Estela Jacinto
Helped define mTORC2 and its rapamycin-insensitive control of Akt
PhD, UC San Diego · postdoc, Biozentrum, University of Basel (Michael Hall lab) · Professor of Biochemistry & Molecular Biology, Rutgers Robert Wood Johnson Medical School
Portrait: Jacinto Lab, Rutgers
Estela Jacinto did her postdoctoral training with Michael Hall at the Biozentrum in Basel, one of the labs that pioneered TOR biology, where she helped identify and characterize the second, rapamycin-insensitive mTOR complex, mTORC2.
Her 2004 and 2006 papers established that mTORC2 contains rictor and the scaffold protein SIN1/MIP1, and that this complex — distinct from the raptor-containing mTORC1 — controls the actin cytoskeleton and phosphorylates Akt at a site required for its full activation. That work set up mTORC2 as a parallel signalling arm alongside mTORC1, now studied for its own roles in metabolism, cancer and immunity. She now runs her own lab at Rutgers, studying how mTORC1 and mTORC2 together shape metabolism in cancer, aging and immune cells.
The timeline below follows Jacinto's contributions gathered in this Atlas.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2004 | M | Mammalian TOR complex 2 controls the actin cytoskeleton and is rapamycin insensitive JAC2004 Shows mammalian TOR complex 2 (mTORC2) controls the actin cytoskeleton and, unlike mTORC1, is not directly inhibited by rapamycin. |
| 2006 | M | SIN1/MIP1 maintains rictor-mTOR complex integrity and regulates Akt phosphorylation and substrate specificity JAC2006 Shows SIN1/MIP1 is required to maintain rictor-mTOR (mTORC2) complex integrity and its control of Akt phosphorylation and substrate specificity. |
| 2021 | R | Regulation and metabolic functions of mTORC1 and mTORC2 SZW2021 Reviews the distinct regulation and metabolic functions of mTORC1 and mTORC2. |