ArticleJournal of molecular cell biology2016
Yin Yang 1 promotes mTORC2-mediated AKT phosphorylation.
Article in Journal of molecular cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Intrinsic mechanotransduction during apical constriction licenses lineage competence in pluripotent stem cells.bioRxiv : the preprint server for biology · 2025Article
- Clinical Significance of Nuclear Yin-Yang Overexpression Evaluated by Immunohistochemistry in Tissue Microarrays and Digital Pathology Analysis: A Useful Prognostic Tool for Breast Cancer.International journal of molecular sciences · 2025Article
- Yin Yang 1: Role in Leishmaniasis.Cells · 2025Review
- Article
- Leishmania regulates host YY1: Comparative proteomic analysis identifies infection modulated YY1 dependent proteins.PloS one · 2025Article
- Yin Yang 1 expression predicts a favourable survival in diffuse large B-cell lymphoma.Heliyon · 2024Article
- Clinical Potential of YY1-Hypoxia Axis for Vascular Normalization and to Improve Immunotherapy.Cancers · 2024Review
- Review
- Targeting Transcription Factor YY1 for Cancer Treatment: Current Strategies and Future Directions.Cancers · 2023Review
- PLAU is associated with cell migration and invasion and is regulated by transcription factor YY1 in cervical cancer.Oncology reports · 2023Article
- A histidine cluster determines YY1-compartmentalized coactivators and chromatin elements in phase-separated enhancer clusters.Nucleic acids research · 2022Article
- Yin Yang 1 regulates ITGAV and ITGB1, contributing to improved prognosis of colorectal cancer.Oncology reports · 2022Article
- YY1 Oligomerization Is Regulated by Its OPB Domain and Competes with Its Regulation of Oncoproteins.Cancers · 2022Article
- YY1 activates EMI2 and promotes the progression of cholangiocarcinoma through the PI3K/Akt signaling axis.Cancer cell international · 2021Article
- The Protective Role of Yin-Yang 1 in Cardiac Injury and Remodeling After Myocardial Infarction.Journal of the American Heart Association · 2021Article
- Disruption of YY1-EZH2 Interaction Using Synthetic Peptides Inhibits Breast Cancer Development.Cancers · 2021Article
- Biological roles of Yin Yang 2: Its implications in physiological and pathological events.Journal of cellular and molecular medicine · 2020Review
- Transcriptional Factor Yin Yang 1 Promotes the Stemness of Breast Cancer Cells by Suppressing miR-873-5p Transcriptional Activity.Molecular therapy. Nucleic acids · 2020Article
- The biological implications of Yin Yang 1 in the hallmarks of cancer.Theranostics · 2020Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Yin Yang 1 (YY1) regulates both gene expression and protein modifications, and has shown a proliferative role in cancers. In this study, we demonstrate that YY1 promotes AKT phosphorylation at S473, a marker of AKT activation. YY1 expression positively correlated with AKT(S473) phosphorylation in a tissue microarray and cultured cells of breast cancer, but negatively associated with the distant metastasis-free survival of 166 breast cancer patients. YY1 promotes AKT phosphorylation at S473 through direct interaction with AKT, and the AKT-binding site is mapped to the residues G201-S226 on YY1. These residues are also involved in YY1 interaction with Mdm2, Ezh2, and E1A, and thus are designated as the oncogene protein binding (OPB) domain. YY1-promoted AKT phosphorylation relies on the OPB domain but is independent of either transcriptional activity of YY1 or the activity of phosphoinositide-3-kinases. We also determine that YY1-promoted mTORC2 access to AKT leads to its phosphorylation at S473. Importantly, a peptide based on the OPB domain blocks YY1 interaction with AKT and reduces AKT phosphorylation and cell proliferation. Thus, we demonstrate for the first time that YY1 promotes mTORC2-mediated AKT activation and disrupting YY1-AKT interaction by OPB domain-based peptide may represent a potential strategy for cancer therapy.
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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.