Evidence map›Paper›PMID 17551829›Full record

ArticleNeurochemical research2007

Glia maturation factor regulation of STAT expression: a novel mechanism in experimental autoimmune encephalomyelitis.

Smita Zaheer, Yanghong Wu, Jon Bassett, Baoli Yang, Asgar Zaheer

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Next Generation Precision Medicine: CRISPR-mediated Genome Editing for the Treatment of Neurodegenerative Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Review
  4. CRISPR/Cas9 Editing of Glia Maturation Factor Regulates Mitochondrial Dynamics by Attenuation of the NRF2/HO-1 Dependent Ferritin Activation in Glial Cells.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Article
  5. Glia Maturation Factor in the Pathogenesis of Alzheimer's disease.Open access journal of neurology & neurosurgery · 2019
    Article
  6. Article
  7. Review
  8. Review
  9. Involvement of the janus kinase/signal transducer and activator of transcription signaling pathway in multiple sclerosis and the animal model of experimental autoimmune encephalomyelitis.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. IL-9: basic biology, signaling pathways in CD4+ T cells and implications for autoimmunity.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010
    Review
  18. 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 2 institutions in 1 country.

Smita ZaheerVeterans Affairs Medical Center, Iowa City, IA, USA. asgar-zaheer@uiowa.edu
Yanghong Wu
Jon Bassett
Baoli Yang
Asgar Zaheer
University of Iowa · USVeterans Health Administration · US

Funding

GMF in CNS inflammationR01NS047145 · NINDS · UNIVERSITY OF IOWA · PI ZAHEER, ASGAR · 2004 to 2013
$2.9M
NINDS NIH HHS NS-47145
6 · The paper itself

Abstract

Inflammatory cytokines are implemented in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. We previously demonstrated that glia maturation factor (GMF), a brain protein, isolated, sequenced and cloned in our laboratory, induce expression of proinflammatory cytokine/chemokine in the central nervous system (CNS). We found GMF-deficient (knockout) mice relatively resistant to EAE development after immunization with encephalitogenic MOG peptide 35-55. Consistent with these findings, the expression of proinflammatory cytokines in CNS of mice with EAE differed profoundly between wild type and GMF-knockout mice. In the present study we examined the expressions of six murine signal transducers and activators of transcription (STATs) genes, which are known to regulate the cytokine-dependent signal transduction pathways in autoimmune inflammation. The expressions of STATs genes were evaluated in the brains and spinal cords of wild type and GMF-knockout mice at the peak of EAE by quantitative real-time RT-PCR. Compared to GMF-knockout mice, the expressions of STAT1, STAT2, STAT3, STAT4, STAT5, and STAT6 genes were significantly (P < 0.001) upregulated in the wild type mice exhibiting EAE symptoms. The results are consistent with the diminished development of EAE in the GMF-knockout mice. A significant suppression of STATs expression in GMF-knockout mice suggests GMF as an upstream effector of JAK/STAT signaling.

Indexed as

AnimalsBlotting, WesternCytokinesEncephalomyelitis, Autoimmune, ExperimentalEnzyme-Linked Immunosorbent AssayGlia Maturation FactorImmunoprecipitationJanus KinasesMiceMice, KnockoutMyelin SheathPhosphorylationReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSignal TransductionSTAT Transcription FactorsCytokinesGlia Maturation FactorJanus KinasesRNA, MessengerSTAT Transcription FactorsSuppressor of Cytokine Signaling Proteins

Identifiers

PMID17551829
OpenAlexW2128246468

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.