Evidence map›Paper›PMID 29046349›Full record

ArticleThe Journal of biological chemistry2017

Differential regulation of the Rac1 GTPase-activating protein (GAP) BCR during oxygen/glucose deprivation in hippocampal and cortical neurons.

Katharine R Smith, Dipen Rajgor, Jonathan G Hanley

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 2 pooled it
1.0field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. TRPM2 and CaMKII Signaling Drives Excessive GABAergic Synaptic Inhibition Following Ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  6. Review
  7. Article
  8. Article
  9. TRP Channels Regulation of Rho GTPases in Brain Context and Diseases.Frontiers in cell and developmental biology · 2020
    Review
  10. 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 1 institution in 2 countries.

Katharine R SmithCentre for Synaptic Plasticity and School of Biochemistry, Biomedical Sciences Building, University of Bristol, University Walk, Bristol BS8 1TD, United Kingdom; Department of Pharmacology, University of Colorado Denver School of Medicine, Aurora, Colorado 80045. Electronic address: katharine.r.smith@ucdenver.edu.
Dipen RajgorCentre for Synaptic Plasticity and School of Biochemistry, Biomedical Sciences Building, University of Bristol, University Walk, Bristol BS8 1TD, United Kingdom.
Jonathan G HanleyCentre for Synaptic Plasticity and School of Biochemistry, Biomedical Sciences Building, University of Bristol, University Walk, Bristol BS8 1TD, United Kingdom.
University of Bristol · GB

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research Council MR/L011131/1Wellcome Trust
6 · The paper itself

Abstract

Brain ischemia causes oxygen and glucose deprivation (OGD) in neurons, triggering a cascade of events leading to synaptic accumulation of glutamate. Excessive activation of glutamate receptors causes excitotoxicity and delayed cell death in vulnerable neurons. Following global cerebral ischemia, hippocampal CA1 pyramidal neurons are more vulnerable to injury than their cortical counterparts, but the mechanisms that underlie this difference are unclear. Signaling via Rho-family small GTPases, their upstream guanine nucleotide exchange factors, and GTPase-activating proteins (GAPs) is differentially dysregulated in response to OGD/ischemia in hippocampal and cortical neurons. Increased Rac1 activity caused by OGD/ischemia contributes to neuronal death in hippocampal neurons via diverse effects on NADPH oxidase activity and dendritic spine morphology. The Rac1 guanine nucleotide exchange factor Tiam1 mediates an OGD-induced increase in Rac1 activity in hippocampal neurons; however, the identity of an antagonistic GAP remains elusive. Here we show that the Rac1 GAP breakpoint cluster region (BCR) associates with NMDA receptors (NMDARs) along with Tiam1 and that this protein complex is more abundant in hippocampal compared with cortical neurons. Although total BCR is similar in the two neuronal types, BCR is more active in hippocampal compared with cortical neurons. OGD causes an NMDAR- and Ca

Indexed as

Gene Expression RegulationHypoxiaAnimalsBrain IschemiaCells, CulturedCerebral CortexGlucoseGTPase-Activating ProteinsHippocampusNeuronsOxygenrac1 GTP-Binding ProteinRatsRats, WistarReceptors, N-Methyl-D-AspartateT-Lymphoma Invasion and Metastasis-inducing Protein 1Bcr protein, ratGlucoseGTPase-Activating ProteinsOxygenrac1 GTP-Binding ProteinRac1 protein, ratReceptors, N-Methyl-D-AspartateTiam1 protein, ratT-Lymphoma Invasion and Metastasis-inducing Protein 1BCRcortexGTPase-activating protein (GAP)guanine nucleotide exchange factor (GEF)hippocampusischemiaNMDA receptor (NMDAR)OGDTiam1

Identifiers

PMID29046349
PMCPMC5724004
OpenAlexW2766288854

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.