Evidence map›Paper›PMID 11717354›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Phosphorylation of cAMP response element-binding protein in hippocampal neurons as a protective response after exposure to glutamate in vitro and ischemia in vivo.

T Mabuchi, K Kitagawa, K Kuwabara, K Takasawa, T Ohtsuki, Z Xia, D Storm, T Yanagihara, M Hori, M Matsumoto

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

99 citing papers in PubMed, 265 citations in OpenAlex.

  1. Article
  2. Review
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  4. β-Actin: An Emerging Biomarker in Ischemic Stroke.Cellular and molecular neurobiology · 2023
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  9. Cofilin Signaling in the CNS Physiology and Neurodegeneration.International journal of molecular sciences · 2021
    Review
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  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

39 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 3 countries.

T MabuchiDivision of Strokology, Department of Internal Medicine, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan.
K Kitagawa
K Kuwabara
K Takasawa
T Ohtsuki
Z Xia
D Storm
T Yanagihara
M Hori
M Matsumoto
Osaka University · JPEnvironmental Health · GBUniversity of Washington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although accumulating evidence indicates that cAMP response element-binding protein (CREB) phosphorylation mediates not only synaptic plasticity but also survival of certain neurons, it remains uncertain whether CREB phosphorylation induced after metabolic insult leads to CRE-mediated gene transcription and is involved in cell survival or not. In the present study, we clarified that (1) CREB phosphorylation and ischemic tolerance induced after preconditioning ischemia in the hippocampal neurons was abolished by MK801 administration in gerbil global ischemia model, (2) CREB phosphorylation induced after exposure to glutamate in cultured neurons was inhibited by removal of extracellular calcium, by MK801 and by an inhibitor of calcium-calmodulin-dependent protein kinase (CaMK) II and IV, (3) inhibitor of CaMK II-IV or CRE-decoy oligonucleotide suppressed upregulation of BCL-2 expression and accelerated neuronal damage after exposure to glutamate, and (4) CREB phosphorylation induced in the hippocampal neurons after ischemia and in cultured neurons after exposure to glutamate was followed by CRE-mediated gene transcription in transgenic mice with a CRE-LacZ reporter. Our results suggest that CREB phosphorylation in neurons after ischemia and exposure to glutamate is induced by NMDA receptor-gated calcium influx and subsequent activation of CaMK II-IV and that CREB phosphorylation after metabolic stress might show a neuroprotective response through CRE-mediated gene induction.

Indexed as

AnimalsBrain IschemiaCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium-Calmodulin-Dependent Protein Kinase Type 4Cells, CulturedCell SurvivalCyclic AMP Response Element-Binding ProteinDizocilpine MaleateEnzyme InhibitorsExcitatory Amino Acid AntagonistsGene Expression RegulationGenes, ReporterGerbillinaeGlutamic AcidCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium-Calmodulin-Dependent Protein Kinase Type 4Camk4 protein, mouseCyclic AMP Response Element-Binding ProteinDizocilpine MaleateEnzyme InhibitorsExcitatory Amino Acid AntagonistsGlutamic AcidOligonucleotidesProto-Oncogene Proteins c-bcl-2

Identifiers

PMID11717354
PMCPMC6763920
OpenAlexW1614322283

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.