ArticleThe Journal of biological chemistry2009
NF-YC complexity is generated by dual promoters and alternative splicing.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Alternative Splicing of the NF-Y Subunit, NF-YA, in Neuroblastoma Phenotype Heterogeneity.Cancers · 2026Review
- The role(s) of NF-Y in development and differentiation.Cell death and differentiation · 2025Review
- ATRX guards against aberrant differentiation in mesenchymal progenitor cells.Nucleic acids research · 2024Article
- The pancancer overexpressed NFYC Antisense 1 controls cell cycle mitotic progression through in cis and in trans modes of action.Cell death & disease · 2024Article
- NF-Y subunits overexpression in gastric adenocarcinomas (STAD).Scientific reports · 2021Article
- Alternative splicing of NF-YA promotes prostate cancer aggressiveness and represents a new molecular marker for clinical stratification of patients.Journal of experimental & clinical cancer research : CR · 2021Article
- NF-Y Subunits Overexpression in HNSCC.Cancers · 2021Article
- Live cell dynamics of the NF-Y transcription factor.Scientific reports · 2021Article
- NF-Y Overexpression in Liver Hepatocellular Carcinoma (HCC).International journal of molecular sciences · 2020Article
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- NF-YA Overexpression in Lung Cancer: LUAD.Genes · 2020Article
- Discovery, characterization and potential roles of a novel NF-YAx splice variant in human neuroblastoma.Journal of experimental & clinical cancer research : CR · 2019Article
- NF-YA Overexpression in Lung Cancer: LUSC.Genes · 2019Article
- Overexpression and alternative splicing of NF-YA in breast cancer.Scientific reports · 2019Article
- Prognostic role of NF-YA splicing isoforms and Lamin A status in low grade endometrial cancer.Oncotarget · 2017Article
- Specific inhibition of NF-Y subunits triggers different cell proliferation defects.Nucleic acids research · 2011Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The CCAAT box is a DNA element present in the majority of human promoters, bound by the trimeric NF-Y, composed of NF-YA, NF-YB, and NF-YC subunits. We describe and characterize novel isoforms of one of the two histone-like subunits, NF-YC. The locus generates a minimum of four splicing products, mainly located within the Q-rich activation domain. The abundance of each isoform is cell-dependent; only one major NF-YC isoform is present in a given cell type. The 37- and 50-kDa isoforms are mutually exclusive, and preferential pairings with NF-YA isoforms possess different transcriptional activities, with specific combinations being more active on selected promoters. The transcriptional regulation of the NF-YC locus is also complex, and mRNAs arise from the two promoters P1 and P2. Transient transfections, chromatin immunoprecipitations, and reverse transcription-PCRs indicate that P1 has a robust housekeeping activity; P2 possesses a lower basal activity, but it is induced in response to DNA damage in a p53-dependent way. Alternative promoter usage directly affects NF-YC splicing, with the 50-kDa transcript being excluded from P2. Specific functional inactivation of the 37-kDa isoform affects the basal levels of G(1)/S blocking and pro-apoptotic genes but not G(2)/M promoters. In summary, our data highlight an unexpected degree of complexity and regulation of the NF-YC gene, demonstrating the existence of a discrete cohort of NF-Y trimer subtypes resulting from the functional diversification of Q-rich transactivating subunits and a specific role of the 37-kDa isoform in suppression of the DNA damage-response under growing conditions.
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