ArticleMolecular and cellular biology2006
Only Akt1 is required for proliferation, while Akt2 promotes cell cycle exit through p21 binding.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 175 citations in OpenAlex.
- Characterization of myogenesis in European sea bass (Dicentrarchus labrax) using primary white muscle cell cultures.Scientific reports · 2025Article
- Phosphorylation of plectin by Akt3 promotes triple-negative breast cancer cell invasive migration.iScience · 2025Article
- Research progress on the mechanism of common inflammatory pathways in the pathogenesis and development of lymphoma.Annals of medicine · 2024Review
- Calorie restriction and rapamycin distinctly mitigate aging-associated protein phosphorylation changes in mouse muscles.Communications biology · 2024Article
- Role of EGFR and FASN in breast cancer progression.Journal of cell communication and signaling · 2023Review
- Differential activation of AKT isoforms by growth factors in human myotubes.Physiological reports · 2023Article
- Interfering with the Ubiquitin-Mediated Regulation of Akt as a Strategy for Cancer Treatment.International journal of molecular sciences · 2023Review
- Finnish-specific AKT2 gene variant leads to impaired insulin signalling in myotubes.Journal of molecular endocrinology · 2023Article
- The role of phosphoinositide 3-kinases in immune-inflammatory responses: potential therapeutic targets for abdominal aortic aneurysm.Cell cycle (Georgetown, Tex.) · 2022Review
- Article
- Targeting Akt in cancer for precision therapy.Journal of hematology & oncology · 2021Review
- Akt Isoforms: A Family Affair in Breast Cancer.Cancers · 2021Review
- The structural basis of Akt PH domain interaction with calmodulin.Biophysical journal · 2021Article
- Key Genes Regulating Skeletal Muscle Development and Growth in Farm Animals.Animals : an open access journal from MDPI · 2021Review
- Neurotrophin-3 stimulates stem Leydig cell proliferation during regeneration in rats.Journal of cellular and molecular medicine · 2020Article
- Akt isoform-specific effects on thyroid cancer development and progression in a murine thyroid cancer model.Scientific reports · 2020Article
- Article
- Regulation of the Mammalian SWI/SNF Family of Chromatin Remodeling Enzymes by Phosphorylation during Myogenesis.Biology · 2020Review
- AKT2 maintains brain endothelial claudin-5 expression and selective activation of IR/AKT2/FOXO1-signaling reverses barrier dysfunction.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020Article
- Knockdown of Death-Associated Protein Expression Induces Global Transcriptome Changes in Proliferating and Differentiating Muscle Satellite Cells.Frontiers in physiology · 2020Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein kinase B (PKB/Akt) is an important modulator of insulin signaling, cell proliferation, and survival. Using small interfering RNA duplexes in nontransformed mammalian cells, we show that only Akt1 is essential for cell proliferation, while Akt2 promotes cell cycle exit. Silencing Akt1 resulted in decreased cyclin A levels and inhibition of S-phase entry, effects not seen with Akt2 knockdown and specifically rescued by microinjection of Akt1, not Akt2. In differentiating myoblasts, Akt2 knockout prevented myoblasts from exiting the cell cycle and showed sustained cyclin A expression. In contrast, overexpression of Akt2 reduced cyclin A and hindered cell cycle progression in M-G1 with increased nuclear p21. p21 is a major target in the differential effects of Akt isoforms, with endogenous Akt2 and not Akt1 binding p21 in the nucleus and increasing its level. Accordingly, Akt2 knockdown cells, and not Akt1 knockdown cells, showed reduced levels of p21. A specific Akt2/p21 interaction can be reproduced in vitro, and the Akt2 binding site on p21 is similar to that in cyclin A spanning T145 to T155, since (i) prior incubation with cyclin A prevents Akt2 binding, (ii) T145 phosphorylation on p21 by Akt1 prevents Akt2 binding, and (iii) binding Akt2 prevents phosphorylation of p21 by Akt1. These data show that specific interaction of the Akt2 isoform with p21 is key to its negative effect on normal cell cycle progression.
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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.