ArticleMolecular and cellular biology1996
Expression of dominant-negative mutant DP-1 blocks cell cycle progression in G1.
Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 138 citations in OpenAlex.
- Bypassing the guardian: regulated cell death pathways in p53-mutant cancers.Cellular & molecular biology letters · 2025Review
- Genome-wide ATAC-see screening identifies TFDP1 as a modulator of global chromatin accessibility.Nature genetics · 2024Article
- Biphasic JNK-Erk signaling separates the induction and maintenance of cell senescence after DNA damage induced by topoisomerase II inhibition.Cell systems · 2023Article
- Normal cell cycle progression requires negative regulation of E2F1 by Groucho during S phase and its relief at G2 phase.Development (Cambridge, England) · 2023Article
- Chromatin-bound RB targets promoters, enhancers, and CTCF-bound loci and is redistributed by cell-cycle progression.Molecular cell · 2022Article
- Active RB causes visible changes in nuclear organization.The Journal of cell biology · 2022Article
- Loss of dE2F compromises mitochondrial function.Developmental cell · 2013Article
- LXCXE-independent chromatin remodeling by Rb/E2f mediates neuronal quiescence.Cell cycle (Georgetown, Tex.) · 2013Article
- Identification of E2F target genes that are rate limiting for dE2F1-dependent cell proliferation.Developmental dynamics : an official publication of the American Association of Anatomists · 2012Article
- The retinoblastoma protein is essential for survival of postmitotic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- The RIP140 gene is a transcriptional target of E2F1.PloS one · 2012Article
- Adenovirus E1A directly targets the E2F/DP-1 complex.Journal of virology · 2011Article
- Context-dependent requirement for dE2F during oncogenic proliferation.PLoS genetics · 2008Article
- Phosphorylation of pRb by cyclin D kinase is necessary for development of cardiac hypertrophy.Cell proliferation · 2008Article
- A small-molecule E2F inhibitor blocks growth in a melanoma culture model.Cancer research · 2008Article
- p110 CUX1 cooperates with E2F transcription factors in the transcriptional activation of cell cycle-regulated genes.Molecular and cellular biology · 2008Article
- Molecular signature of CD34(+) hematopoietic stem and progenitor cells of patients with CML in chronic phase.Leukemia · 2007Article
- Reduction of total E2F/DP activity induces senescence-like cell cycle arrest in cancer cells lacking functional pRB and p53.The Journal of cell biology · 2005Article
- The helix-loop-helix protein ID1 localizes to centrosomes and rapidly induces abnormal centrosome numbers.Oncogene · 2004Article
- Autorepression of c-myc requires both initiator and E2F-binding site elements and cooperation with the p107 gene product.Oncogene · 2004Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Unregulated expression of the transcription factor E2F promotes the G1-to-S phase transition in cultured mammalian cells. However, there has been no direct evidence for an E2F requirement in this process. To demonstrate that E2F is obligatory for cell cycle progression, we attempted to inactivate E2F by overexpressing dominant-negative forms of one of its heterodimeric partners, DP-1. We dissected the functional domains of DP-1 and separated the region that facilitate heterodimer DNA binding from the E2F dimerization domain. Various DP-1 mutants were introduced into cells via transfection, and the cell cycle profile of the transfected cells was analyzed by flow cytometry. Expression of wild-type DP-1 or DP-1 mutants that bind to both DNA and E2F drove cells into S phase. In contrast, DP-1 mutants that retained E2F binding but lost DNA binding arrested cells in the G1 phase of the cell cycle. The DP-1 mutants that were unable to bind DNA resulted in transcriptionally inactive E2F complexes, suggesting that the G1 arrest is caused by formation of defective E2F heterodimers. Furthermore, the G1 arrest instigated by these DP-1 mutants could be rescued by coexpression of wild-type E2F or DP protein. These experiments define functional domains of DP and demonstrate a requirement for active E2F complexes in cell cycle progression.
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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.