Evidence map›Paper›PMID 21975601›Full record

ArticleJournal of molecular neuroscience : MN2012

STC1 induction by PACAP is mediated through cAMP and ERK1/2 but not PKA in cultured cortical neurons.

Yvonne Holighaus, Eberhard Weihe, Lee E Eiden

Abstract read
In one paragraph

Article in Journal of molecular neuroscience : MN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Expression, function and clinical application of stanniocalcin-1 in cancer.Journal of cellular and molecular medicine · 2020
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
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  10. Review
  11. Signaling through the neuropeptide GPCR PAC₁ induces neuritogenesis via a single linear cAMP- and ERK-dependent pathway using a novel cAMP sensor.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012
    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

3 authors at 2 institutions in 2 countries.

Yvonne HolighausSection on Molecular Neuroscience, Laboratory of Cellular and Molecular Regulation, National Institute of Mental Health, Bethesda, MD 20892, USA.
Eberhard Weihe
Lee E Eiden
National Institute of Mental Health · USPhilipps University of Marburg · DE

Funding

Chemical Coding Of NeurotransmissionZIAMH002386 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI EIDEN, LEE E. · 2009 to 2025
$25.6M
NEUROSECRETORY VESICLED PROTEINS AND CHEMICAL CODING OF NEUROTRANSMISSIONZ01MH002386 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI EIDEN, LEE E. · 1987 to 2008
$3.6M
Intramural NIH HHS Z01 MH002386Intramural NIH HHS ZIA MH002386
6 · The paper itself

Abstract

The neuroprotective actions of PACAP (pituitary adenylate cyclase-activating polypeptide) in vitro and in vivo suggest that activation of its cognate G protein coupled receptor PAC1 or downstream signaling molecules,and thus activation of PACAP target genes, could be of therapeutic benefit. Here, we show that cultured rat cortical neurons predominantly expressed the PAC1hop and null variants. PACAP receptor activation resulted in the elevation of the two second messengers cAMP and Ca(2+) and expression of the putative neuroprotectant stanniocalcin 1(STC1). PACAP signaling to the STC1 gene proceeded through the extracellular signal-regulated kinases 1 and 2(ERK1/2), but not through the cAMP-dependent protein kinase (PKA), and was mimicked by the adenylate cyclase activator forskolin. PACAP- and forskolin-mediated activation of ERK1/2 occurred through cAMP, but not PKA.These results suggest that STC1 gene induction proceeds through cAMP and ERK1/2, independently of PKA, the canonical cAMP effector. In contrast, PACAP signaling to the BDNF gene proceeded through PKA, suggesting that two different neuroprotective cAMP pathways co-exist in differentiated cortical neurons. The selective activation of a potentially neuroprotective cAMP-dependent pathway different from the canonical cAMP pathway used in many physiological processes, such as memory storage, has implications for pharmacological activation of neuroprotection in vivo.

Indexed as

AnimalsCell DifferentiationCerebral CortexCyclic AMPCyclic AMP-Dependent Protein KinasesExtracellular Signal-Regulated MAP KinasesFemaleGlycoproteinsMAP Kinase Signaling SystemNeuronsPituitary Adenylate Cyclase-Activating PolypeptidePrimary Cell CultureRatsRats, WistarReceptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type ITranscriptional ActivationCyclic AMPCyclic AMP-Dependent Protein KinasesExtracellular Signal-Regulated MAP KinasesGlycoproteinsPituitary Adenylate Cyclase-Activating PolypeptideReceptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type Iteleocalcin

Identifiers

PMID21975601
PMCPMC3256285
OpenAlexW1988146686

What OpenQuestion holds

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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.