Oliver's mTOR Atlas Evidence Platform
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Valeria Facchinetti

First author of the study showing that mTORC2 phosphorylates the turn motif of Akt and conventional PKC as the proteins are made, which helps them fold and stay stable

Department of Immunology, MD Anderson Cancer Center, Houston (2008; listed again at MD Anderson in 2018) · worked with Bing Su (MD Anderson, then Yale) and Estela Jacinto · current position not confirmed

Valeria Facchinetti is first author of FAC2008, written at MD Anderson Cancer Center with Estela Jacinto and Bing Su as senior authors. Cells lacking the mTORC2 components mTOR, SIN1 or rictor lost phosphorylation of Akt and conventional PKC at the turn motif. This phosphorylation did not depend on growth factors and was also found in yeast. It helped newly made Akt and PKC fold and stay stable; without it, Akt was held by Hsp90. mTORC2 controlled the Akt turn-motif and hydrophobic-motif (Ser473) sites independently.

She was also a co-author of two 2010 follow-up papers: one from Su's lab at Yale on Sin1–mTORC2 and Akt2 in B-cell development, and one from Jacinto's lab showing that mTORC2 can sit on ribosomes and phosphorylate the Akt turn motif while the protein is still being made. A 2018 JCI paper on galectin-9 in lupus models again lists her at MD Anderson. Her current position could not be confirmed from the sources checked here.

Milestones in the Atlas

A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.

YearEvidenceStudy
2008 M The mammalian target of rapamycin complex 2 controls folding and stability of Akt and protein kinase C FAC2008 First author: mTORC2 phosphorylates the turn motif of Akt and conventional PKC, which controls their folding and stability.

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