Evidence map›Paper›PMID 28790888›Full record

ArticleFrontiers in molecular neuroscience2017

Amyloid β1-42 (Aβ1-42) Induces the CDK2-Mediated Phosphorylation of Tau through the Activation of the mTORC1 Signaling Pathway While Promoting Neuronal Cell Death.

Ki Hoon Lee, Sei-Jung Lee, Hyun Jik Lee, Gee Euhn Choi, Young Hyun Jung, Dah Ihm Kim, Amr Ahmed Gabr, Jung Min Ryu, Ho Jae Han

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

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  16. Molecular crosstalk between cancer and neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2020
    Review
  17. Review
  18. Neuroprotective effects of urolithin A on HNutrition research and practice · 2020
    Article
  19. Article
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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 4 institutions in 2 countries.

Ki Hoon LeeDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science and BK21 PLUS Program for Creative Veterinary Science Research Center, Seoul National UniversitySeoul, South Korea.
Sei-Jung LeeDepartment of Pharmaceutical Engineering, Daegu Haany UniversityGyeongsan, South Korea.
Hyun Jik LeeDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science and BK21 PLUS Program for Creative Veterinary Science Research Center, Seoul National UniversitySeoul, South Korea.
Gee Euhn ChoiDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science and BK21 PLUS Program for Creative Veterinary Science Research Center, Seoul National UniversitySeoul, South Korea.
Young Hyun JungDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science and BK21 PLUS Program for Creative Veterinary Science Research Center, Seoul National UniversitySeoul, South Korea.
Dah Ihm KimDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science and BK21 PLUS Program for Creative Veterinary Science Research Center, Seoul National UniversitySeoul, South Korea.
Amr Ahmed GabrDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science and BK21 PLUS Program for Creative Veterinary Science Research Center, Seoul National UniversitySeoul, South Korea.
Jung Min RyuDepartment of Veterinary Physiology, College of Veterinary Medicine, Chonnam National UniversityGwangju, South Korea.
Ho Jae HanDepartment of Veterinary Physiology, College of Veterinary Medicine, Research Institute for Veterinary Science and BK21 PLUS Program for Creative Veterinary Science Research Center, Seoul National UniversitySeoul, South Korea.
Seoul National University · KRCairo University · EGChonnam National University · KRDaegu Haany University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder, characterized by cognitive impairment and memory loss. Amyloid β1-42 (Aβ) and hyper-phosphorylation of microtubule-associated protein tau have been considered as major histological features in AD. However, the mechanism of how Aβ induces the hyper-phosphorylation of tau remains to be clarified. In the present study, we investigated the underlying cellular mechanisms of Aβ with regard to the cell cycle regulatory protein-mediated phosphorylation of tau in promoting neuronal cell death. The oligomer Aβ (5 μM) significantly increased the level of caspase 3 cleavage and has the ability to induce cytotoxicity in human neuroblastoma SK-N-MC cells. Aβ induced the degree of extracellular calcium influx via the L-type channel to facilitate the production of reactive oxygen species (ROS). Aβ signaling through ROS production is uniquely mediated by the activation of PI3K/Akt, which is in turn required for mammalian target of rapamycin complex 1 (mTORC1) phosphorylation. mTORC1 activated by Aβ further increased the phosphorylation of eukaryotic translation initiation factor 4E (eIF4E), a binding protein (4E-BP1) and p70S6K1 to stimulate the HIF1α synthesis responsible for the induction of cyclinD

Indexed as

Alzheimer’s diseasecyclin dependent kinase 2mammalian target of rapamycinneuronal cell deathtauopathy

Identifiers

PMID28790888
PMCPMC5522873
OpenAlexW2739316300

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.