ReviewBiochemical pharmacology2018
A partnership with the proteasome; the destructive nature of GSK3.
Review in Biochemical pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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.
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Who cites it
52 citing papers in PubMed, 94 citations in OpenAlex.
- The ZBTB16/CUL3/ROC1 ubiquitin ligase drives the degradation of pathogenic pendrin (SLC26A4) protein variants.Journal of biomedical science · 2026Article
- Divergent transcriptomic pathways underlie sex-biased cognitive rescue by developmental GSK3B inhibition in a mouse model of 22q11.2 deletion syndrome.Translational psychiatry · 2026Article
- Dual modulation of Wnt and inflammatory pathways by Gingerenone a inhibits colorectal tumorigenesis.Molecular biology reports · 2026Article
- Article
- βTrCP facilitates MRN complex localization on chromatin to enhance DNA repair.Communications biology · 2025Article
- Inhibition of virally induced TFEB proteasomal degradation as a host-centric therapeutic approach for coronaviral infection.Science advances · 2025Article
- The Yeast Gsk-3 Kinase Mck1 Is Necessary for Cell Wall Remodeling in Glucose-Starved and Cell Wall-Stressed Cells.International journal of molecular sciences · 2025Article
- Bioinformatics analysis of PSAT1 loss identifies downstream pathways regulated in EGFR mutant NSCLC and a selective gene signature for predicting the risk of relapse.Oncology letters · 2025Article
- Article
- GSK3-Driven Modulation of Inflammation and Tissue Integrity in the Animal Model.International journal of molecular sciences · 2024Review
- Inhibition of mitochondrial cyclophilin D, a downstream target of glycogen synthase kinase 3α, improves sperm motility.Reproductive biology and endocrinology : RB&E · 2024Article
- The anti-inflammatory cytokine IL-37 improves the NK cell-mediated anti-tumor response.Oncoimmunology · 2024Article
- The SGK3-Catalase antioxidant signaling axis drives cervical cancer growth and therapy resistance.Redox biology · 2023Article
- Sex differences in the cardiac stress response following SARS-CoV-2 infection of ferrets.American journal of physiology. Heart and circulatory physiology · 2023Article
- Review
- Regulation of ABC transporters by sex steroids may explain differences in drug resistance between sexes.Journal of physiology and biochemistry · 2023Review
- Mechanisms of NURR1 Regulation: Consequences for Its Biological Activity and Involvement in Pathology.International journal of molecular sciences · 2023Review
- Signal Pathways and microRNAs in Osteosarcoma Growth and the Dual Role of Mesenchymal Stem Cells in Oncogenesis.International journal of molecular sciences · 2023Review
- Nrf2 in TIME: The Emerging Role of Nuclear Factor Erythroid 2-Related Factor 2 in the Tumor Immune Microenvironment.Molecules and cells · 2023Review
- Glycogen Synthase Kinase-3 Isoform Variants and Their Inhibitory Phosphorylation in Human Testes and Spermatozoa.The world journal of men's health · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Glycogen Synthase Kinase-3 (GSK3) was originally reported as a key enzyme of glucose homeostasis through regulation of the rate of glycogen synthesis. It has subsequently been found to influence most cellular processes, including growth, differentiation and death, as part of its role in modulating response to hormonal, nutritional and cellular stress stimuli. More than 100 protein targets for GSK3 have been proposed although only a small fraction of these have been convincingly validated in physiological cell systems. The effects of GSK3 phosphorylation on substrates include alteration of enzyme activity, protein localisation, protein:protein interaction and protein stability. This latter form of regulation of GSK3 substrates is the focus of this review. There is an ever-growing list of GSK3 substrates that upon phosphorylation are targeted to the beta-transducin repeat containing protein (β-TrCP), thereby allowing ubiquitination of bound protein by cullin-1 and so initiating destruction at the proteasome. We propose the existence of a GSK3-β-TrCP 'destruction hit-list' that allows co-ordinated removal (or stabilisation) of a set of proteins with a common physiological purpose, through control of GSK3. We identify 29 proteins where there is relatively strong evidence for regulation by a GSK3-β-TrCP axis and note common features of regulation and pathophysiology. Furthermore, we assess the potential of pre-phosphorylation (priming) of these targets (normally a prerequisite for GSK3 recognition) to provide a second layer of regulation delineated by the priming kinase that allows GSK3 to mark them for destruction. Finally, we discuss whether this knowledge improves options for therapeutic intervention.
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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.