ArticleThe Journal of biological chemistry2008
DEC1, a basic helix-loop-helix transcription factor and a novel target gene of the p53 family, mediates p53-dependent premature senescence.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
81 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.
- Pooled it
- BHLHE40 as a transcriptional rheostat: decoding microenvironmental signals in context-dependent tumor plasticity.Science China. Life sciences · 2026Review
- Overview of molecular signatures of senescence and associated resources: pros and cons.FEBS open bio · 2026Review
- DEC1 Deficiency Attenuates Breast Cancer-Induced Osteolytic Destruction by Suppression of Cancer-Associated Fibroblast Differentiation.Cancer medicine · 2026Article
- Article
- TAp63γ is the primary isoform of TP63 for tumor suppression but not development.Cell death discovery · 2025Article
- The Common Hallmarks and Interconnected Pathways of Aging, Circadian Rhythms, and Cancer: Implications for Therapeutic Strategies.Research (Washington, D.C.) · 2025Review
- Decoding senescence of aging single cells at the nexus of biomaterials, microfluidics, and spatial omics.npj aging · 2024Review
- The clock gene BHLHE40 and atypical CCNG2 control androgen-induced cellular senescence as a novel tumor suppressive pathway in prostate cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- Antagonizing Activin A/p15Cells · 2024Article
- Article
- GSDMD gene knockout alleviates hyperoxia-induced hippocampal brain injury in neonatal mice.Journal of neuroinflammation · 2023Article
- Isoform-specific disruption of theeLife · 2023Article
- GSDMD gene knockout alleviates hyperoxia-induced hippocampal brain injury in neonatal mice.Research square · 2023Article
- Differentiated Embryo-Chondrocyte Expressed Gene1 and Parkinson's Disease: New Insights and Therapeutic Perspectives.Current neuropharmacology · 2023Review
- A senescence-associated signature refines the classification of different modification patterns and characterization of tumor immune microenvironment infiltration in triple-negative breast cancer.Frontiers in pharmacology · 2023Article
- Cellular Senescence: Molecular Targets, Biomarkers, and Senolytic Drugs.International journal of molecular sciences · 2022Review
- DEC1 promotes progression of Helicobacter pylori-positive gastric cancer by regulating Akt/NF-κB pathway.Journal of cellular and molecular medicine · 2022Article
- Article
- Fine-tuning p53 activity by modulating the interaction between eukaryotic translation initiation factor eIF4E and RNA-binding protein RBM38.Genes & development · 2021Article
21 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
4 authors at 3 institutions in 1 country.
Funding
Abstract
Cellular senescence plays an important role in tumor suppression. p53 tumor suppressor has been reported to be crucial in cellular senescence. However, the underlying mechanism is poorly understood. In this regard, a cDNA microarray assay was performed to identify p53 targets involved in senescence. Among the many candidates is DEC1, a basic helix-loop-helix transcription factor that has been recently shown to be up-regulated in K-ras-induced premature senescence. However, it is not clear whether DEC1 is capable of inducing senescence. Here, we found that DEC1 is a novel target gene of the p53 family and mediates p53-dependent premature senescence. Specifically, we showed that DEC1 is induced by the p53 family and DNA damage in a p53-dependent manner. We also found that the p53 family proteins bind to, and activate, the promoter of the DEC1 gene. In addition, we showed that overexpression of DEC1 induces G(1) arrest and promotes senescence. Moreover, we found that targeting endogenous DEC1 attenuates p53-mediated premature senescence in response to DNA damage. Furthermore, overexpression of DEC1 induces cellular senescence in p53-knockdown cells, albeit to a lesser extent. Finally, we showed that DEC1-induced senescence is p21-independent. Taken together, our data provided strong evidence that DEC1 is one of the effectors downstream of p53 to promote premature senescence.
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What OpenQuestion holds
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.