ArticleMolecular carcinogenesis2010
AMPK-mediated phosphorylation of murine p27 at T197 promotes binding of 14-3-3 proteins and increases p27 stability.
Article in Molecular carcinogenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- Chrono-Pharmacology for Cancer: Harnessing Circadian Regulations of the Cell Cycle and Immune Response Dynamics for Precision Therapy.ACS pharmacology & translational science · 2025Review
- Crosstalk between the circadian clock, intestinal stem cell niche, and epithelial cell fate decision.Genes & diseases · 2025Review
- Alpha lipoic acid diminishes migration and invasion in hepatocellular carcinoma cells through an AMPK-p53 axis.Scientific reports · 2024Article
- 14-3-3 Protein-Protein Interactions: From Mechanistic Understanding to Their Small-Molecule Stabilization.Chembiochem : a European journal of chemical biology · 2024Review
- Single-cell landscape analysis unravels molecular programming of the human B cell compartment in chronic GVHD.JCI insight · 2023Article
- Deregulation of the cyclin-dependent kinase inhibitor p27 as a putative candidate for transformation inAIMS microbiology · 2023Article
- p27 controls autophagic vesicle trafficking in glucose-deprived cells via the regulation of ATAT1-mediated microtubule acetylation.Cell death & disease · 2021Article
- p27 controls Ragulator and mTOR activity in amino acid-deprived cells to regulate the autophagy-lysosomal pathway and coordinate cell cycle and cell growth.Nature cell biology · 2020Article
- PCK1 negatively regulates cell cycle progression and hepatoma cell proliferation via the AMPK/p27Journal of experimental & clinical cancer research : CR · 2019Article
- The tuberous sclerosis complex subunit TBC1D7 is stabilized by Akt phosphorylation-mediated 14-3-3 binding.The Journal of biological chemistry · 2018Article
- AMPKα2 Regulates Bladder Cancer Growth through SKP2-Mediated Degradation of p27.Molecular cancer research : MCR · 2016Article
- Inhibitory effect of NBL1 on PDGF-BB-induced human PASMC proliferation through blockade of PDGFβ-p38MAPK pathway.Bioscience reports · 2016Article
- Minireview: hey U(PS): metabolic and proteolytic homeostasis linked via AMPK and the ubiquitin proteasome system.Molecular endocrinology (Baltimore, Md.) · 2014Review
- 14-3-3-β and -{varepsilon} contribute to activation of the osmoprotective transcription factor NFAT5 by increasing its protein abundance and its transactivating activity.Physiological reports · 2014Article
- AMP-activated protein kinase suppresses the in vitro and in vivo proliferation of hepatocellular carcinoma.PloS one · 2014Article
- Fbxl12 triggers G1 arrest by mediating degradation of calmodulin kinase I.Cellular signalling · 2013Article
- Phosphorylation of serine 1137/1138 of mouse insulin receptor substrate (IRS) 2 regulates cAMP-dependent binding to 14-3-3 proteins and IRS2 protein degradation.The Journal of biological chemistry · 2013Article
- Assembly, activation, and substrate specificity of cyclin D1/Cdk2 complexes.Biochemistry · 2013Article
- Activation of AMP-activated protein kinase inhibits the proliferation of human endothelial cells.The Journal of pharmacology and experimental therapeutics · 2012Article
- Consequences of interrupted Rheb-to-AMPK feedback signaling in tuberous sclerosis complex and cancer.Small GTPases · 2011Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
The tuberous sclerosis complex 2 (Tsc2) gene product, tuberin, acts as a negative regulator of mTOR signaling, and loss of tuberin function leads to tumors of the brain, skin, kidney, heart, and lungs. Previous studies have shown that loss of tuberin function affects the stability and subcellular localization of the cyclin-dependent kinase inhibitor (CKI) p27, although the mechanism(s) by which tuberin modulates p27 stability has/have not been elucidated. Previous studies have also shown that AMP-activated protein kinase (AMPK), which functions in an energy-sensing pathway in the cell, becomes activated in the absence of tuberin. Here we show that in Tsc2-null tumors and cell lines, AMPK activation correlates with an increase in p27 levels, and inhibition of AMPK signaling decreases p27 levels in these cells. In addition, activation of AMPK led to phosphorylation of p27 at the conserved terminal threonine residue of murine p27 (T197) in both in vitro kinase assays and in cells. Phosphorylation of p27 at T197 led to increased interaction between p27 and 14-3-3 proteins and increased the protein stability of p27. Furthermore, activation of AMPK signaling promoted the interaction between p27 and 14-3-3 proteins and increased the stability of the p27 protein in a manner that was dependent on T197. These data identify a conserved mechanism for the regulation of p27 stability via phosphorylation at the terminal threonine (mT197/hT198) and binding of 14-3-3 proteins, which when AMPK is activated results in stabilization of the p27 protein.
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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 Socratic graph.