Evidence map›Paper›PMID 33339170›Full record

ReviewBiomolecules2020

GSK3α: An Important Paralog in Neurodegenerative Disorders and Cancer.

Octavio Silva-García, Ricarda Cortés-Vieyra, Francisco N Mendoza-Ambrosio, Guillermo Ramírez-Galicia, Víctor M Baizabal-Aguirre

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Interactomes of Glycogen Synthase Kinase-3 Isoforms.Journal of proteome research · 2023
    Article
  4. Article
  5. Article
  6. Targets and mechanisms ofFrontiers in aging neuroscience · 2022
    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

5 authors at 3 institutions in 1 country.

Octavio Silva-GarcíaDepartamento de Química Teórica, Universidad del Papaloapan, Oaxaca 68301, Mexico.
Ricarda Cortés-VieyraCentro de Investigación Biomédica de Michoacán, Instituto Mexicano del Seguro Social, Michoacán 58000, Mexico.
Francisco N Mendoza-AmbrosioDepartamento de Química Teórica, Universidad del Papaloapan, Oaxaca 68301, Mexico.
Guillermo Ramírez-GaliciaDepartamento de Química Teórica, Universidad del Papaloapan, Oaxaca 68301, Mexico.
Víctor M Baizabal-AguirreCentro Multidisciplinario de Estudios en Biotecnología, Facultad de Medicina Veterinaria y Zootecnia, Universidad Michoacana de San Nicolás de Hidalgo, Michoacán 58893, Mexico.
Universidad del Papaloapan · MXMexican Social Security Institute · MXUniversidad Michoacana de San Nicolás de Hidalgo · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The biological activity of the enzyme glycogen synthase kinase-3 (GSK3) is fulfilled by two paralogs named GSK3α and GSK3β, which possess both redundancy and specific functions. The upregulated activity of these proteins is linked to the development of disorders such as neurodegenerative disorders (ND) and cancer. Although various chemical inhibitors of these enzymes restore the brain functions in models of ND such as Alzheimer's disease (AD), and reduce the proliferation and survival of cancer cells, the particular contribution of each paralog to these effects remains unclear as these molecules downregulate the activity of both paralogs with a similar efficacy. Moreover, given that GSK3 paralogs phosphorylate more than 100 substrates, the simultaneous inhibition of both enzymes has detrimental effects during long-term inhibition. Although the GSK3β kinase function has usually been taken as the global GSK3 activity, in the last few years, a growing interest in the study of GSK3α has emerged because several studies have recognized it as the main GSK3 paralog involved in a variety of diseases. This review summarizes the current biological evidence on the role of GSK3α in AD and various types of cancer. We also provide a discussion on some strategies that may lead to the design of the paralog-specific inhibition of GSK3α.

Indexed as

Alzheimer DiseaseAnimalsBrain NeoplasmsCarcinoma, Pancreatic DuctalFemaleGlycogen Synthase Kinase 3HL-60 CellsHumansInhibitory Concentration 50Leukemia, Myeloid, AcuteLung NeoplasmsMaleMolecular Docking SimulationMultiple MyelomaNeurodegenerative DiseasesPhosphorylationGlycogen Synthase Kinase 3glycogen synthase kinase 3 alphaProtein Serine-Threonine KinasesAlzheimer’s diseasecancerGSK3GSK3 structureGSK3αGSK3β

Identifiers

PMID33339170
PMCPMC7765659
OpenAlexW3112569863

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.