ArticleCell cycle (Georgetown, Tex.)2016
cMyc-p53 feedback mechanism regulates the dynamics of T lymphocytes in the immune response.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Metabolic reprogramming of Th17/Treg imbalance in autoimmune thyroid diseases.Cell communication and signaling : CCS · 2026Review
- Role of B1 antisense RNA on the proliferation and killing tumor ability of aged mouse spleen lymphocytes.Scientific reports · 2025Article
- Metabolic and proteomic signatures differentiate inflammatory phenotypes from cancer and predict treatment response in patient sera.Bioengineering & translational medicine · 2025Article
- Ubiquitination in the T Cell Metabolism-Based Immunotherapy in Diseases.Advances in experimental medicine and biology · 2024Review
- The Expression of P53, MDM2, c-myc, and P14Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2020Article
- Inhibition of p53 inhibitors: progress, challenges and perspectives.Journal of molecular cell biology · 2019Review
- VPS33B interacts with NESG1 to modulate EGFR/PI3K/AKT/c-Myc/P53/miR-133a-3p signaling and induce 5-fluorouracil sensitivity in nasopharyngeal carcinoma.Cell death & disease · 2019Article
- Immunosuppressive circuits in tumor microenvironment and their influence on cancer treatment efficacy.Virchows Archiv : an international journal of pathology · 2019Review
- Protoporphyrin IX is a dual inhibitor of p53/MDM2 and p53/MDM4 interactions and induces apoptosis in B-cell chronic lymphocytic leukemia cells.Cell death discovery · 2019Article
- Oncogenes in immune cells as potential therapeutic targets.ImmunoTargets and therapy · 2018Review
- Clinical significance of costimulatory molecules CD40/CD40L and CD134/CD134L in coronary heart disease: A case-control study.Medicine · 2017Observational
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6 authors.
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Abstract
Activation and proliferation of T cells are tightly regulated during the immune response. We show here that kinetics of proliferation of PHA activated T cells follows the expression of cMyc. Expression of p53 is also elevated and remains high several days after activation. To investigate the role of p53 in activated T cells, its expression was further elevated with nultin-3 treatment, a small molecule that dissociates the E3 ubiquitin protein ligase MDM2 from p53. Concomitantly, cMyc expression and proliferation decreased. At the other end of the cMyc-p53 axis, inhibition of cMyc with 10058-F4 led to down regulation of p53, likely through the lower level of cMyc induced p14ARF, which is also known to dissociate the p53-MDM2 complex. Both compounds induced cell cycle arrest and apoptosis. We conclude that the feedback regulation between cMyc and p53 is important for the T cell homeostasis. We also show that the two compounds modulating p53 and cMyc levels inhibited proliferation without abolishing the cytotoxic function, thus demonstrating the dichotomy between proliferation and cytotoxicity in activated T cells.
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