ArticleThe Journal of biological chemistry2014
Retinoblastoma protein and MyoD function together to effect the repression of Fra-1 and in turn cyclin D1 during terminal cell cycle arrest associated with myogenesis.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Analysing Differential Alternative Splicing Events and Their Impact on Retinoblastoma Progression Using RNA-seq Metadata.Asian Pacific journal of cancer prevention : APJCP · 2025Pooled it
- Fra-1 promotes gastric cancer progression by regulating macrophage polarization and transcriptionally activating HMGA2 expression.Cell death discovery · 2025Article
- MyoD1 promotes the transcription of BIK and plays an apoptosis-promoting role in the development of gastric cancer.Cell cycle (Georgetown, Tex.) · 2024Article
- RBL2-E2F-GCN5 guide cell fate decisions during tissue specification by regulating cell-cycle-dependent fluctuations of non-cell-autonomous signaling.Cell reports · 2023Article
- Comprehensive Analysis of Genes Associated With Sudden Infant Death Syndrome.Frontiers in pediatrics · 2021Article
- Beyond What Your Retina Can See: Similarities of Retinoblastoma Function between Plants and Animals, from Developmental Processes to Epigenetic Regulation.International journal of molecular sciences · 2020Review
- Involvement of Fra-1 in Retinal Ganglion Cell Apoptosis in Rat Light-Induced Retina Damage Model.Cellular and molecular neurobiology · 2017Article
- Cell cycle regulation of embryonic stem cells and mouse embryonic fibroblasts lacking functional Pax7.Cell cycle (Georgetown, Tex.) · 2016Article
- Inhibitory effect of MyoD on the proliferation of breast cancer cells.Oncology letters · 2016Article
- Contextualizing the Genes Altered in Bladder Neoplasms in Pediatric andTeen Patients Allows Identifying Two Main Classes of Biological ProcessesInvolved and New Potential Therapeutic Targets.Current genomics · 2016Article
- β-Arrestin scaffolds and signaling elements essential for the obestatin/GPR39 system that determine the myogenic program in human myoblast cells.Cellular and molecular life sciences : CMLS · 2016Article
- MiR-492 contributes to cell proliferation and cell cycle of human breast cancer cells by suppressing SOX7 expression.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- MiR-615 inhibited cell proliferation and cell cycle of human breast cancer cells by suppressing of AKT2 expression.International journal of clinical and experimental medicine · 2015Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The acquisition of skeletal muscle-specific function and terminal cell cycle arrest represent two important features of the myogenic differentiation program. These cellular processes are distinct and can be separated genetically. The lineage-specific transcription factor MyoD and the retinoblastoma protein pRb participate in both of these cellular events. Whether and how MyoD and pRb work together to effect terminal cell cycle arrest is uncertain. To address this question, we focused on cyclin D1, whose stable repression is required for terminal cell cycle arrest and execution of myogenesis. MyoD and pRb are both required for the repression of cyclin D1; their actions, however, were found not to be direct. Rather, they operate to regulate the immediate early gene Fra-1, a critical player in mitogen-dependent induction of cyclin D1. Two conserved MyoD-binding sites were identified in an intronic enhancer of Fra-1 and shown to be required for the stable repression of Fra-1 and, in turn, cyclin D1. Localization of MyoD alone to the intronic enhancer of Fra-1 in the absence of pRb was not sufficient to elicit a block to Fra-1 induction; pRb was also recruited to the intronic enhancer in a MyoD-dependent manner. These observations suggest that MyoD and pRb work together cooperatively at the level of the intronic enhancer of Fra-1 during terminal cell cycle arrest. This work reveals a previously unappreciated link between a lineage-specific transcription factor, a tumor suppressor, and a proto-oncogene in the control of an important facet of myogenic differentiation.
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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.