ArticleGenes & development1999
Control of cell cycle progression by c-Jun is p53 dependent.
Article in Genes & development, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 272 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
272 citing papers in PubMed, 574 citations in OpenAlex.
- c-JUN controls microbial colonization via selective phagocytosis in the sea anemone Nematostella.Nature communications · 2026Article
- KIF7 promotes the proliferation of clear cell renal cell carcinoma by activating the WNT/β-catenin signaling pathway.Clinical and experimental medicine · 2026Article
- Review
- AP1 Transcription Factor in the Regulation of the Urokinase Plasminogen Activation System.Biomolecules · 2026Review
- Enhancing the potency of CAR-T cells against solid tumors through transcription factor engineering.JCI insight · 2025Review
- c-Jun promotes neuroblastoma cell differentiation by inhibiting APC formation via CDC16 and reduces neuroblastoma malignancy.Biology direct · 2025Article
- Morphogenesis and regeneration share a conserved core transition cell state program that controls lung epithelial cell fate.Developmental cell · 2025Article
- Exosome-Mediated Lectin Pathway and Resistin-MIF-AA Metabolism Axis Drive Immune Dysfunction in Immune Thrombocytopenia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Inactivation of JNK signalling results in polarity loss and cell senescence of Sertoli cell.Cell proliferation · 2025Article
- Identification of biomarkers associated with coronary artery disease and non-alcoholic fatty liver disease by bioinformatics analysis and machine learning.Scientific reports · 2025Article
- c-JUN: a chromatin repressor that limits mesoderm differentiation in human pluripotent stem cells.Nucleic acids research · 2025Article
- The role of cell cycle-related genes in the tumorigenesis of adrenal and thyroid neuroendocrine tumors.Heliyon · 2025Review
- Article
- Kojic Acid Derivative as an Antimitotic Agent That Selectively Kills Tumour Cells.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Identification of Estrogen-Responsive Proteins in Mouse Seminal Vesicles Through Mass Spectrometry-Based Proteomics.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Sequences within and upstream of the mouse Ets1 gene drive high level expression in B cells, but are not sufficient for consistent expression in T cells.bioRxiv : the preprint server for biology · 2024Article
- Implications of neonatal absence of innate immune mediated NFκB/AP1 signaling in the murine liver.Pediatric research · 2024Article
- Andrographolide inhibits Burkitt's lymphoma by binding JUN and CASP3 proteins.Cancer chemotherapy and pharmacology · 2024Article
- H9N2 Avian Influenza Virus Downregulates FcRY Expression in Chicken Macrophage Cell Line HD11 by Activating the JNK MAPK Pathway.International journal of molecular sciences · 2024Article
- Targeting Oral Squamous Cell Carcinoma with Combined Polo-Like-Kinase-1 Inhibitors and γ-Radiation Therapy.Biomedicines · 2024Article
212 more citing papers are in PubMed but not listed here.
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 5 institutions in 3 countries.
Funding
Abstract
The c-jun proto-oncogene encodes a component of the mitogen-inducible immediate-early transcription factor AP-1 and has been implicated as a positive regulator of cell proliferation and G1-to-S-phase progression. Here we report that fibroblasts derived from c-jun-/- mouse fetuses exhibit a severe proliferation defect and undergo a prolonged crisis before spontaneous immortalization. The cyclin D1- and cyclin E-dependent kinases (CDKs) and transcription factor E2F are poorly activated, resulting in inefficient G1-to-S-phase progression. Furthermore, the absence of c-Jun results in elevated expression of the tumor suppressor gene p53 and its target gene, the CDK inhibitor p21, whereas overexpression of c-Jun represses p53 and p21 expression and accelerates cell proliferation. Surprisingly, protein stabilization, the common mechanism of p53 regulation, is not involved in up-regulation of p53 in c-jun-/- fibroblasts. Rather, c-Jun regulates transcription of p53 negatively by direct binding to a variant AP-1 site in the p53 promoter. Importantly, deletion of p53 abrogates all defects of cells lacking c-Jun in cell cycle progression, proliferation, immortalization, and activation of G1 CDKs and E2F. These results demonstrate that an essential, rate-limiting function of c-Jun in fibroblast proliferation is negative regulation of p53 expression, and establish a mechanistic link between c-Jun-dependent mitogenic signaling and cell-cycle regulation.
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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.