Evidence map›Paper›PMID 22387108›Full record

ArticleNeuroscience2012

c-Jun N-terminal kinase controls a negative loop in the regulation of glial fibrillary acidic protein expression by retinoic acid.

F Herrera, P Maher, D Schubert

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 48% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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.

F HerreraCellular Neurobiology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.
P Maher
D Schubert
Salk Institute for Biological Studies · US

Funding

Redox Sensitive Proteins in Aging and NeurodegenerationR01AG025337 · NIA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI SCHUBERT, DAVID R · 2004 to 2006
$1.2M
NIA NIH HHS AG025337NIA NIH HHS R01 AG025337
6 · The paper itself

Abstract

Glial fibrillary acidic protein (GFAP) is a protein widely used as a molecular marker for astroglial differentiation and mature astrocytes. We and others have shown previously that retinoic acid and specific cytokines induce the expression of GFAP in neural precursor cells by activating the phosphatidylinositol-4,5-bisphosphate-3-kinase (PI3K) phosphorylation pathway. Here, we extend our previous work and show that retinoic acid also activates specifically the c-Jun N-terminal kinase (JNK) phosphorylation pathway, which in turn inhibits GFAP expression. Our results suggest the existence of a negative self-regulatory loop in the phosphorylation pathways that regulates GFAP expression. This loop is constitutively repressed by the PI3K pathway. Our results could be relevant for disorders involving sustained GFAP overexpression in precursor cells, such as glioblastoma and Alexander disease.

Indexed as

AnimalsAstrocytesBlotting, WesternCytokinesElectrophoresis, Gel, Two-DimensionalEnzyme ActivationEnzyme InhibitorsGene Expression RegulationGlial Fibrillary Acidic ProteinHippocampusImmunohistochemistryJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein KinasesNerve Tissue ProteinsNeural Stem CellsPhosphatidylinositol 3-KinasesCytokinesEnzyme InhibitorsGlial Fibrillary Acidic ProteinJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein KinasesNerve Tissue ProteinsPhosphatidylinositol 3-KinasesTretinoin

Identifiers

PMID22387108
PMCPMC4539028
OpenAlexW2040299445

What OpenQuestion holds

Textmetadata
LicenceTDM
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.