ArticleMolecular and cellular biology1999
Distinct cellular factors regulate the c-myb promoter through its E2F element.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- MYB: A Key Transcription Factor in the Hematopoietic System Subject to Many Levels of Control.Advances in experimental medicine and biology · 2024Review
- LIN28 and histone H3K4 methylase induce TLR4 to generate tumor-initiating stem-like cells.iScience · 2023Article
- Leprosy drug clofazimine activates peroxisome proliferator-activated receptor-γ and synergizes with imatinib to inhibit chronic myeloid leukemia cells.Haematologica · 2020Article
- CDCA7 is a critical mediator of lymphomagenesis that selectively regulates anchorage-independent growth.Haematologica · 2018Article
- MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter.Nucleic acids research · 2017Article
- Early B Cell Progenitors Deficient for GON4L Fail To Differentiate Due to a Block in Mitotic Cell Division.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- New Insights on COX-2 in Chronic Inflammation Driving Breast Cancer Growth and Metastasis.Journal of mammary gland biology and neoplasia · 2015Review
- ISMARA: automated modeling of genomic signals as a democracy of regulatory motifs.Genome research · 2014Article
- Analysis of genetic aberrations on chromosomal region 8q21-24 identifies E2F5 as an oncogene with copy number gain in prostate cancer.Medical oncology (Northwood, London, England) · 2013Article
- E2F4 plays a key role in Burkitt lymphoma tumorigenesis.Leukemia · 2012Article
- E2F-1 has dual roles depending on the cell cycle.International journal of biological sciences · 2010Article
- E2F1 expression is deregulated and plays an oncogenic role in sporadic Burkitt's lymphoma.Cancer research · 2009Article
- Overexpression of E2F-5 correlates with a pathological basal phenotype and a worse clinical outcome.British journal of cancer · 2009Article
- Mechanisms involved in Burkitt's tumor formation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2008Review
- The histone deacetylase inhibitor trichostatin A induces GADD45 gamma expression via Oct and NF-Y binding sites.Oncogene · 2008Article
- Expression of Dmp1 in specific differentiated, nonproliferating cells and its regulation by E2Fs.Oncogene · 2006Article
- Functional evolution of the vertebrate Myb gene family: B-Myb, but neither A-Myb nor c-Myb, complements Drosophila Myb in hemocytes.Genetics · 2005Article
- Identification of a negative regulatory element in the Epstein-Barr virus Zta transactivation domain that is regulated by the cell cycle control factors c-Myc and E2F1.Journal of virology · 2004Article
- Control of cyclin G2 mRNA expression by forkhead transcription factors: novel mechanism for cell cycle control by phosphoinositide 3-kinase and forkhead.Molecular and cellular biology · 2004Article
- GATA-1 and c-myb crosstalk during red blood cell differentiation through GATA-1 binding sites in the c-myb promoter.Oncogene · 2003Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Most E2F-driven promoters are transiently activated around the G(1)/S transition. Although the promoter for the c-myb proto-oncogene harbors an E2F element, it is induced early in G(1) following entry into the cell cycle. Furthermore, this promoter remains active throughout subsequent cell cycles. Since E2F sites function as repressor elements during G(1) (due to the association of pRb with E2F factors), we investigated whether the E2F element in the c-myb promoter is regulated differently than E2F elements in promoters that are repressed during G(1). By gel shift analysis, the E2F element from the c-myb promoter was found to form a unique complex, referred to as E2Fmyb-sp, which was not observed with E2F elements from several other promoters. Antibodies to DP-1, E2F1 to -5, p107, or pRb failed to either supershift or block E2Fmyb-sp complex formation. Methylation interference experiments indicate that the DNA contact residues for the E2Fmyb-sp complex are distinct from but overlapping with residues required for the binding of E2F proteins. In addition to the identification of E2Fmyb-sp, we have found that SP-1 binds to the c-myb E2F element. Functional studies revealed that E2Fmyb-sp and/or SP-1 are required to achieve full activation of the c-myb promoter in different cell types and to maintain elevated expression of the c-myb promoter during G(1) in NIH 3T3 cells. These studies demonstrate that E2F elements can be regulated differently through the binding of unique sets of proteins.
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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.