ArticleOncogene1999
Down-regulation of cyclin B1 gene transcription in terminally differentiated skeletal muscle cells is associated with loss of functional CCAAT-binding NF-Y complex.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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.
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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
53 citing papers in PubMed, 110 citations in OpenAlex.
- Rev-Erb co-regulates muscle regeneration via tethered interaction with the NF-Y cistrome.Molecular metabolism · 2017Trial
- Genetic tracing and topography of spontaneous and stimulated cardiac regeneration in mice.Nature cardiovascular research · 2025Article
- The role(s) of NF-Y in development and differentiation.Cell death and differentiation · 2025Review
- Kinase-inactivated CDK6 preserves the long-term functionality of adult hematopoietic stem cells.Blood · 2024Article
- Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during mouse fetal heart development.Developmental cell · 2023Article
- Myo-differentiation reporter screen reveals NF-Y as an activator of PAX3-FOXO1 in rhabdomyosarcoma.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Cell Cycle Regulation by NF-YC inInternational journal of molecular sciences · 2023Article
- mTOR Driven Gene Transcription Is Required for Cholesterol Production in Neurons of the Developing Cerebral Cortex.International journal of molecular sciences · 2021Article
- MITO-Luc/GFP zebrafish model to assess spatial and temporal evolution of cell proliferation in vivo.Scientific reports · 2021Article
- Application of the RBBP9 Serine Hydrolase Inhibitor, ML114, Decouples Human Pluripotent Stem Cell Proliferation and Differentiation.International journal of molecular sciences · 2020Article
- Article
- Functional Analysis of Nuclear Factor Y in the Wing-Dimorphic Brown Planthopper,Frontiers in genetics · 2020Article
- NF-YA Overexpression in Lung Cancer: LUSC.Genes · 2019Article
- Combinatory RNA-Sequencing Analyses Reveal a Dual Mode of Gene Regulation by ADAR1 in Gastric Cancer.Digestive diseases and sciences · 2018Article
- The animal nuclear factor Y: an enigmatic and important heterotrimeric transcription factor.American journal of cancer research · 2018Review
- Single-cell, single-mRNA analysis of Ccnb1 promoter regulation.Scientific reports · 2017Article
- NF-Y (CBF) regulation in specific cell types and mouse models.Biochimica et biophysica acta. Gene regulatory mechanisms · 2017Review
- The laminA/NF-Y protein complex reveals an unknown transcriptional mechanism on cell proliferation.Oncotarget · 2017Article
- NF-YB Regulates Spermatogonial Stem Cell Self-Renewal and Proliferation in the Planarian Schmidtea mediterranea.PLoS genetics · 2016Article
- Nuclear Factor-Y is an adipogenic factor that regulates leptin gene expression.Molecular metabolism · 2015Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The observation that cyclin B1 protein and mRNAs are down-regulated in terminally differentiated (TD) C2C12 cells, suggested us to investigate the transcriptional regulation of the cyclin B1 gene in these cells. Transfections of cyclin B1 promoter constructs indicate that two CCAAT boxes support cyclin B1 promoter activity in proliferating cells. EMSAs demonstrate that both CCAAT boxes are recognized by the trimeric NF-Y complex in proliferating but not in TD cells. Transfecting a dominant-negative mutant of NF-YA we provide evidence that NF-Y is required for maximal promoter activity. Addition of recombinant NF-YA to TD C2C12 nuclear extracts restores binding activity in vitro, thus indicating that the loss of NF-YA in TD cells is responsible for the lack of the NF-Y binding to the CCAAT boxes. Consistent with this, we found that the NF-YA protein is absent in TD C2C12 cells. In conclusion, our data demonstrate that NF-Y is required for cyclin B1 promoter activity. We also demonstrate that cyclin B1 expression is regulated at the transcriptional level in TD C2C12 cells and that the switch-off of cyclin B1 promoter activity in differentiated cells depends upon the loss of a functional NF-Y complex. In particular the loss of NF-YA protein is most likely responsible for its inactivation.
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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.