ArticleNature communications2024
Mst1-mediated phosphorylation of FoxO1 and C/EBP-β stimulates cell-protective mechanisms in cardiomyocytes.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Carboxypeptidase A6 contributes to bovine enterovirus F production through apoptosis-associated PI3K/AKT/FOXO1 signaling.Virulence · 2026Article
- Perm1 enhances Nrf2-driven antioxidant defense through Keap1 oxidation during myocardial ischemia/reperfusion injury.JCI insight · 2026Article
- Gadd45α silencing alleviates cerebral ischemia-reperfusion injury by suppressing FOXO1 signaling.Scientific reports · 2026Article
- Dynamic monitoring of cognitive impairment and prognostic recurrence risk in patients with stroke by serum HDAC3 and FOXO1: A potential diagnostic approach.Journal of medical biochemistry · 2026Article
- FOXO1 Inhibition and FADD Knockdown Have Opposing Effects on Anticancer Drug-Induced Cytotoxicity and p21 Expression in Osteosarcoma Cells.International journal of molecular sciences · 2026Article
- Transcription factor CEBPA suppresses sepsis induced lung injury by activating SIRT4 transcription.Scientific reports · 2025Article
- Silicate-based therapy for inflammatory dilated cardiomyopathy by inhibiting the vicious cycle of immune inflammation via FOXO signaling.Science advances · 2025Article
- p21-Activated Kinase 1 (Pak1) as an Element in Functional and Dysfunctional Interplay Among the Myocardium, Adipose Tissue, and Pancreatic Beta Cells.Comprehensive Physiology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The molecular mechanisms by which FoxO transcription factors mediate diametrically opposite cellular responses, namely death and survival, remain unknown. Here we show that Mst1 phosphorylates FoxO1 Ser209/Ser215/Ser218/Thr228/Ser232/Ser243, thereby inhibiting FoxO1-mediated transcription of proapoptotic genes. On the other hand, Mst1 increases FoxO1-C/EBP-β interaction and activates C/EBP-β by phosphorylating it at Thr299, thereby promoting transcription of prosurvival genes. Myocardial ischemia/reperfusion injury is larger in cardiac-specific FoxO1 knockout mice than in control mice. However, the concurrent presence of a C/EBP-β T299E phospho-mimetic mutation reduces infarct size in cardiac-specific FoxO1 knockout mice. The C/EBP-β phospho-mimetic mutant exhibits greater binding to the promoter of prosurvival genes than wild type C/EBP-β. In conclusion, phosphorylation of FoxO1 by Mst1 inhibits binding of FoxO1 to pro-apoptotic gene promoters but enhances its binding to C/EBP-β, phosphorylation of C/EBP-β, and transcription of prosurvival genes, which stimulate protective mechanisms in the heart.
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