ArticleCellular and molecular life sciences : CMLS2011
B-MYB delays cell aging by repressing p16 (INK4α) transcription.
Article in Cellular and molecular life sciences : CMLS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Cell cycle regulator MYBL2 is a distinct vulnerability in acute myeloid leukemia.Cell death discovery · 2025Article
- Metabolism and metabolomics in senescence, aging, and age-related diseases: a multiscale perspective.Frontiers of medicine · 2025Review
- Integrative transcriptome analysis identifies MYBL2 as a poor prognosis marker for osteosarcoma and a pan-cancer marker of immune infiltration.Genes & diseases · 2024Article
- Common factors among three types of cells aged in mice.Biogerontology · 2023Article
- Biomarkers of aging.Science China. Life sciences · 2023Review
- Antisense Oligonucleotide Induction of the hnRNPA1b Isoform Affects Pre-mRNA Splicing ofInternational journal of molecular sciences · 2022Article
- p300/Sp1-Mediated High Expression of p16 Promotes Endothelial Progenitor Cell Senescence Leading to the Occurrence of Chronic Obstructive Pulmonary Disease.Mediators of inflammation · 2021Article
- Identification of nine key genes by bioinformatics analysis for predicting poor prognosis in smoking-induced lung adenocarcinoma.Lung cancer management · 2020Article
- RNA sequencing identifies common pathways between cigarette smoke exposure and replicative senescence in human airway epithelia.BMC genomics · 2019Article
- c-Myb and C/EBPβ regulate OPN and other senescence-associated secretory phenotype factors.Oncotarget · 2018Article
- The Role of p16International journal of molecular sciences · 2017Review
- MYBL2 (B-Myb): a central regulator of cell proliferation, cell survival and differentiation involved in tumorigenesis.Cell death & disease · 2017Review
- Downregulation of B-myb promotes senescence via the ROS-mediated p53/p21 pathway, in vascular endothelial cells.Cell proliferation · 2017Article
- MYBL2 is an independent prognostic marker that has tumor-promoting functions in colorectal cancer.American journal of cancer research · 2015Article
- Cellular senescence and aging: the role of B-MYB.Aging cell · 2014Review
- MicroRNA-29 induces cellular senescence in aging muscle through multiple signaling pathways.Aging · 2014Article
- The molecular balancing act of p16(INK4a) in cancer and aging.Molecular cancer research : MCR · 2014Review
- MYBL2 haploinsufficiency increases susceptibility to age-related haematopoietic neoplasia.Leukemia · 2013Article
- B-Myb, cancer, senescence, and microRNAs.Cancer research · 2011Review
- Regulatory mechanisms of tumor suppressor P16(INK4A) and their relevance to cancer.Biochemistry · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
p16 ( INK4α ), an inhibitor of cyclin-dependent kinase 4 and 6, has been proposed to play an important role in cellular aging and in premature senescence. The expression of the p16 ( INK4α ) is primarily under transcriptional control. Our previous data showed that a negative regulation element lies in its promoter. In that element, a MYB-binding site (MBS) was uncovered by transcription analysis. Here, we report that MBS is a negative regulation element and B-MYB binds to this site in vivo. In human embryonic lung fibroblast cells, B-MYB downregulated p16 ( INK4α ) expression, whereas knocking down of B-MYB upregulated it. Evidence also showed that overexpression of B-MYB in cells could increase the number of utmost passage and decrease G1 block, whereas knocking down of B-MYB could impair their replicative ability. This study provides evidence of the capacity of B-MYB not only to regulate p16 ( INK4α ) expression but also the phenotypic consequence on cellular senescence.
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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.