Evidence map›Paper›PMID 14973226›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Neuroprotective role of a proline-rich Akt substrate in apoptotic neuronal cell death after stroke: relationships with nerve growth factor.

Atsushi Saito, Purnima Narasimhan, Takeshi Hayashi, Shuzo Okuno, Michel Ferrand-Drake, Pak H Chan

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 109 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Minocycline-preconditioned neural stem cells enhance neuroprotection after ischemic stroke in rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 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

6 authors at 1 institution in 1 country.

Atsushi SaitoDepartment of Neurosurgery, Stanford University School of Medicine, Stanford, California 94305-5487, USA.
Purnima Narasimhan
Takeshi Hayashi
Shuzo Okuno
Michel Ferrand-Drake
Pak H Chan
Stanford University · US

Funding

Transgenic Animal CoreP50NS014543 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI GIFFARD, RONA G · 1990 to 2007
$8.2M
Reperfusion and Neurovascular Injury in StrokeR01NS025372 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CHAN, PAK H · 1988 to 2015
$5.0M
Cell Death/Survival After Global Cerebral IschemiaR01NS038653 · NINDS · STANFORD UNIVERSITY · PI CHAN, PAK H · 1998 to 2013
$4.5M
OXYGEN RADICALS AND NEURONAL APOPTOSIS IN FOCAL STROKER01NS036147 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CHAN, PAK H · 1997 to 2010
$3.8M
NINDS NIH HHS P50 NS014543NINDS NIH HHS P50NS14543NINDS NIH HHS R01 NS025372NINDS NIH HHS R01 NS036147NINDS NIH HHS R01 NS038653NINDS NIH HHS R01NS25372NINDS NIH HHS R01NS36147NINDS NIH HHS R01NS38653
6 · The paper itself

Abstract

The Akt signaling pathway contributes to regulation of apoptosis after a variety of cell death stimuli. A novel proline-rich Akt substrate (PRAS) was recently detected and found to be involved in apoptosis. In our study, Akt activation was modulated by growth factors, and treatment with nerve growth factor (NGF) reduced apoptotic cell death after ischemic injury. However, the role of the PRAS pathway in apoptotic neuronal cell death after ischemia remains unknown. Phosphorylated PRAS (pPRAS) and the binding of pPRAS/phosphorylated Akt (pPRAS/pAkt) to 14-3-3 (pPRAS/14-3-3) were detected, and their expression transiently decreased in mouse brains after transient focal cerebral ischemia (tFCI). Liposome-mediated pPRAS cDNA transfection induced overexpression of pPRAS, promoted pPRAS/14-3-3, and inhibited apoptotic neuronal cell death after tFCI. The expression of pPRAS, pPRAS/pAkt, and pPRAS/14-3-3 increased in NGF-treated mice but decreased with inhibition of phosphatidylinositol-3 kinase and the NGF receptor after tFCI. These results suggest that PRAS phosphorylation and its interaction with pAkt and 14-3-3 might play an important role in neuroprotection mediated by NGF in apoptotic neuronal cell death after tFCI.

Indexed as

Protein Serine-Threonine Kinases14-3-3 ProteinsAdaptor Proteins, Signal TransducingAnimalsAntibody SpecificityApoptosisBlotting, WesternCaspase 3CaspasesCell SurvivalDisease Models, AnimalEnzyme InhibitorsGene Expression RegulationGene Transfer TechniquesInfarction, Middle Cerebral ArteryMale14-3-3 ProteinsAdaptor Proteins, Signal TransducingAKT1S1 protein, humanCASP3 protein, humanCasp3 protein, mouseCaspase 3CaspasesEnzyme InhibitorsNerve Growth FactorNeuroprotective AgentsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphoproteinsProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktTyrosine 3-Monooxygenase

Identifiers

PMID14973226
PMCPMC6730448
OpenAlexW2072523093

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.