ArticleOncogene2018
NFκB regulates p21 expression and controls DNA damage-induced leukemic differentiation.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed.
- Ploidy-Dependent Response to Anticancer Drugs of Human Embryonic Stem Cells.Cell proliferation · 2026Article
- Autonomous Oscillations of NF-κB.Advances in experimental medicine and biology · 2026Review
- The lncRNA ELDR suppresses tumorigenicity of AML by interfering with DNA replication and chromatin accessibility.Blood advances · 2025Article
- First Direct Evidence of Accelerated Molecular Aging in Intracranial Aneurysmal Tissue.Aging cell · 2025Article
- Norchelerythrine fromInternational journal of oncology · 2025Article
- The alternative polyadenylation regulator CFIm25 promotes macrophage differentiation and activates the NF-κB pathway.Cell communication and signaling : CCS · 2025Article
- Therapeutic Potential ofInternational journal of molecular sciences · 2025Article
- Contribution of p53-dependent and -independent mechanisms to upregulation of p21 in Fanconi anemia.PLoS genetics · 2024Article
- Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation.Cell communication and signaling : CCS · 2024Article
- Bleomycin-treated myoblasts undergo p21-associated cellular senescence and have severely impaired differentiation.GeroScience · 2024Article
- Osmolar Modulation Drives Reversible Cell Cycle Exit and Human Pluripotent Cell Differentiation via NF-κВ and WNT Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Comprehensive review of CRISPR-based gene editing: mechanisms, challenges, and applications in cancer therapy.Molecular cancer · 2024Review
- The mechanism of gut-lung axis in pulmonary fibrosis.Frontiers in cellular and infection microbiology · 2024Review
- Colchicine prevents oxidative stress-induced endothelial cell senescence via blocking NF-κB and MAPKs: implications in vascular diseases.Journal of inflammation (London, England) · 2023Article
- Article
- Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells.Antioxidants (Basel, Switzerland) · 2023Article
- DAPL1 prevents epithelial-mesenchymal transition in the retinal pigment epithelium and experimental proliferative vitreoretinopathy.Cell death & disease · 2023Article
- TLR4 downregulation by the RNA-binding protein PUM1 alleviates cellular aging and osteoarthritis.Cell death and differentiation · 2022Article
- Transcription Factor Activation Profiles (TFAP) identify compounds promoting differentiation of Acute Myeloid Leukemia cell lines.Cell death discovery · 2022Article
- Thyroid hormones act as modulators of inflammation through their nuclear receptors.Frontiers in endocrinology · 2022Review
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.
Funding
Abstract
DNA damage exposure is a major modifier of cell fate in both normal and cancer tissues. In response to DNA damage, myeloid leukemia cells activate a poorly understood terminal differentiation process. Here, we show that the NFκB pathway directly activates expression of the proliferation inhibitor p21 in response to DNA damage in myeloid leukemia cells. In order to understand the role of this unexpected regulatory event, we ablated the NFκB binding site we identified in the p21 promoter, using CRISPR/Cas9-mediated genome editing. We found that NFκB-mediated p21 activation controls DNA damage-induced myeloid differentiation. Our results uncover a p53-independent pathway for p21 activation involved in controlling hematopoietic cell fate.
Indexed as
Identifiers
29622796What 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.