ReviewBiochimica et biophysica acta. Molecular cell research2020
Glycogen synthase kinase (GSK)-3 and the double-strand RNA-dependent kinase, PKR: When two kinases for the common good turn bad.
Review in Biochimica et biophysica acta. Molecular cell research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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.
Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Association Between CDH1 Downregulation and Lymphocyte Cell-Cycle Dysfunction in Alzheimer's Disease and Mild Cognitive Impairment.Cellular and molecular neurobiology · 2026Article
- NF-κB signaling pathway in osteosarcoma: from signaling networks to targeted therapy.Frontiers in oncology · 2025Review
- Activation of protein kinase receptor (PKR) plays a pro-viral role in mammarenavirus-infected cells.Journal of virology · 2024Article
- Isoform-Directed Control of c-Myc Functions: Understanding the Balance from Proliferation to Growth Arrest.International journal of molecular sciences · 2023Review
- Interferon regulates neural stem cell function at all ages by orchestrating mTOR and cell cycle.EMBO molecular medicine · 2023Article
- Innate Immunity: A Balance between Disease and Adaption to Stress.Biomolecules · 2022Review
- Revisiting the Role of GSK3, A Modulator of Innate Immunity, in Idiopathic Inclusion Body Myositis.Cells · 2021Review
- Review
- Activation of GSK3 Prevents Termination of TNF-Induced Signaling.Journal of inflammation research · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycogen synthase kinase (GSK)-3α/β and the double-stranded RNA-dependent kinase PKR are two sentinel kinases that carry-out multiple similar yet distinct functions in both the cytosol and the nucleus. While these kinases belong to separate signal transduction cascades, they demonstrate an uncanny propensity to regulate many of the same proteins either through direct phosphorylation or by altering transcription/translation, including: c-MYC, NF-κB, p53 and TAU, as well as each another. A significant number of studies centered on the GSK3 kinases have led to the identification of the GSK3 interactome and a number of substrates, which link GSK3 activity to metabolic control, translation, RNA splicing, ribosome biogenesis, cellular division, DNA repair and stress/inflammatory signaling. Interestingly, many of these same pathways and processes are controlled by PKR, but unlike the GSK3 kinases, a clear picture of proteins interacting with PKR and a complete listing of its substrates is still missing. In this review, we take a detailed look at what is known about the PKR and GSK3 kinases, how these kinases interact to influence common cellular processes (innate immunity, alternative splicing, translation, glucose metabolism) and how aberrant activation of these kinases leads to diseases such as Alzheimer's disease (AD), diabetes mellitus (DM) and cancer.
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Identifiers
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Registered trials
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.