 virus (NY-1V) is ubiquitinated and proteasomally degraded (E. Geimonen, I. Fernandez, I. N. Gavrilovskaya, and E. R. Mackow, J. Virol. 77: 10760-10768, 2003). Here we report that the G1 cytoplasmic tails of pathogenic Andes (HPS) and Hantaan (HFRS) viruses are also degraded by the proteasome and that, in contrast, the G1 tail of nonpathogenic Prospect Hill virus (PHV) is stable and not proteasomally degraded. We determined that the signals which direct NY-1V G1 tail degradation are present in a hydrophobic region within the C-terminal 30 residues of the protein. In contrast to that of PHV, the NY-1V hydrophobic domain directs the proteasomal degradation of green fluorescent protein and constitutes an autonomous degradation signal, or "degron," within the NY-1V G1 tail. Replacing 4 noncontiguous residues of the NY-1V G1 tail with residues present in the stable PHV G1 tail resulted in a NY-1V G1 tail that was not degraded by the proteasome. In contrast, changing a different but overlapping set of 4 PHV residues to corresponding NY-1V residues directed proteasomal degradation of the PHV G1 tail. The G1 tails of pathogenic, but not nonpathogenic, hantaviruses contain intervening hydrophilic residues within the C-terminal hydrophobic domain, and amino acid substitutions that alter the stability or degradation of NY-1V or PHV G1 tails result from removing or adding intervening hydrophilic residues. Our results identify residues that selectively direct the proteasomal degradation of pathogenic hantavirus G1 tails. Although a role for the proteasomal degradation of the G1 tail in HPS or HFRS is unclear, these findings link G1 tail degradation to viral pathogenesis and suggest that degrons within hantavirus G1 tails are potential virulence determinants.

Indexed as

Amino Acid MotifsAmino Acid SubstitutionGenes, ReporterGreen Fluorescent ProteinsHantaan virusHumansHydrophobic and Hydrophilic InteractionsOrthohantavirusProteasome Endopeptidase ComplexProtein Structure, TertiaryViral Envelope ProteinsVirulenceenhanced green fluorescent proteinglycoprotein G1, HantavirusGreen Fluorescent ProteinsProteasome Endopeptidase ComplexViral Envelope Proteins

Identifiers

PMID17267477
PMCPMC1866138
OpenAlexW2139050070

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.