ArticleMolecular and cellular biochemistry2006
Hypertonicity activates GSK3beta in tumor cells.
Article in Molecular and cellular biochemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- How do kinases contribute to tonicity-dependent regulation of the transcription factor NFAT5?World journal of nephrology · 2016Review
- Quantitative molecular phenotyping of gill remodeling in a cichlid fish responding to salinity stress.Molecular & cellular proteomics : MCP · 2013Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Responses to perturbations in the composition of the extracellular environment are crucial to maintain cell and tissue homeostasis. In hypertonic conditions cell lines derived from kidney epithelium initiate a variety of stress responses to maintain cell viability that include activation of Mitogen Activated Protein Kinases (MAPK). We previously showed that NaCl also regulates MAPK in different tumor cell lines and we now show that when hypertonic conditions induced with NaCl and other osmolytes were used to stimulate several tumor cell lines, Glycogen Synthase Kinase 3beta (GSK3beta) was rapidly dephosphorylated at serine 9 and its kinase activity was increased. This response was both time- and dose-dependent, it was independent of the Akt signaling pathway and did not increase steady state levels of phosphorylation of beta-catenin, although the data suggested that activated GSK3beta could regulate the activity of ERK1/2.
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Registered trials
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