Mustafa Sahin
Senior author of the studies showing that mTOR signalling reaches the circadian clock through BMAL1, and a physician-scientist focused on tuberous sclerosis, the classic disease of overactive mTOR.
Neurologist-in-Chief (chair since 2024), Department of Neurology, Boston Children's Hospital, and Professor of Neurology, Harvard Medical School · residencies in pediatrics (Children's Hospital of Philadelphia) and child neurology (Boston Children's, 2000) · MD, PhD in Neurobiology, Yale University School of Medicine (1995)
Sahin Lab, Rosamund Stone Zander and Hansjoerg Wyss Translational Neuroscience Center, Department of Neurology, Boston Children's Hospital and Harvard Medical School (Boston, Massachusetts, USA) ↗ Lab lineage1 direct trainee →
Portrait: Rosamund Stone Zander and Hansjoerg Wyss Translational Neuroscience Center, Boston Children's Hospital
Sahin's lab showed that S6K1, downstream of mTORC1, phosphorylates the clock protein BMAL1, which lets it act as a translation factor and gives protein synthesis a daily rhythm (LIP2015). In mouse models of tuberous sclerosis, where mTOR is stuck on, his team found raised BMAL1 levels and disturbed circadian behaviour that improved when BMAL1 was genetically lowered (LIP2017).
He earned his MD and PhD at Yale and trained in pediatrics and child neurology in Philadelphia and Boston. He directs the Translational Neuroscience Center at Boston Children's Hospital, became chair of its Department of Neurology in 2024, cares for children with tuberous sclerosis and was elected to the National Academy of Medicine in 2023.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2015 | A | The Circadian Protein BMAL1 Regulates Translation in Response to S6K1-Mediated Phosphorylation LIP2015 Senior author: S6K1 phosphorylates BMAL1, making it a translation factor that links mTOR to the circadian clock. |
| 2017 | A | Aberrant Proteostasis of BMAL1 Underlies Circadian Abnormalities in a Paradigmatic mTOR-opathy LIP2017 Senior author: mTOR overactivity in tuberous sclerosis models deregulates BMAL1 and disrupts circadian rhythms. |
Co-authors in the Atlas
People with a profile here who share at least one study with Mustafa Sahin.
- Ashwin Nathan 2 shared studies Co-author on both Boston Children's Hospital studies linking mTOR signalling to the circadian clock protein BMAL1.
- Elizabeth D. Yuan 2 shared studies Second author on the study showing that S6K1 phosphorylates BMAL1 to link mTOR signalling with circadian protein synthesis, and co-author on the follow-up in tuberous sclerosis models.
- Fred C. Davis 2 shared studies Circadian biologist from Northeastern University who brought expertise on the brain's master clock to two studies linking mTOR and the clock protein BMAL1.
- Jonathan O. Lipton 2 shared studies First author of the two studies that tie mTOR signalling to the circadian clock protein BMAL1: S6K1 phosphorylates BMAL1 to drive translation, and constant mTOR activity in tuberous sclerosis disturbs the clock.
- Lara M. Boyle 2 shared studies Research assistant at Boston Children's Hospital who co-authored both studies linking mTOR to the clock protein BMAL1, including the tuberous sclerosis study where she was second author.
- John M. Asara Mass-spectrometry specialist whose core facility supplied metabolomics and proteomics for several mTOR studies, including measurements of purine, pyrimidine and SAM metabolism downstream of mTORC1.
Every researcher with a profile →
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