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Class II PI3K

Characterization of the signalling and physiological roles of the class II PI3Ks

Total Cost €


EC-Contrib. €






 Class II PI3K project word cloud

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Project "Class II PI3K" data sheet

The following table provides information about the project.


Organization address
city: LONDON
postcode: WC1E 6BT
website: n.a.

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 United Kingdom [UK]
 Project website
 Total cost 183˙454 €
 EC max contribution 183˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2014
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-02-01   to  2018-01-31


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITY COLLEGE LONDON UK (LONDON) coordinator 183˙454.00


 Project objective

Phosphoinositide 3-kinases (PI3Ks) are lipid kinases that generate intracellular second messengers in signal transduction and membrane trafficking pathways and are important drug targets. This proposal seeks to delineate the roles and mechanism of action of a group of PI3Ks which have remained enigmatic ever since their discovery over a decade ago. The PI3K family comprises eight members in three subclasses. Class I PI3Ks signal downstream of growth factor and G protein-coupled receptors, are amongst the most commonly mutated genes in cancer and are being exploited as drug targets. The class II and III PI3Ks have in part emerged as regulators of membrane trafficking pathways but their physiological roles remain poorly understood. We aim to identify the physiological roles of the class II PI3K-C2α and β and to characterize the impact of their kinase activity on signalling pathways. To analyse the roles of class II PI3K activity in vivo, the Host Laboratory has created constitutive global and conditional knock-in kinase-inactive mice (unpublished). In contrast to PI3K gene knockout models, these mouse lines allow us to specifically address kinase-dependent functions and hence are an ideal model to evaluate the potential of class II PI3Ks as drug targets. The class II PI3K-C2α (C2α) is involved in endo- and exocytosis as well as endocytic recycling, whereas PI3K-C2β (C2β) has been implicated in cell migration. However, their influence on cellular signalling is unknown. As an initial approach, the Host Laboratory performed a screen for proteins interacting with C2α or C2β (unpublished). We will explore hits from this screen using the kinase-inactive knock-in mice and cells derived thereof as discovery tools. The combination of my expertise in membrane traffic and phosphoinositide regulation with the mouse and signalling studies of the Host Laboratory form an excellent and timely basis to uncover the roles of the class II PI3Ks in mammalian biology.

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