Evidence map›Paper›PMID 11885780›Full record

ArticleNeurochemical research2001

Effects of glia maturation factor overexpression in primary astrocytes on MAP kinase activation, transcription factor activation, and neurotrophin secretion.

A Zaheer, M A Yorek, R Lim

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

40 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. The role of the immune system during regeneration of the central nervous system.Journal of immunology and regenerative medicine · 2020
    Article
  10. 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
  11. Article
  12. Article
  13. Article
  14. Glia Maturation Factor in the Pathogenesis of Alzheimer's disease.Open access journal of neurology & neurosurgery · 2019
    Article
  15. Article
  16. GMF as an Actin Network Remodeling Factor.Trends in cell biology · 2018
    Review
  17. Cross-Talk between Glia, Neurons and Mast Cells in Neuroinflammation Associated with Parkinson's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018
    Article
  18. Article
  19. Review
  20. Review
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

3 authors at 1 institution in 1 country.

A ZaheerDepartment of Neurology, Veterans Affairs Medical Center and the University of Iowa College of Medicine, Iowa City 52242, USA.
M A Yorek
R Lim
University of Iowa · US

Funding

SITE SPECIFIC ANTIINSULIN RECEPTOR ANTIBODIESP30DK025295 · NIDDK · UNIVERSITY OF IOWA · PI SIGMUND, CURT DANIEL · 1986 to 2002
$2.6M
NIDDK NIH HHS DK-25295
6 · The paper itself

Abstract

Using the replication-defective adenovirus vector, we overexpressed rat glia maturation factor (GMF) in primary astrocyte cultures derived from embryonic rat brains. Among the three isoforms of MAP kinase, there was a big increase in the phosphorylation of p38, as detected with Western blotting using the phosphospecific antibody. Likewise, there was a substantial increase in the phosphorylation of the transcription factor CREB. Using the electrophoretic mobility shift assay (EMSA), we found a stimulation in the transcription factor NF-kappaB. The activations of CREB and NF-kappaB were blocked by inhibitors of either p38 (SB-203580) or MEK (PD-098059), suggesting that they were events downstream of MAK kinase. There was an increased secretion of BDNF and NGF into the conditioned medium, along with an increase in their messenger RNA. The inductions of BDNF and NGF were also blocked by inhibitors of p38 and MEK, as well as by the inhibition of NF-kappaB with a decoy DNA sequence. Taken together, the results suggest that GMF functions intracellularly in astrocytes as a modulator of MAP kinase signal transduction, leading to a series of downstream events including CREB and NF-kappaB activation, resulting in the induction and secretion of the neurotrophins.

Indexed as

AnimalsAstrocytesBrain-Derived Neurotrophic FactorCells, CulturedCyclic AMP Response Element-Binding ProteinEnzyme ActivationFetusGlia Maturation FactorMitogen-Activated Protein KinasesNerve Growth FactorsNF-kappa Bp38 Mitogen-Activated Protein KinasesRatsTranscription FactorsBrain-Derived Neurotrophic FactorCyclic AMP Response Element-Binding ProteinGlia Maturation FactorMitogen-Activated Protein KinasesNerve Growth FactorsNF-kappa Bp38 Mitogen-Activated Protein KinasesTranscription Factors

Identifiers

PMID11885780
OpenAlexW1564344417

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.