ArticleCell cycle (Georgetown, Tex.)2011
A GSK-3-mediated transcriptional network maintains repression of immediate early genes in quiescent cells.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
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- Activation of the Mevalonate Pathway in Response to Anti-cancer Treatments Drives Glioblastoma Recurrences Through Activation of Rac-1.Cancer research communications · 2024Article
- Network model of skeletal muscle cell signalling predicts differential responses to endurance and resistance exercise training.Experimental physiology · 2024Article
- A large-scale transgenic RNAi screen identifies transcription factors that modulate myofiber size in Drosophila.PLoS genetics · 2021Article
- Glycogen synthase kinase-3β inhibitor SB216763 promotes DNA repair in ischemic retinal neurons.Neural regeneration research · 2021Article
- Activation of GSK3 Prevents Termination of TNF-Induced Signaling.Journal of inflammation research · 2021Article
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- GSK3β inhibition attenuates LPS-induced IL-6 expression in porcine adipocytes.Scientific reports · 2018Article
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- Transcriptional regulation of pig GYS1 gene by glycogen synthase kinase 3β (GSK3β).Molecular and cellular biochemistry · 2017Article
- GSK-3 as potential target for therapeutic intervention in cancer.Oncotarget · 2014Review
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- Polo-like kinase 4 transcription is activated via CRE and NRF1 elements, repressed by DREAM through CDE/CHR sites and deregulated by HPV E7 protein.Nucleic acids research · 2014Article
- The Mck1 GSK-3 kinase inhibits the activity of Clb2-Cdk1 post-nuclear division.Cell cycle (Georgetown, Tex.) · 2012Article
- Coordinating Gene Expression and Axon Assembly to Control Axon Growth: Potential Role of GSK3 Signaling.Frontiers in molecular neuroscience · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Glycogen synthase kinase-3 (GSK-3) plays a central role in cell survival and proliferation, in part by the regulation of transcription. Unlike most protein kinases, GSK-3 is active in quiescent cells in the absence of growth factor signaling. In a recent series of studies, we employed a systems-level approach to understanding the transcription network regulated by GSK-3 in a quiescent cell model. We identified a group of immediate early genes that were upregulated in quiescent cells solely by the inhibition of GSK-3 in the absence of growth factor stimulation. Computational analysis of the upstream sequences of these genes identified statistically over-represented binding sites for the transcription factors CREB, NFκB and AP-1, and the roles of these factors in regulating expression of GSK-3 target genes were verified by chromatin immunoprecipitation and RNA interference. In quiescent cells, GSK-3 inhibits CREB, NFκB and AP-1, thereby maintaining repression of their target genes and contributing to maintenance of cell cycle arrest.
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Registered trials
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