ArticleMolecular and cellular biology1997
Identification of positively and negatively acting elements regulating expression of the E2F2 gene in response to cell growth signals.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 212 citations in OpenAlex.
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- Unraveling MYC's Role in Orchestrating Tumor Intrinsic and Tumor Microenvironment Interactions Driving Tumorigenesis and Drug Resistance.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Review
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- Sulfopin is a covalent inhibitor of Pin1 that blocks Myc-driven tumors in vivo.Nature chemical biology · 2021Article
- MYC: a multipurpose oncogene with prognostic and therapeutic implications in blood malignancies.Journal of hematology & oncology · 2021Review
- Gene Transactivation and Transrepression in MYC-Driven Cancers.International journal of molecular sciences · 2021Review
- Molecular Analysis of the E2F/DP Gene Family ofFrontiers in plant science · 2021Article
- Blockade of CDK7 Reverses Endocrine Therapy Resistance in Breast Cancer.International journal of molecular sciences · 2020Article
- Regulation of Cell Cycle Entry and Exit: A Single Cell Perspective.Comprehensive Physiology · 2019Review
- Strategies to generate functionally normal neutrophils to reduce infection and infection-related mortality in cancer chemotherapy.Pharmacology & therapeutics · 2019Review
- JMJD6 is a tumorigenic factor and therapeutic target in neuroblastoma.Nature communications · 2019Article
- Long noncoding RNA EMS connects c-Myc to cell cycle control and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- A positive role of c-Myc in regulating androgen receptor and its splice variants in prostate cancer.Oncogene · 2019Article
- Estrogen-independent Myc overexpression confers endocrine therapy resistance on breast cancer cells expressing ERαY537S and ERαD538G mutations.Cancer letters · 2019Article
- Post-translational modification localizes MYC to the nuclear pore basket to regulate a subset of target genes involved in cellular responses to environmental signals.Genes & development · 2018Article
- Cell Proliferation in Neuroblastoma.Cancers · 2016Review
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- Redeployment of Myc and E2f1-3 drives Rb-deficient cell cycles.Nature cell biology · 2015Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mammalian cell growth is governed by regulatory activities that include the products of genes such as c-myc and ras that act early in G1, as well as the E2F family of transcription factors that accumulate later in G1 to regulate the expression of genes involved in DNA replication. Previous work has shown that the expression of the E2F1, E2F2, and E2F3 gene products is tightly regulated by cell growth. To further explore the mechanisms controlling accumulation of E2F activity, we have isolated genomic sequences flanking the 5' region of the E2F2 coding sequence. Various assays demonstrate promoter activity in this sequence that reproduces the normal control of E2F2 expression during a growth stimulation. Sequence comparison reveals the presence of a variety of known transcription factor binding sites, including E-box elements that are consensus Myc binding sites, as well as E2F binding sites. We demonstrate that the E-box elements, which we show can function as Myc-responsive sites, contribute in a positive fashion to promoter function. We also find that E2F-dependent negative regulation in quiescent cells plays a significant role in the cell growth-dependent control of the promoter, similar to the regulation of the E2F1 gene promoter.
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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.