ArticleCell cycle (Georgetown, Tex.)2013
LXCXE-independent chromatin remodeling by Rb/E2f mediates neuronal quiescence.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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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.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.Nature communications · 2024Article
- HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes.bioRxiv : the preprint server for biology · 2023Article
- Genetics in ophthalmology: molecular blueprints of retinoblastoma.Human genomics · 2023Review
- Rb deficiency, neuronal survival and neurodegeneration: In search of the perfect mouse model.Current research in neurobiology · 2023Review
- The pro-death role of Cited2 in stroke is regulated by E2F1/4 transcription factors.The Journal of biological chemistry · 2019Article
- Differential impact of RB status on E2F1 reprogramming in human cancer.The Journal of clinical investigation · 2018Article
- "Till Death Do Us Part": A Potential Irreversible Link Between Aberrant Cell Cycle Control and Neurodegeneration in the Adult Olfactory Bulb.Frontiers in neuroscience · 2018Review
- Inhibition of pluripotency networks by the Rb tumor suppressor restricts reprogramming and tumorigenesis.Cell stem cell · 2015Article
- Transcriptional control of stem cell fate by E2Fs and pocket proteins.Frontiers in genetics · 2015Review
- Defining a new vision for the retinoblastoma gene: report from the 3rd International Rb Meeting.Cell division · 2013Article
- Rb and chromatin remodeling in the maintenance of the post-mitotic state of neurons.Cell cycle (Georgetown, Tex.) · 2013Article
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5 authors at 2 institutions in 1 country.
Funding
Abstract
Neuronal survival is dependent upon the retinoblastoma family members, Rb1 (Rb) and Rb2 (p130). Rb is thought to regulate gene repression, in part, through direct recruitment of chromatin modifying enzymes to its conserved LXCXE binding domain. We sought to examine the mechanisms that Rb employs to mediate cell cycle gene repression in terminally differentiated cortical neurons. Here, we report that Rb loss converts chromatin at the promoters of E2f-target genes to an activated state. We established a mouse model system in which Rb-LXCXE interactions could be induciblely disabled. Surprisingly, this had no effect on survival or gene silencing in neuronal quiescence. Absence of the Rb LXCXE-binding domain in neurons is compatible with gene repression and long-term survival, unlike Rb deficiency. Finally, we are able to show that chromatin activation following Rb deletion occurs at the level of E2fs. Blocking E2f-mediated transcription downstream of Rb loss is sufficient to maintain chromatin in an inactive state. Taken together our results suggest a model whereby Rb-E2f interactions are sufficient to maintain gene repression irrespective of LXCXE-dependent chromatin remodeling.
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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.