Thomas Porstmann
Cell biologist who, as a researcher in Almut Schulze's laboratory at the Cancer Research UK London Research Institute, showed that the growth kinase Akt drives fat synthesis through SREBP and that this route runs through mTORC1
Gene Expression Analysis Laboratory, Cancer Research UK London Research Institute, London (papers 2005–2009, at the time of the study)
Thomas Porstmann was first author of a 2008 Cell Metabolism paper (POR2008) that connected two big ideas about cell growth. A growing cell has to make more membrane as well as more protein, and membranes are built from fats. SREBP is a family of transcription factors, proteins that switch on genes, and they control the genes for making fatty acids and cholesterol. The study showed in human cells that when the kinase Akt is switched on, the active form of SREBP1 builds up in the nucleus, and that this needs mTORC1, the growth-control complex. Rapamycin, which blocks mTORC1, stopped it.
Blocking SREBP did more than lower fat production. It also stopped Akt from making cells bigger, and in fruit flies loss of SREBP reduced cell and organ size. So mTORC1 also orders the lipids for new membranes, on top of speeding up protein production. The work was done in cultured cells and in flies.
The paper grew out of Porstmann's earlier first-author study in Oncogene (2005) in the same laboratory, which used gene-expression arrays to find that Akt switches on cholesterol and fatty acid enzymes through SREBP. In 2009 Porstmann and colleagues summarised the SREBP and mTORC1 link in a Biochemical Society Transactions review. All three papers list the Gene Expression Analysis Laboratory led by Almut Schulze at the Cancer Research UK London Research Institute, now part of the Francis Crick Institute. A current position could not be confirmed.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2008 | M | SREBP activity is regulated by mTORC1 and contributes to Akt-dependent cell growth POR2008 First author: showed that Akt-driven activation of SREBP and fat synthesis needs mTORC1, and that SREBP is required for Akt to make cells grow. |
Co-authors in the Atlas 1
People with a profile here who share at least one study with Thomas Porstmann.
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- Almut Schulze Studies how growth signaling, including PI3K/Akt and mTORC1, drives the metabolism that cancer cells need, notably fat synthesis through SREBP.
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