Yann‐Gaël Gangloff

Université Claude Bernard Lyon 1 — France

Biochemistry, Genetics and Molecular Biology · Life Sciences

22h-index2.7kcitations33works4.02yr avg
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Research Topics

Genomics and Chromatin Dynamics(11), Muscle Physiology and Disorders(11), RNA Research and Splicing(9), RNA and protein synthesis mechanisms(3), Autophagy in Disease and Therapy(3)

Publications33 total

Muscle mTOR controls iron homeostasis and ferritinophagy via NRF2, HIFs and AKT/PKB signaling pathways
Cellular and Molecular Life Sciences·2025· 8 citedOpen Access
Combining SMN2 splicing modifiers with HDAC6 inhibition greatly improves muscle function and survival in Spinal Muscular Atrophy
2025
H syndrome mimicking Erdheim Chester disease: new entity and therapeutic perspectives
Haematologica·2023· 6 citedOpen Access
Pharmacological inhibition of HDAC6 improves muscle phenotypes in dystrophin-deficient mice by downregulating TGF-β via Smad3 acetylation
Nature Communications·2022· 40 citedOpen Access
Pharmacological inhibition of HDAC6 downregulates TGF-β via Smad2/3 acetylation and improves dystrophin-deficient muscles
2022· 3 citedOpen Access
The ESCRT-0 subcomplex component Hrs/Hgs is a master regulator of myogenesis via modulation of signaling and degradation pathways
BMC Biology·2021· 14 citedOpen Access
Additional file 11 of The ESCRT-0 subcomplex component Hrs/Hgs is a master regulator of myogenesis via modulation of signaling and degradation pathways
Figshare·2021Open Access
H2A.Z is dispensable for both basal and activated transcription in post-mitotic mouse muscles
Nucleic Acids Research·2020· 33 citedOpen Access
Lack of muscle mTOR kinase activity causes early onset myopathy and compromises whole‐body homeostasis
Journal of Cachexia Sarcopenia and Muscle·2018· 28 citedOpen Access
Increased Serpina3n release into circulation during glucocorticoid‐mediated muscle atrophy
Journal of Cachexia Sarcopenia and Muscle·2018· 71 citedOpen Access
Increased release of Serpina3n into circulation during glucocorticoid-mediated muscle atrophy
HAL (Le Centre pour la Communication Scientifique Directe)·2018
Resistance exercise initiates mechanistic target of rapamycin (mTOR) translocation and protein complex co-localisation in human skeletal muscle
Scientific Reports·2017· 116 citedOpen Access
mTOR inactivation in myocardium from infant mice rapidly leads to dilated cardiomyopathy due to translation defects and p53/JNK-mediated apoptosis
Journal of Molecular and Cellular Cardiology·2016· 51 cited
S6K1 controls pancreatic β cell size independently of intrauterine growth restriction
Journal of Clinical Investigation·2015· 24 citedOpen Access
0452 : MTOR inactivation during early postnatal development of mice myocardium leads to severe dilated cardiomyopathy due to altered translational efficiency and hypoxia-induced apoptosis
Archives of Cardiovascular Diseases Supplements·2015
The metabolic checkpoint kinase mTOR is essential for IL-15 signaling during the development and activation of NK cells
Nature Immunology·2014· 586 citedOpen Access
Arrest of Myelination and Reduced Axon Growth When Schwann Cells Lack mTOR
Journal of Neuroscience·2012· 138 citedOpen Access
Myopathy caused by mammalian target of rapamycin complex 1 (mTORC1) inactivation is not reversed by restoring mitochondrial function
Proceedings of the National Academy of Sciences·2011· 43 cited
Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy
The Journal of Experimental Medicine·2009· 17 cited
Muscle inactivation of mTOR causes metabolic and dystrophin defects leading to severe myopathy
The Journal of Cell Biology·2009· 368 citedOpen Access
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Frequent Co-authors

Laurent Schaeffer(16), Irwin Davidson(11), Christophe Romier(8), Pascal Leblanc(7), Laetitia Mazelin(6), Vincent Moncollin(6), Agnès Conjard‐Duplany(6), Alexis Osseni(6), Sebastiaan Werten(5), Edwige Belotti(5), Matthias Mueller(4), George Thomas(4), Sara C. Kozma(4), Valérie Risson(4), Dominique Baas(4), Sylvie Thuault(4), L Carré(4), Dino Moras(4), Klaas Romanino(3), Markus A. Rüegg(3)