ArticleThe Journal of biological chemistry2011
The E-box binding factors Max/Mnt, MITF, and USF1 act coordinately with FoxO to regulate expression of proapoptotic and cell cycle control genes by phosphatidylinositol 3-kinase/Akt/glycogen synthase kinase 3 signaling.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- O-GlcNAcylation of MITF regulates its activity and CDK4/6 inhibitor resistance in breast cancer.Nature communications · 2024Article
- Mitf regulates gene expression networks implicated in B cell homeostasis, germinal center responses, and tolerance.Frontiers in immunology · 2024Article
- Article
- Upstream Stimulatory Factors Regulate HIV-1 Latency and Are Required for Robust T Cell Activation.Viruses · 2023Article
- FTO Alleviates CdClInternational journal of molecular sciences · 2022Article
- Mnt Represses Epithelial Identity To Promote Epithelial-to-Mesenchymal Transition.Molecular and cellular biology · 2021Article
- Review
- miR-139-5p Regulates the Proliferation of Acute Promyelocytic Leukemia Cells by Targeting MNT.Journal of oncology · 2021Article
- MYC-Associated Factor MAX is a Regulator of the Circadian Clock.International journal of molecular sciences · 2020Article
- The MNT transcription factor autoregulates its expression and supports proliferation in MYC-associated factor X (MAX)-deficient cells.The Journal of biological chemistry · 2020Article
- Article
- Requirement of GSK-3 for PUMA induction upon loss of pro-survival PI3K signaling.Cell death & disease · 2018Article
- MNT and Emerging Concepts of MNT-MYC Antagonism.Genes · 2017Article
- The rise and fall of insulin signaling in Alzheimer's disease.Metabolic brain disease · 2016Review
- Phosphorylation of GSK3α/β correlates with activation of AKT and is prognostic for poor overall survival in acute myeloid leukemia patients.BBA clinical · 2015Article
- MITF in melanoma: mechanisms behind its expression and activity.Cellular and molecular life sciences : CMLS · 2015Review
- The transcription factor MITF is a critical regulator of GPNMB expression in dendritic cells.Cell communication and signaling : CCS · 2015Article
- Protein kinases as switches for the function of upstream stimulatory factors: implications for tissue injury and cancer.Frontiers in pharmacology · 2015Article
- GSK3β-dependent phosphorylation alters DNA binding, transactivity and half-life of the transcription factor USF2.PloS one · 2014Article
- Unbiased proteomic analysis of proteins interacting with the HIV-1 5'LTR sequence: role of the transcription factor Meis.Nucleic acids research · 2012Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Phosphatidylinositol (PI) 3-kinase/Akt signaling plays a critical role in cell proliferation and survival, partly by regulation of FoxO transcription factors. Previous work using global expression profiling indicated that inhibition of PI 3-kinase in proliferating cells led to induction of genes that promote cell cycle arrest and apoptosis. The upstream regulatory regions of these genes had binding sites not only for FoxO, but also for Myc/Max transcription factors. In the present study, we have addressed the role of Myc family members and related E-box-binding proteins in the regulation of these genes. Chromatin immunoprecipitations and RNA interference indicated that transcription was repressed by Max-Mnt-Sin3a-histone deacetylase complexes in proliferating cells. Inhibition of PI 3-kinase led to a loss of Max/Mnt binding and transcriptional induction by MITF and USF1, as well as FoxO. Both MITF and USF1 were activated by glycogen synthase kinase (GSK) 3, with GSK3 phosphorylation sites on USF1 identified as the previously described activating site threonine 153 as well as serine 186. siRNA against MITF as well as against FoxO3a protected cells from apoptosis following PI 3-kinase inhibition. These results define a novel E-box-regulated network that functions coordinately with FoxO to regulate transcription of apoptotic and cell cycle regulatory genes downstream of PI 3-kinase/Akt/GSK3 signaling.
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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.