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LYSOKIN SIGNED

Architecture and regulation of PI3KC2β lipid kinase complex for nutrient signaling at the lysosome

Total Cost €

EC-Contrib. €

Partnership

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LYSOKIN project word cloud

Explore the words cloud of the LYSOKIN project. It provides you a very rough idea of what is the project "LYSOKIN" about.

biology lysosome precise machinery governs survival proteins diabetes organelle lipid mtorc1 degradative phosphoinositide cancer regulation terminus controls biochemical metabolism beta endosomes diverse functions recruited proliferation protein mechanisms pi structural dissecting pi3kc2 suite lyles cell signaling interaction eukaryotic kinase repressed raptor signalling turnover sensing revealed subunit combat starvation class coordinates p2 diseases lyle molecular ranging depending dictates unknown host nutrient lysosomes pave

Project "LYSOKIN" data sheet

The following table provides information about the project.

Coordinator	FORSCHUNGSVERBUND BERLIN EV Organization address address: RUDOWER CHAUSSEE 17 city: BERLIN postcode: 12489 website: www.fv-berlin.de contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.
Coordinator Country	Germany [DE]
Total cost	162˙806 €
EC max contribution	162˙806 € (100%)
Programme	1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
Code Call	H2020-MSCA-IF-2018
Funding Scheme	MSCA-IF-EF-ST
Starting year	2020
Duration (year-month-day)	from 2020-04-15 to 2022-04-14

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	FORSCHUNGSVERBUND BERLIN EV FORSCHUNGSVERBUND BERLIN EV Organization address address: RUDOWER CHAUSSEE 17 city: BERLIN postcode: 12489 website: www.fv-berlin.de contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	DE (BERLIN)	coordinator	162˙806.00

Map

Project objective

The lysosome is a eukaryotic organelle that coordinates degradative pathways with nutrient sensing and signalling. It therefore dictates cell growth and survival depending on nutrient availability. Dissecting the molecular machinery that enables these functions is of key importance to cell biology. The mTORC1 complex controls cell proliferation and metabolism by nutrient sensing at lysosomes and late endosomes (LyLEs). Recent work from the host revealed that during nutrient starvation, mTORC1 is repressed by the lipid PI(3,4)P2 at LyLEs which is produced by the class II phosphoinositide 3-kinase PI3KC2β. PI3KC2β is recruited to LyLEs via an interaction of its N-terminus with the Raptor subunit of mTORC1. The precise mechanisms of PI3KC2β regulation at LyLEs are unknown. Using a diverse suite of structural and biochemical methods, I propose to define how complex formation of PI3KC2β with mTORC1 and other LyLE associated proteins governs nutrient signaling and protein turnover at LyLEs. The proposed research may pave the way to combat diseases ranging from diabetes to cancer.

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The information about "LYSOKIN" are provided by the European Opendata Portal: CORDIS opendata.