ArticleScience signaling2013
BSTA promotes mTORC2-mediated phosphorylation of Akt1 to suppress expression of FoxC2 and stimulate adipocyte differentiation.
Article in Science signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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
30 citing papers in PubMed, 4 citations in OpenAlex.
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- Metabolic Reprogramming in Urological Tumors: New Perspectives from Tumor Metabolic Phenotypes to Therapeutic Targets.International journal of biological sciences · 2025Review
- Article
- Research Progress on the Mechanism of Milk Fat Synthesis in Cows and the Effect of Conjugated Linoleic Acid on Milk Fat Metabolism and Its Underlying Mechanism: A Review.Animals : an open access journal from MDPI · 2024Review
- Dlk2 interacts with Syap1 to activate Akt signaling pathway during osteoclast formation.Cell death & disease · 2023Article
- Regulation and metabolic functions of mTORC1 and mTORC2.Physiological reviews · 2021Review
- Control of adipogenic commitment by a STAT3-VSTM2A axis.American journal of physiology. Endocrinology and metabolism · 2021Article
- Bovine Pre-adipocyte Adipogenesis Is Regulated by bta-miR-150 Through mTOR Signaling.Frontiers in genetics · 2021Article
- Endogenous Cyclin D1 Promotes the Rate of Onset and Magnitude of Mitogenic Signaling via Akt1 Ser473 Phosphorylation.Cell reports · 2020Article
- Molecular Mechanism of Stem Cell Differentiation into Adipocytes and Adipocyte Differentiation of Malignant Tumor.Stem cells international · 2020Review
- The Epithelial to Mesenchymal Transition Promotes Glutamine Independence by SuppressingCancers · 2019Article
- An essential role of the mouse synapse-associated protein Syap1 in circuits for spontaneous motor activity and rotarod balance.Biology open · 2019Article
- Brown fat organogenesis and maintenance requires AKT1 and AKT2.Molecular metabolism · 2019Article
- Lab review: Molecular dissection of the signal transduction pathways associated with PTEN deletion-induced optic nerve regeneration.Restorative neurology and neuroscience · 2019Review
- mTOR and Tumor Cachexia.International journal of molecular sciences · 2018Review
- Role of mTOR in Glucose and Lipid Metabolism.International journal of molecular sciences · 2018Review
- Coordination of Necessary and Permissive Signals by PTEN Inhibition for CNS Axon Regeneration.Frontiers in neuroscience · 2018Review
- Initial characterization of a Syap1 knock-out mouse and distribution of Syap1 in mouse brain and cultured motoneurons.Histochemistry and cell biology · 2016Article
- The Mechanistic Target of Rapamycin: The Grand ConducTOR of Metabolism and Aging.Cell metabolism · 2016Review
- Recent Advances in Adipose mTOR Signaling and Function: Therapeutic Prospects.Trends in pharmacological sciences · 2016Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Phosphorylation and activation of Akt1 is a crucial signaling event that promotes adipogenesis. However, neither the complex multistep process that leads to activation of Akt1 through phosphorylation at Thr³⁰⁸ and Ser⁴⁷³ nor the mechanism by which Akt1 stimulates adipogenesis is fully understood. We found that the BSD domain-containing signal transducer and Akt interactor (BSTA) promoted phosphorylation of Akt1 at Ser⁴⁷³ in various human and murine cells, and we uncovered a function for the BSD domain in BSTA-Akt1 complex formation. The mammalian target of rapamycin complex 2 (mTORC2) facilitated the phosphorylation of BSTA and its association with Akt1, and the BSTA-Akt1 interaction promoted the association of mTORC2 with Akt1 and phosphorylation of Akt1 at Ser⁴⁷³ in response to growth factor stimulation. Furthermore, analyses of bsta gene-trap murine embryonic stem cells revealed an essential function for BSTA and phosphorylation of Akt1 at Ser⁴⁷³ in promoting adipocyte differentiation, which required suppression of the expression of the gene encoding the transcription factor FoxC2. These findings indicate that BSTA is a molecular switch that promotes phosphorylation of Akt1 at Ser⁴⁷³ and reveal an mTORC2-BSTA-Akt1-FoxC2-mediated signaling mechanism that is critical for adipocyte differentiation.
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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.