Evidence map›Paper›PMID 12134038›Full record

ArticleJournal of virology2002

Critical role for protein tyrosine phosphatase SHP-1 in controlling infection of central nervous system glia and demyelination by Theiler's murine encephalomyelitis virus.

Paul T Massa, Stacie L Ropka, Sucharita Saha, Karen L Fecenko, Kathryn L Beuler

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.1field-weighted citation impact, top 51% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. SHP-1-dependent macrophage differentiation exacerbates virus-induced myositis.Journal of immunology (Baltimore, Md. : 1950) · 2015
    Article
  4. Article
  5. Article
  6. Article
  7. Article
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  9. Macrophages of multiple sclerosis patients display deficient SHP-1 expression and enhanced inflammatory phenotype.Laboratory investigation; a journal of technical methods and pathology · 2009
    Article
  10. Article
  11. Article
  12. Article
  13. SHP-1 deficiency and increased inflammatory gene expression in PBMCs of multiple sclerosis patients.Laboratory investigation; a journal of technical methods and pathology · 2008
    Article
  14. Article
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 1 institution in 1 country.

Paul T MassaDepartment of Neurology, Upstate Medical University, State University of New York, Syracuse 13210, USA. massap@upstate.edu
Stacie L Ropka
Sucharita Saha
Karen L Fecenko
Kathryn L Beuler
SUNY Upstate Medical University · US

Funding

REGULATION OF INTERFERON ACTIVITY BY SHP-1 IN THE CNSR01NS041593 · NINDS · UPSTATE MEDICAL UNIVERSITY · PI MASSA, PAUL T · 2001 to 2007
$1.2M
NINDS NIH HHS NS41593-01NINDS NIH HHS R01 NS041593
6 · The paper itself

Abstract

We previously characterized the expression and function of the protein tyrosine phosphatase SHP-1 in the glia of the central nervous system (CNS). In the present study, we describe the role of SHP-1 in virus infection of glia and virus-induced demyelination in the CNS. For in vivo studies, SHP-1-deficient mice and their normal littermates received an intracerebral inoculation of an attenuated strain of Theiler's murine encephalomyelitis virus (TMEV). At various times after infection, virus replication, TMEV antigen expression, and demyelination were monitored. It was found that the CNS of SHP-1-deficient mice uniquely displayed demyelination and contained substantially higher levels of virus than did that of normal littermate mice. Many infected astrocytes and oligodendrocytes were detected in both brains and spinal cords of SHP-1-deficient but not normal littermate mice, showing that the virus replicated and spread at a much higher rate in the glia of SHP-1-deficient animals. To ascertain whether the lack of SHP-1 in the glia was primarily responsible for these differences, glial samples from these mice were cultured in vitro and infected with TMEV. As in vivo, infected astrocytes and oligodendrocytes of SHP-1-deficient mice were much more numerous and produced more virus than did those of normal littermate mice. These findings indicate that SHP-1 is a critical factor in controlling virus replication in the CNS glia and virus-induced demyelination.

Indexed as

AnimalsAstrocytesBrainCardiovirus InfectionsCentral Nervous System InfectionsDemyelinating DiseasesIntracellular Signaling Peptides and ProteinsMiceMice, Inbred C3HMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsNeurogliaOligodendrogliaParalysisProtein Tyrosine Phosphatase, Non-Receptor Type 6Intracellular Signaling Peptides and ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesPtpn6 protein, mouse

Identifiers

PMID12134038
PMCPMC155140
OpenAlexW2157501261

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.