ArticleMolecular and cellular biology2010
A G1 checkpoint mediated by the retinoblastoma protein that is dispensable in terminal differentiation but essential for senescence.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 55 citations in OpenAlex.
- One hotspotFrontiers in oncology · 2026Article
- Epstein-Barr virus replication within differentiated epithelia requires pRb sequestration of activator E2F transcription factors.Journal of virology · 2024Article
- The Inhibitors of CDK4/6 from a Library of Marine Compound Database: A Pharmacophore, ADMET, Molecular Docking and Molecular Dynamics Study.Marine drugs · 2022Article
- An RB-Condensin II Complex Mediates Long-Range Chromosome Interactions and Influences Expression at Divergently Paired Genes.Molecular and cellular biology · 2020Article
- Differentiation-Induced Remodelling of Store-Operated Calcium Entry Is Independent of Neuronal or Glial Phenotype but Modulated by Cellular Context.Molecular neurobiology · 2019Article
- CDK4/6 Inhibition in Cancer: Beyond Cell Cycle Arrest.Trends in cell biology · 2018Review
- Autochthonous tumors driven byProceedings of the National Academy of Sciences of the United States of America · 2018Article
- The Retinoblastoma (RB) Tumor Suppressor: Pushing Back against Genome Instability on Multiple Fronts.International journal of molecular sciences · 2017Review
- Multiple molecular interactions redundantly contribute to RB-mediated cell cycle control.Cell division · 2017Article
- Roles of pRB in the Regulation of Nucleosome and Chromatin Structures.BioMed research international · 2016Review
- Deficiencies in Cellular Processes Modulated by the Retinoblastoma Protein Do Not Account for Reduced Human Cytomegalovirus Replication in Its Absence.Journal of virology · 2015Article
- Review
- Novel mutations in the RB1 gene from Chinese families with a history of retinoblastoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Structural and functional characterization of the acidic region from the RIZ tumor suppressor.Biochemistry · 2015Article
- Inhibition of pluripotency networks by the Rb tumor suppressor restricts reprogramming and tumorigenesis.Cell stem cell · 2015Article
- Retinoblastoma protein (RB) interacts with E2F3 to control terminal differentiation of Sertoli cells.Cell death & disease · 2014Article
- A retinoblastoma allele that is mutated at its common E2F interaction site inhibits cell proliferation in gene-targeted mice.Molecular and cellular biology · 2014Article
- Targeting tumor suppressor networks for cancer therapeutics.Current drug targets · 2014Article
- Complete senescence: RB and PML share the task.Cell cycle (Georgetown, Tex.) · 2014Article
- Dystonia, facial dysmorphism, intellectual disability and breast cancer associated with a chromosome 13q34 duplication and overexpression of TFDP1: case report.BMC medical genetics · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Terminally differentiated cell types are needed to live and function in a postmitotic state for a lifetime. Cellular senescence is another type of permanent arrest that blocks the proliferation of cells in response to genotoxic stress. Here we show that the retinoblastoma protein (pRB) uses a mechanism to block DNA replication in senescence that is distinct from its role in permanent cell cycle exit associated with terminal differentiation. Our work demonstrates that a subtle mutation in pRB that cripples its ability to interact with chromatin regulators impairs heterochromatinization and repression of E2F-responsive promoters during senescence. In contrast, terminally differentiated nerve and muscle cells bearing the same mutation fully exit the cell cycle and block E2F-responsive gene expression by a different mechanism. Remarkably, this reveals that pRB recruits chromatin regulators primarily to engage a stress-responsive G(1) arrest program.
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What OpenQuestion holds
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.