Evidence map›Paper›PMID 28179579›Full record

ArticleOncotarget2017

Designing of dual inhibitors for GSK-3β and CDK5: Virtual screening and in vitro biological activities study.

Hongbo Xie, Haixia Wen, Denan Zhang, Lei Liu, Bo Liu, Qiuqi Liu, Qing Jin, Kehui Ke, Ming Hu, Xiujie Chen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. GSK3β and Tau Protein in Alzheimer's Disease and Epilepsy.Frontiers in cellular neuroscience · 2020
    Article
  11. Review
  12. 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 at 1 institution in 1 country.

Hongbo XieDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, P. R. China.
Haixia WenDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, P. R. China.
Denan ZhangDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, P. R. China.
Lei LiuDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, P. R. China.
Bo LiuDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, P. R. China.
Qiuqi LiuDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, P. R. China.
Qing JinDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, P. R. China.
Kehui KeDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, P. R. China.
Ming HuDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, P. R. China.
Xiujie ChenDepartment of Pharmacogenomics, College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150086, P. R. China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease is a multifactorial neurodegenerative disorder with many drug targets contributing to its etiology. Despite the devastating effects of this disease, therapeutic methods for treating Alzheimer's disease remain limited. The multifactorial nature of Alzheimer's disease strongly supports a multi-target rationale as a drug design strategy. Glycogen synthase kinase-3 beta and cyclin-dependent kinase 5 have been identified as being involved in the pathological hyperphosphorylation of tau proteins, which leads to the formation of neurofibrillary tangles and causes Alzheimer's disease. In this study, using a molecular docking method to screen a virtual library, we discovered molecules that can simultaneously inhibit Glycogen synthase kinase-3 beta and cyclin-dependent kinase 5 as lead compounds for the treatment of Alzheimer's disease. The docking results revealed the key residues in the substrate binding sites of both Glycogen synthase kinase-3 beta and cyclin-dependent kinase 5. A receiver operating characteristic curve indicated that the docking model consistently and selectively scored the majority of active compounds above decoys. The pre-treatment of cells with screened compounds protected them against Aβ25-35- induced cell death by up to 80%. Collectively, these findings suggest that some compounds have potential to be promising multifunctional agents for Alzheimer's disease treatment.

Indexed as

Alzheimer DiseaseDrug DesignCell LineCyclin-Dependent Kinase 5Enzyme InhibitorsGlycogen Synthase Kinase 3 betaHumansMolecular Docking SimulationNeuronsNeuroprotective AgentsROC CurveCDK5 protein, humanCyclin-Dependent Kinase 5Enzyme InhibitorsGlycogen Synthase Kinase 3 betaNeuroprotective AgentsAlzheimer’s diseaseCDK5GSK-3βmulti-target

Identifiers

PMID28179579
PMCPMC5392312
OpenAlexW2585381782

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.