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The activation of mTor complex 1 in the cell is central to many vital processes in the body such as cell growth and metabolism. Overactivity of this signaling pathway can result in diseases such as in diabetic insulin resistance and cancer. A team led by the scientist Volker Haucke (Leibniz—Forschungsinstitut für Molekulare Pharmakologie and Freie Universität Berlin) has now discovered how inactivation of a certain lipid kinase promotes mTor complex 1 activity, and may therefore constitute a new point of attack for the treatment of diabetes and cancer. The results have just been published in the renowned journal Nature Cell Biology.
The signaling pathways in somatic cells are highly complex, and specific mechanisms can only be triggered if several switches are flipped in a fixed sequence. However, given the high number of substances and substance complexes involved in the cellular signal transmission, finding these switches and identifying their role is a real challenge. The question of how mTor complex 1 can be deactivated in the cell has also been long unresolved. Even so, FMP researchers were able to shed light on this switch as early as 2017, revealing that a certain lipid kinase (PI3KC2ß) acts as a natural brake for the mTor protein and ensures that the mTor complex 1 is switched off, for example, when certain hormonal signals such as insulin are absent.
Team - FMP - Researcher - Alexander - Wallroth
Now, a team led by FMP researcher Alexander Wallroth from Volker Haucke's research group has been scrutinizing how this lipid kinase is regulated. Wallroth says, "We manipulated the lipid kinase in various ways and looked at the effects these manipulations had on mTOR and activity on cell growth." This work has allowed the researchers to uncover a mechanism for inactivating the PI3KC2ß lipid kinase. Another kinase that plays a key role...
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