ReviewAging cell2014
Cellular senescence and aging: the role of B-MYB.
Review in Aging cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
44 citing papers in PubMed, 79 citations in OpenAlex.
- Oxidative stress promotes the progression of age-related macular degeneration by up-regulating Spp1 to activate the JAK/STAT signaling pathway.Scientific reports · 2026Article
- Integrated single-cell multi-omics profiling reveals a senescence-associated hematopoietic landscape and regulatory network in aging bone marrow.Biogerontology · 2025Article
- Cell cycle regulator MYBL2 is a distinct vulnerability in acute myeloid leukemia.Cell death discovery · 2025Article
- Hypoxic HPV-Positive Cancer Cells Are Particularly Sensitive to the Pro-Senescent Effects of B-MYB Repression Due to the Lack of Compensatory A-MYB Induction.Journal of medical virology · 2025Article
- Replicative senescence in amniotic fluid-derived mesenchymal stem cells and its impact on their immunomodulatory properties.Histochemistry and cell biology · 2025Article
- Increased PTCHD4 expression via m6A modification of PTCHD4 mRNA promotes senescent cell survival.Nucleic acids research · 2024Article
- Bioinformatics Approach to Identify the Influences of COVID-19 on Ischemic Stroke.Biochemical genetics · 2023Article
- Porokeratoses-A Comprehensive Review on the Genetics and Metabolomics, Imaging Methods and Management of Common Clinical Variants.Metabolites · 2023Review
- OverexpressedJournal of thoracic disease · 2023Article
- Common factors among three types of cells aged in mice.Biogerontology · 2023Article
- ESCCdb: A comprehensive database and key regulator exploring platform based on cross dataset comparisons for esophageal squamous cell carcinoma.Computational and structural biotechnology journal · 2023Article
- LncRNA-MALAT1 Regulates Cancer Glucose Metabolism in Prostate Cancer via MYBL2/mTOR Axis.Oxidative medicine and cellular longevity · 2022Article
- Intricate crosstalk between MYB and noncoding RNAs in cancer.Cancer cell international · 2021Review
- Licochalcone A activation of glycolysis pathway has an anti-aging effect on human adipose stem cells.Aging · 2021Article
- B-Myb accelerates colorectal cancer progression through reciprocal feed-forward transactivation of E2F2.Oncogene · 2021Article
- WNT inhibition creates a BRCA-like state in Wnt-addicted cancer.EMBO molecular medicine · 2021Article
- Association between B-Oncology letters · 2021Review
- Cellular senescence in the aging retina and developments of senotherapies for age-related macular degeneration.Journal of neuroinflammation · 2021Review
- Common Genes Involved in Autophagy, Cellular Senescence and the Inflammatory Response in AMD and Drug Discovery Identified via Biomedical Databases.Translational vision science & technology · 2021Article
- Impact of Acrylamide on Cellular Senescence Response and Cell Cycle Distribution via an In-vitro Study.Iranian journal of pharmaceutical research : IJPR · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Cellular senescence is a stable cell cycle arrest, caused by insults, such as: telomere erosion, oncogene activation, irradiation, DNA damage, oxidative stress, and viral infection. Extrinsic stimuli such as cell culture stress can also trigger this growth arrest. Senescence is thought to have evolved as an example of antagonistic pleiotropy, as it acts as a tumor suppressor mechanism during the reproductive age, but can promote organismal aging by disrupting tissue renewal, repair, and regeneration later in life. The mechanisms underlying the senescence growth arrest are broadly considered to involve p16(INK4A) -pRB and p53-p21(CIP1/WAF1/SDI1) tumor suppressor pathways; but it is not known what makes the senescence arrest stable and what the critical downstream targets are, as they are likely to be key to the establishment and maintenance of the senescent state. MYB-related protein B (B-MYB/MYBL2), a member of the myeloblastosis family of transcription factors, has recently emerged as a potential candidate for regulating entry into senescence. Here, we review the evidence which indicates that loss of B-MYB expression has an important role in causing senescence growth arrest. We discuss how B-MYB acts, as the gatekeeper, to coordinate transit through the cell cycle, in conjunction with the multivulval class B (MuvB) complex and FOXM1 transcription factors. We also evaluate the evidence connecting B-MYB to the mTOR nutrient signaling pathway and suggest that inhibition of this pathway leading to an extension of healthspan may involve activation of B-MYB.
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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.