ArticleNucleic acids research2017
MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- MAZ regulates fetal hemoglobin repression by activating MYB transcription.Scientific reports · 2025Article
- Genome-wide functional integration identified MAZ-controlled RPS14 dysregulation in hepatocellular carcinoma.Archives of toxicology · 2024Article
- MYB: A Key Transcription Factor in the Hematopoietic System Subject to Many Levels of Control.Advances in experimental medicine and biology · 2024Review
- Increased retinoic acid signaling decreases lung metastasis in salivary adenoid cystic carcinoma by inhibiting the noncanonical Notch1 pathway.Experimental & molecular medicine · 2023Article
- Construction of a breast cancer prognosis model based on alternative splicing and immune infiltration.Discover oncology · 2022Article
- Downregulation ofGenes & diseases · 2022Article
- Cell cycle gene regulation dynamics revealed by RNA velocity and deep-learning.Nature communications · 2022Article
- Analyses of the circadian clock genes expression in whole embryos and maternal major tissues of mice.Journal of molecular histology · 2022Article
- Myc-associated zinc-finger protein promotes clear cell renal cell carcinoma progression through transcriptional activation of the MAP2K2-dependent ERK pathway.Cancer cell international · 2021Article
- CDCA7 finely tunes cytoskeleton dynamics to promote lymphoma migration and invasion.Haematologica · 2020Article
- CDCA7 is a critical mediator of lymphomagenesis that selectively regulates anchorage-independent growth.Haematologica · 2018Article
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most E2F-binding sites repress transcription through the recruitment of Retinoblastoma (RB) family members until the end of the G1 cell-cycle phase. Although the MYB promoter contains an E2F-binding site, its transcription is activated shortly after the exit from quiescence, before RB family members inactivation, by unknown mechanisms. We had previously uncovered a nuclear factor distinct from E2F, Myb-sp, whose DNA-binding site overlapped the E2F element and had hypothesized that this factor might overcome the transcriptional repression of MYB by E2F-RB family members. We have purified Myb-sp and discovered that Myc-associated zinc finger proteins (MAZ) are major components. We show that various MAZ isoforms are present in Myb-sp and activate transcription via the MYB-E2F element. Moreover, while forced RB or p130 expression repressed the activity of a luciferase reporter driven by the MYB-E2F element, co-expression of MAZ proteins not only reverted repression, but also activated transcription. Finally, we show that MAZ binds the MYB promoter in vivo, that its binding site is critical for MYB transactivation, and that MAZ knockdown inhibits MYB expression during the exit from quiescence. Together, these data indicate that MAZ is essential to bypass MYB promoter repression by RB family members and to induce MYB expression.
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