ArticlePloS one2011
E2F1 regulates cellular growth by mTORC1 signaling.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 813 citations in OpenAlex.
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- The multifaceted role of cell cycle regulators in the coordination of growth and metabolism.The FEBS journal · 2021Review
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- FAK activates AKT-mTOR signaling to promote the growth and progression of MMTV-Wnt1-driven basal-like mammary tumors.Breast cancer research : BCR · 2020Article
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- Comprehensive Analysis of Zinc Derivatives Pro-proliferative, Anti-Apoptotic and Antimicrobial Effect on Human Fibroblasts and Keratinocytes in a Simulated, Nutrient-deficient EnvironmentInternational journal of molecular and cellular medicine · 2020Article
- Phosphofructokinases Axis Controls Glucose-Dependent mTORC1 Activation Driven by E2F1.iScience · 2019Article
- CDK4 Regulates Lysosomal Function and mTORC1 Activation to Promote Cancer Cell Survival.Cancer research · 2019Article
- Adult neural stem cell dysfunction in the subventricular zone of the lateral ventricle leads to diabetic olfactory defects.Neural regeneration research · 2017Article
- Information-dependent enrichment analysis reveals time-dependent transcriptional regulation of the estrogen pathway of toxicity.Archives of toxicology · 2017Article
- E2F1 somatic mutation within miRNA target site impairs gene regulation in colorectal cancer.PloS one · 2017Article
- Mutations of RagA GTPase in mTORC1 Pathway Are Associated with Autosomal Dominant Cataracts.PLoS genetics · 2016Article
- Decreased MicroRNA-26a expression causes cisplatin resistance in human non-small cell lung cancer.Cancer biology & therapy · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During cell proliferation, growth must occur to maintain homeostatic cell size. Here we show that E2F1 is capable of inducing growth by regulating mTORC1 activity. The activation of cell growth and mTORC1 by E2F1 is dependent on both E2F1's ability to bind DNA and to regulate gene transcription, demonstrating that a gene induction expression program is required in this process. Unlike E2F1, E2F3 is unable to activate mTORC1, suggesting that growth activity could be restricted to individual E2F members. The effect of E2F1 on the activation of mTORC1 does not depend on Akt. Furthermore, over-expression of TSC2 does not interfere with the effect of E2F1, indicating that the E2F1-induced signal pathway can compensate for the inhibitory effect of TSC2 on Rheb. Immunolocalization studies demonstrate that E2F1 induces the translocation of mTORC1 to the late endosome vesicles, in a mechanism dependent of leucine. E2F1 and leucine, or insulin, together affect the activation of S6K stronger than alone suggesting that they are complementary in activating the signal pathway. From these studies, E2F1 emerges as a key protein that integrates cell division and growth, both of which are essential for cell proliferation.
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