Marina K. Holz
Cell biologist who, as a postdoc with John Blenis, showed how mTOR and S6K1 trade places on eIF3 to start protein synthesis, and who now studies mTOR in breast cancer and the rare lung disease LAM at New York Medical College
Graduate School of Biomedical Sciences and Department of Cell and Molecular Physiology, New York Medical College (2026) · Department of Cell Biology and Anatomy, New York Medical College (from 2018) · Department of Biology, Stern College for Women, Yeshiva University, and Albert Einstein Cancer Center (papers to 2017) · Department of Cell Biology, Harvard Medical School, John Blenis lab (2005)
Marina Holz is first author of the Atlas study HOL2005, done in John Blenis's lab at Harvard Medical School. It answered a basic question: how does mTOR, once switched on by growth signals, get the cell's protein-making machinery started? The answer centred on eIF3, a large protein platform that helps ribosomes find the start of a messenger RNA. In resting cells the kinase S6K1 sits on eIF3 in an inactive state. When the cell is stimulated, mTOR arrives with its partner raptor, phosphorylates S6K1, and S6K1 lets go of eIF3 to phosphorylate its own targets, which helps assemble the complex that begins translation. The paper turned a list of phosphorylation events into an ordered sequence on one scaffold. It was done in cultured human cells.
After Harvard, Holz set up a lab in the Department of Biology at Stern College for Women of Yeshiva University, with a link to the Albert Einstein Cancer Center. The group studied how estrogen and mTOR signalling feed each other in breast cancer: mTOR and S6K1 together with the MAPK pathway phosphorylate estrogen receptor alpha (2010), estrogen raises S6K1 levels in a loop that drives breast cancer cell growth (2012), and estrogen tunes the eIF3 subunit eIF3f through mTORC1 (2018).
A second line of work is lymphangioleiomyomatosis (LAM), a rare lung disease of women caused by overactive mTORC1. In mice carrying TSC2-deficient tumours, rapamycin combined with resveratrol switched on cell death (2015), and Holz was senior author of a small clinical study of resveratrol plus sirolimus in LAM patients (2023). At New York Medical College in Valhalla, Holz's recent papers report that CDK4/6 inhibitors suppress mTOR activity in LAM cells (2026) and that education level affects how quickly LAM patients are diagnosed and treated (2026).
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2005 | M | mTOR and S6K1 mediate assembly of the translation preinitiation complex through dynamic protein interchange and ordered phosphorylation events HOL2005 First author: showed in cultured cells that mTOR/raptor and S6K1 swap places on the eIF3 complex in an ordered sequence that starts translation. |
Co-authors in the Atlas 2
People with a profile here who share at least one study with Marina K. Holz.
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- John Blenis Showed early on that rapamycin blocks S6 kinase, then worked out how mTORC1 drives cell growth through its two main translation targets, S6K1 and 4E-BP1. His lab also found, in parallel with the Sabatini lab, that mTORC1 phosphorylates Grb10, a feedback brake on insulin signalling
- Steven P. Gygi Mass-spectrometry scientist whose Harvard lab builds large-scale proteomics methods, including the BioPlex human protein-interaction map, and contributed proteomics to the discoveries of the CASTOR and SAMTOR nutrient sensors
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