ArticleDifferentiation; research in biological diversity2009
Non-canonical role for the TRAIL receptor DR5/FADD/caspase pathway in the regulation of MyoD expression and skeletal myoblast differentiation.
Article in Differentiation; research in biological diversity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Sublethal Caspase-8 Activation Drives Radiation-Induced Genetic Instability and Oncogenic Transformation Through Endonuclease G and Non-Canonical NF-κB Signaling.International journal of molecular sciences · 2026Article
- Regulation of Myogenic Cell Apoptosis, UPS, and Autophagy During Mammalian Skeletal Myogenesis.Cells · 2026Review
- Review
- Death receptor 5 is required for intestinal stem cell activity during intestinal epithelial renewal at homoeostasis.Cell death & disease · 2024Article
- TRAIL and its receptors in cardiac diseases.Frontiers in physiology · 2023Review
- TRAIL/DR5 pathway promotes AKT phosphorylation, skeletal muscle differentiation, and glucose uptake.Cell death & disease · 2021Article
- Muscle-derived TRAIL negatively regulates myogenic differentiation.Experimental cell research · 2020Article
- Basal Signalling Through Death Receptor 5 and Caspase 3 Activates p38 Kinase to Regulate Serum Response Factor (SRF)-Mediated MyoD Transcription.Journal of molecular signaling · 2020Article
- Death receptor 5 contributes to cardiomyocyte hypertrophy through epidermal growth factor receptor transactivation.Journal of molecular and cellular cardiology · 2019Article
- Review
- Mitophagy regulates mitochondrial network signaling, oxidative stress, and apoptosis during myoblast differentiation.Autophagy · 2019Article
- The muscle regulatory transcription factor MyoD participates with p53 to directly increase the expression of the pro-apoptotic Bcl2 family member PUMA.Apoptosis : an international journal on programmed cell death · 2017Article
- Surviving apoptosis: life-death signaling in single cells.Trends in cell biology · 2015Review
- Regulating TRAIL receptor-induced cell death at the membrane : a deadly discussion.Recent patents on anti-cancer drug discovery · 2011Review
- Caspase-3, myogenic transcription factors and cell cycle inhibitors are regulated by leukemia inhibitory factor to mediate inhibition of myogenic differentiation.Skeletal muscle · 2011Article
- TRAIL-R4 promotes tumor growth and resistance to apoptosis in cervical carcinoma HeLa cells through AKT.PloS one · 2011Article
- Stress-induced C/EBP homology protein (CHOP) represses MyoD transcription to delay myoblast differentiation.PloS one · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We report herein that the TRAIL receptor DR5/FADD/caspase pathway plays a role in skeletal myoblast differentiation through modulation of the expression of the muscle regulatory transcription factor MyoD. Specifically, treatment with the selective caspase 3 inhibitor DEVD-fmk or the selective caspase 8 inhibitor IETD-fmk in growth media (GM), prior to culture in differentiation media (DM), inhibited differentiation. Further, this treatment resulted in decreased levels of MyoD message and protein. We next explored a role for the TRAIL receptor DR5/FADD pathway. We found that expression of either dominant negative (dn) FADD or dominant negative (dn) DR5 also resulted in decreased levels of MyoD mRNA and protein and blocked differentiation. This decreased level of MyoD mRNA was not a consequence of altered stability. Treatment with TSA, an inhibitor of histone deacetylases (HDACs), allowed MyoD expression in myoblasts expressing dnDR5. Finally, acetylation of histones associated with the distal regulatory region (DRR) enhancer of MyoD was decreased in myoblasts expressing dnDR5. Thus, our data suggests a non-canonical role for the TRAIL receptor/FADD pathway in the regulation of MyoD expression and skeletal myoblast 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.