Evidence map›Paper›PMID 24583056›Full record

ArticleNeurobiology of disease2014

PRAS40 plays a pivotal role in protecting against stroke by linking the Akt and mTOR pathways.

Xiaoxing Xiong, Rong Xie, Hongfei Zhang, Lijuan Gu, Weiying Xie, Michelle Cheng, Zhihong Jian, Kristina Kovacina, Heng Zhao

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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

52 citing papers in PubMed, 87 citations in OpenAlex.

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  8. Cognitive Impairment in Multiple Sclerosis.Bioengineering (Basel, Switzerland) · 2023
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  15. Article
  16. New Insights for nicotinamide: Metabolic disease, autophagy, and mTOR.Frontiers in bioscience (Landmark edition) · 2020
    Review
  17. PTEN inhibitor VO-OHpic suppresses TSC2Experimental and therapeutic medicine · 2020
    Article
  18. Silencing the lncRNAJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Article
  19. Article
  20. Review
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

9 authors at 1 institution in 2 countries.

Xiaoxing XiongDepartment of Neurosurgery, Stanford University, Stanford, CA 94305, USA.
Rong XieDepartment of Neurosurgery, Stanford University, Stanford, CA 94305, USA; Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai 200040, China.
Hongfei ZhangDepartment of Neurosurgery, Stanford University, Stanford, CA 94305, USA.
Lijuan GuDepartment of Neurosurgery, Stanford University, Stanford, CA 94305, USA.
Weiying XieDepartment of Neurosurgery, Stanford University, Stanford, CA 94305, USA.
Michelle ChengDepartment of Neurosurgery, Stanford University, Stanford, CA 94305, USA.
Zhihong JianDepartment of Neurosurgery, Stanford University, Stanford, CA 94305, USA.
Kristina KovacinaDepartment of Chemical and Systems Biology, Stanford University, Stanford, CA 94305, USA.
Heng ZhaoDepartment of Neurosurgery, Stanford University, Stanford, CA 94305, USA. Electronic address: hzhao@stanford.edu.
Stanford University · US

Funding

Protective mechanisms of ischemic postconditioningR01NS064136 · NINDS · STANFORD UNIVERSITY · PI STEINBERG, GARY K · 2010 to 2020
$3.1M
NINDS NIH HHS 1R01NS064136-01NINDS NIH HHS R01 NS064136
6 · The paper itself

Abstract

The proline-rich Akt substrate of 40kDa (PRAS40) protein is not only a substrate of the protein kinase Akt but also a component of the mTOR complex 1 (mTORC1), thus it links the Akt and the mTOR pathways. We investigated the potential protective role of PRAS40 in cerebral ischemia and its underlying mechanisms by using rats with lentiviral over-expression of PRAS40 and mice with PRAS40 gene knockout (PRAS40 KO). Our results show that gene transfer of PRAS40 reduced infarction size in rats by promoting phosphorylation of Akt, FKHR (FOXO1), PRAS40, and mTOR. In contrast, PRAS40 KO increased infarction size. Although the PRAS40 KO under normal condition did not alter baseline levels of phosphorylated proteins in the Akt and mTOR pathways, PRAS40 KO that underwent stroke exhibited reduced protein levels of p-S6K and p-S6 in the mTOR pathway but not p-Akt, or p-PTEN in the Akt pathway. Furthermore, co-immunoprecipitation suggests that there were less interactive effects between Akt and mTOR in the PRAS40 KO. In conclusion, PRAS40 appears to reduce brain injury by converting cell signaling from Akt to mTOR.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsBrainBrain IschemiaCell DeathCells, CulturedForkhead Box Protein O1Forkhead Transcription FactorsGene Transfer TechniquesMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsNeuronsPhosphoproteinsPhosphorylationProto-Oncogene Proteins c-aktAdaptor Proteins, Signal TransducingAkt1s1 protein, ratForkhead Box Protein O1Forkhead Transcription FactorsFoxo1 protein, mouseFoxo1 protein, ratmTOR protein, mousemTOR protein, ratNerve Tissue ProteinsPhosphoproteinsproline-rich Akt substrate, 40 kDa protein, mouseProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAktFocal cerebral ischemiamTORPRAS40PTENStroke

Identifiers

PMID24583056
PMCPMC4448971
OpenAlexW2019551003

What OpenQuestion holds

Textmetadata
LicenceTDM
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.