Evidence map›Paper›PMID 19690168›Full record

ArticleThe Journal of biological chemistry2009

NF-YC complexity is generated by dual promoters and alternative splicing.

Michele Ceribelli, Paolo Benatti, Carol Imbriano, Roberto Mantovani

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed.

  1. Review
  2. The role(s) of NF-Y in development and differentiation.Cell death and differentiation · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. NF-Y Overexpression in Liver Hepatocellular Carcinoma (HCC).International journal of molecular sciences · 2020
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Michele CeribelliDipartimento di Scienze Biomolecolari e Biotecnologie, Università degli Studi di Milano, Via Celoria 26, 20133 Milano, Italy.
Paolo Benatti
Carol Imbriano
Roberto Mantovani

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Alternative SplicingPromoter Regions, GeneticAmino Acid SequenceBase SequenceCCAAT-Binding FactorCell Line, TumorComputational BiologyDimerizationDNA DamageHeLa CellsHistonesHumansMolecular Sequence DataProtein IsoformsProtein Structure, TertiarySequence Homology, Amino AcidCCAAT-Binding FactorHistonesNFYC protein, humanProtein Isoforms

Identifiers

PMID19690168
PMCPMC2797189

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Registered trials

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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.