Evidence map›Paper›PMID 26526334›Full record

ArticleCellular and molecular neurobiology2016

Ischemia-Induced Changes of PRAS40 and p-PRAS40 Immunoreactivities in the Gerbil Hippocampal CA1 Region After Transient Cerebral Ischemia.

Joon Ha Park, Bich Na Shin, Ji Hyeon Ahn, Jeong-Hwi Cho, In Hye Kim, Dae Won Kim, Moo-Ho Won, Seongkweon Hong, Jun Hwi Cho, Choong-Hyun Lee

Abstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. PRAS40 signaling in tumor.Oncotarget · 2017
    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

10 authors.

Joon Ha ParkDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea.
Bich Na ShinDepartment of Physiology, College of Medicine, Hallym University, Chuncheon, 200-702, South Korea.
Ji Hyeon AhnDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea.
Jeong-Hwi ChoDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea.
In Hye KimDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea.
Dae Won KimDepartment of Biochemistry and Molecular Biology, College of Dentistry, and Research Institute of Oral Sciences, Kangnung-Wonju National University, Gangneung, 210-702, South Korea.
Moo-Ho WonDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea.
Seongkweon HongDepartment of Surgery, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea.
Jun Hwi ChoDepartment of Emergency Medicine, College of Medicine, School of Medicine, Kangwon National University, Chuncheon, 200-701, South Korea. cjhemd@kangwon.ac.kr.
Choong-Hyun LeeDepartment of Pharmacy, College of Pharmacy, Dankook University, Cheonan, 330-714, South Korea. anaphy@dankook.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proline-rich Akt substrate of 40-kDa (PRAS40) is one of the important interactive linkers between Akt and mTOR signaling pathways. The increase of PRAS40 is related with the reduction of brain damage induced by cerebral ischemia. In the present study, we investigated time-dependent changes in PRAS40 and phospho-PRAS40 (p-PRAS40) immunoreactivities in the hippocampal CA1 region of the gerbil after 5 min of transient cerebral ischemia. PRAS40 immunoreactivity in the CA1 region was decreased in pyramidal neurons from 12 h after ischemic insult in a time-dependent manner, and, at 5 days post-ischemia, PRAS40 immunoreactivity was newly expressed in astrocytes. p-PRAS40 immunoreactivity in the CA1 pyramidal neurons was hardly found 12 h and apparently detected again 1 and 2 days after ischemic insult. At 5 days post-ischemia, p-PRAS40 immunoreactivity in the CA1 pyramidal neurons was not found. These results indicate that ischemia-induced changes in PRAS40 and p-PRAS40 immunoreactivities in CA1 pyramidal neurons and astrocytes may be closely associated with delayed neuronal death in the hippocampal CA1 region following transient cerebral ischemia.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAstrocytesCA1 Region, HippocampalCell DeathGerbillinaeImmunohistochemistryIschemic Attack, TransientPyramidal CellsAdaptor Proteins, Signal TransducingAstrocyteDelayed neuronal deathPRAS40Transient global cerebral ischemia

Identifiers

PMID26526334
PMCPMC11482446

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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.