Yonghao Yu
Discovered Grb10 as the mTORC1 substrate that shuts off insulin signaling's own feedback brake
BS Chemistry, Fudan Univ. · PhD Chemistry, UC Berkeley (Julie Leary) · postdoc, Harvard Medical School (Steven Gygi & John Blenis) · Associate Professor, UT Southwestern · now Professor, Columbia University Irving Medical Center
Yu Lab, Columbia University Irving Medical Center ↗
As Blenis-lab postdoc, large-scale phosphoproteomics (YUX2011) identified Grb10 as a direct mTORC1 substrate whose stabilization suppresses PI3K/ERK-MAPK signaling downstream of insulin/IGF-1 receptor — discovered independently and near-simultaneously by Sabatini lab's Peggy Hsu (also in this Atlas).
Trained as a chemist before biology; built labs at UT Southwestern then Columbia, studying covalent protein modifications (phosphorylation, poly-ADP-ribosylation, tyrosine sulfation) and covalent drugs against 'undruggable' targets.
**Poznámka (viz flag výše):** Zadání obsahovalo i druhou 2026 studii (YU2026, sepse/vodík), kterou jsme z highlights vynechali — jde pravděpodobně o jinou osobu stejného jména na Tianjin Medical University (Čína), bez institucionální vazby na tuto osobu.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2011 | M | Phosphoproteomic analysis identifies Grb10 as an mTORC1 substrate that negatively regulates insulin signaling YUX2011 Phosphoproteomics identify Grb10 as a direct mTORC1 substrate creating negative feedback on insulin/PI3K signaling. |
| 2026 | A | High-concentration hydrogen mitigates cognitive impairment in a murine model of Sepsis-associated encephalopathy by enhancing oligodendrocyte maturation and myelination in the mPFC YU2026 In a mouse model of sepsis-associated encephalopathy (SAE), mTOR hyperactivation impairs oligodendrocyte maturation and causes cognitive deficits; hydrogen gas and rapamycin suppress mTOR, restore myelination, and improve cognition in these mice. |