ArticleMolecular and cellular biology2004
RB reversibly inhibits DNA replication via two temporally distinct mechanisms.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- Regulation of cell cycle in plant gametes: when is the right time to divide?Development (Cambridge, England) · 2025Review
- Meiosis-specific cohesin complexes display essential and distinct roles in mitotic embryonic stem cell chromosomes.Genome biology · 2022Article
- The N Terminus of the Retinoblastoma Protein Inhibits DNA Replication via a Bipartite Mechanism Disrupted in Partially Penetrant Retinoblastomas.Molecular and cellular biology · 2015Article
- Recruitment of Pontin/Reptin by E2f1 amplifies E2f transcriptional response during cancer progression.Nature communications · 2015Article
- Inactivation of Rb and E2f8 synergizes to trigger stressed DNA replication during erythroid terminal differentiation.Molecular and cellular biology · 2014Article
- Epigenetic regulation of cardiac myocyte differentiation.Frontiers in genetics · 2014Review
- Article
- RB1, development, and cancer.Current topics in developmental biology · 2011Review
- Prohibitin physically interacts with MCM proteins and inhibits mammalian DNA replication.Cell cycle (Georgetown, Tex.) · 2009Article
- Cyclin-dependent kinase 4/6 activity is a critical determinant of pre-replication complex assembly.Oncogene · 2008Article
- Coordinate regulation of Fanconi anemia gene expression occurs through the Rb/E2F pathway.Oncogene · 2008Article
- The ATR-mediated S phase checkpoint prevents rereplication in mammalian cells when licensing control is disrupted.The Journal of cell biology · 2007Article
- Dynamic assembly of chromatin complexes during cellular senescence: implications for the growth arrest of human melanocytic nevi.Aging cell · 2007Article
- Proapoptotic role of novel gene-expression factors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2007Review
- Cell size checkpoint control by the retinoblastoma tumor suppressor pathway.PLoS genetics · 2006Article
- Distinct action of the retinoblastoma pathway on the DNA replication machinery defines specific roles for cyclin-dependent kinase complexes in prereplication complex assembly and S-phase progression.Molecular and cellular biology · 2006Article
- Review
- CtIP activates its own and cyclin D1 promoters via the E2F/RB pathway during G1/S progression.Molecular and cellular biology · 2006Article
- Review
- cAMP-mediated inhibition of DNA replication and S phase progression: involvement of Rb, p21Cip1, and PCNA.Molecular biology of the cell · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The retinoblastoma (RB) tumor suppressor is a critical negative regulator of cellular proliferation. Repression of E2F-dependent transcription has been implicated as the mechanism through which RB inhibits cell cycle progression. However, recent data have suggested that the direct interaction of RB with replication factors or sites of DNA synthesis may contribute to its ability to inhibit S phase. Here we show that RB does not exert a cis-acting effect on DNA replication. Furthermore, the localization of RB was distinct from replication foci in proliferating cells. While RB activation strongly attenuated the RNA levels of multiple replication factors, their protein expression was not diminished coincident with cell cycle arrest. During the first 24 h of RB activation, components of the prereplication complex, initiation factors, and the clamp loader complex (replication factor C) remained tethered to chromatin. In contrast, the association of PCNA and downstream components of the processive replication machinery was specifically disrupted. This signaling from RB occurred in a manner dependent on E2F-mediated transcriptional repression. Following long-term activation of RB, we observed the attenuation of multiple replication factors, the complete cessation of DNA synthesis, and impaired replicative capacity in vitro. Therefore, functional distinctions exist between the "chronic" RB-mediated arrest state and the "acute" arrest state. Strikingly, attenuation of RB activity reversed both acute and chronic replication blocks. Thus, continued RB action is required for the maintenance of two kinetically and functionally distinct modes of replication inhibition.
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Registered trials
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.