ArticleThe Journal of cell biology2010
Rescue of myogenic defects in Rb-deficient cells by inhibition of autophagy or by hypoxia-induced glycolytic shift.
Article in The Journal of cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 42 citations in OpenAlex.
- Ageing-Associated Dysregulation of Myogenic Differentiation in Inclusion Body Myositis.Journal of cachexia, sarcopenia and muscle · 2026Review
- The tumor suppressor pRb and its relative p130 are required to maintain murine adult skeletal muscle homeostasis.Oncogene · 2025Article
- RB1 controls differentiation through positive regulation of phosphoglycerate mutases.Cell death & disease · 2025Article
- Thinking (Metastasis) outside the (Primary Tumor) Box.Cancers · 2023Article
- Retinoblastoma: present scenario and future challenges.Cell communication and signaling : CCS · 2023Review
- p107 mediated mitochondrial function controls muscle stem cell proliferative fates.Nature communications · 2021Article
- Tumor Milieu Controlled by RB Tumor Suppressor.International journal of molecular sciences · 2020Review
- The RB-IL-6 axis controls self-renewal and endocrine therapy resistance by fine-tuning mitochondrial activity.Oncogene · 2017Article
- Intersection of retinoblastoma tumor suppressor function, stem cells, metabolism, and inflammation.Cancer science · 2017Review
- Loss of p16Oncotarget · 2017Article
- Decreased transcriptional corepressor p107 is associated with exercise-induced mitochondrial biogenesis in human skeletal muscle.Physiological reports · 2017Article
- E2F1, a Novel Regulator of Metabolism.Frontiers in endocrinology · 2017Review
- RB1 deficiency in triple-negative breast cancer induces mitochondrial protein translation.The Journal of clinical investigation · 2016Article
- RB1: a prototype tumor suppressor and an enigma.Genes & development · 2016Review
- Retinoblastoma tumor suppressor functions shared by stem cell and cancer cell strategies.World journal of stem cells · 2016Review
- Changes in Communication between Muscle Stem Cells and their Environment with Aging.Journal of neuromuscular diseases · 2015Article
- Proteomic analysis of pRb loss highlights a signature of decreased mitochondrial oxidative phosphorylation.Genes & development · 2015Article
- Emerging links between E2F control and mitochondrial function.Cancer research · 2015Review
- Repression by RB1 characterizes genes involved in the penultimate stage of erythroid development.Cell cycle (Georgetown, Tex.) · 2015Article
- A retinoblastoma allele that is mutated at its common E2F interaction site inhibits cell proliferation in gene-targeted mice.Molecular and cellular biology · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The retinoblastoma tumor suppressor (pRb) is thought to orchestrate terminal differentiation by inhibiting cell proliferation and apoptosis and stimulating lineage-specific transcription factors. In this study, we show that in the absence of pRb, differentiating primary myoblasts fuse to form short myotubes that never twitch and degenerate via a nonapoptotic mechanism. The shortened myotubes exhibit an impaired mitochondrial network, mitochondrial perinuclear aggregation, autophagic degradation, and reduced adenosine triphosphate production. Bcl-2 and autophagy inhibitors restore mitochondrial function and rescue muscle degeneration, leading to formation of long, twitching myotubes that express normal levels of muscle-specific proteins and stably exit the cell cycle. A hypoxia-induced glycolytic switch also rescues the myogenic defect after either chronic or acute inactivation of Rb in a hypoxia-inducible factor-1 (HIF-1)-dependent manner. These results demonstrate that pRb is required to inhibit apoptosis in myoblasts and autophagy in myotubes but not to activate the differentiation program, and they also reveal a novel link between pRb and cell metabolism.
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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.