Evidence map›Paper›PMID 16421317›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

A signaling mechanism from G alpha q-protein-coupled metabotropic glutamate receptors to gene expression: role of the c-Jun N-terminal kinase pathway.

Lu Yang, Limin Mao, Hai Chen, Michael Catavsan, Jonathan Kozinn, Anish Arora, Xianyu Liu, John Q Wang

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. GaCellular and molecular life sciences : CMLS · 2017
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

8 authors at 2 institutions in 1 country.

Lu YangDepartment of Basic Medical Science, University of Missouri-Kansas City School of Medicine, Kansas City, Missouri 64108, USA.
Limin Mao
Hai Chen
Michael Catavsan
Jonathan Kozinn
Anish Arora
Xianyu Liu
John Q Wang
Division of Undergraduate Education · USUniversity of Missouri–Kansas City · US

Funding

REGULATION OF GENE EXPRESSION IN STRIATAL NEURONSR01MH061469 · NIMH · UNIVERSITY OF MISSOURI KANSAS CITY · PI WANG, QIANG · 2001 to 2024
$7.9M
Metabotropic Glutamate Regulation of Amphetamine ActionR01DA010355 · NIDA · UNIVERSITY OF MISSOURI KANSAS CITY · PI WANG, QIANG · 2003 to 2017
$4.6M
NIDA NIH HHS R01 DA010355NIDA NIH HHS R01DA010355NIMH NIH HHS R01 MH061469NIMH NIH HHS R01MH061469
6 · The paper itself

Abstract

Galphaq-protein-coupled group I metabotropic glutamate receptors (mGluRs) are densely expressed in brain neurons and are actively involved in various cellular activities. In this study, we investigated the role of group I mGluRs in regulating the c-Jun N-terminal kinase (JNK)/stress-activated protein kinase in cultured neurons. We found that selective activation of mGluR5 induced a rapid and transient phosphorylation of JNK. In a series of studies to determine the mechanisms, we found that the conventional mGluR5-associated signaling pathways (inositol-1,4,5-triphosphate-mediated Ca2+ release and activation of protein kinase C) were not involved in the mGluR5 regulation. Instead, ligand stimulation of mGluR5 caused a dynamic transactivation of the epidermal growth factor (EGF) receptor, which in turn triggered a downstream signaling pathway to upregulate JNK phosphorylation. Furthermore, the mGluR5-dependent JNK activation specifically activated c-Jun, but not activating transcription factor-2 or JunD, and increased activator protein-1 (AP-1)-mediated endogenous transcriptional activity. Together, we identified a novel mGluR5-to-nucleus communication through the EGF/JNK pathway, which functions to regulate AP-1-mediated transcription.

Indexed as

AnimalsCells, CulturedDose-Response Relationship, DrugGene Expression RegulationGlutamic AcidGTP-Binding Protein alpha Subunits, Gq-G11JNK Mitogen-Activated Protein KinasesMethoxyhydroxyphenylglycolPhosphorylationRatsReceptor, Metabotropic Glutamate 5Receptors, Metabotropic GlutamateSignal Transduction3,4-dihydroxyphenylglycolGlutamic AcidGrm5 protein, ratGTP-Binding Protein alpha Subunits, Gq-G11JNK Mitogen-Activated Protein KinasesMethoxyhydroxyphenylglycolReceptor, Metabotropic Glutamate 5Receptors, Metabotropic Glutamate

Identifiers

PMID16421317
PMCPMC6675367
OpenAlexW2144498047

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.