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La famille des kinases lipidiques appel\u00e9es phosphoinositide 3-kinases (PI3K) est impliqu\u00e9e dans des fonctions cellulaires majeures telles que la survie, la prolif\u00e9ration, la croissance, la migration, la diff\u00e9renciation cellulaire mais aussi la synth\u00e8se des prot\u00e9ines et le trafic v\u00e9siculaire intracellulaire. Chez les vert\u00e9br\u00e9s, la famille PI3K est divis\u00e9e en trois classes diff\u00e9rentes. Cette classification est bas\u00e9e sur leur structure, leur mode d\u2019activation et la sp\u00e9cificit\u00e9 de leur substrat lipidique in vitro et in vivo. Ces enzymes, cod\u00e9es par 8 g\u00e8nes diff\u00e9rents, phosphorylent le groupement hydroxyle en position 3 du noyau inositol des phosphoinositides, d\u2019o\u00f9 leur nom.<\/p>\n
Seule, la classe I (compos\u00e9e de PI3K\u03b1, PI3K\u03b2, PI3K\u03b3, PI3K\u03b4) peut produire \u00e0 partir du phosphatidylinositol (4,5) -bisphosphate [PtdIns-4,5-P2, PtdIns (4,5) P2, PIP2] du phosphatidylinositol (3,4,5) -trisphosphate [PtdIns-3,4,5-P3, PtdIns (3,4,5) P3, PIP3]. Le substrat des enzymes de classe I est majoritairement localis\u00e9 \u00e0 la membrane cellulaire. Ainsi, l\u2019activation des PI3K de classe I produit un second messager lipidique \u00e0 la membrane plasmique \u00e0 l\u2019interface avec le cytoplasme, ce qui permet la transmission de l\u2019information biochimique dans le cytoplasme et qui conduit \u00e0 une r\u00e9ponse cellulaire.<\/p>\n
Les PI3K de classe II (PI3KC2\u03b1, PI3KC2\u03b2, PI3KC2\u03b3) et de classe III (VPS34) peuvent g\u00e9n\u00e9rer du phosphatidylinositol 3-phosphate [PtdIns-3-P, PtdIns (3) P, PI-3-P]. Les PI3K de classe II peuvent aussi synth\u00e9tiser le phosphatidylinositol (3,4) -bisphosphate [PtdIns-3, 4-P2, PtdIns (3,4) P2]. Les substrats de ces enzymes sont pr\u00e9sents dans les membranes externes des organites \u00e0 l\u2019int\u00e9rieur de la cellule, au niveau des endosomes, des autophagosomes. Ainsi, les PI3K de classe II et III contr\u00f4lent le trafic v\u00e9siculaire intracellulaire.<\/p>\n
La forte activation des PI3K de classe I est consid\u00e9r\u00e9e comme une caract\u00e9ristique du cancer ; cependant, le r\u00f4le de chaque PI3K de classe I dans les diff\u00e9rentes \u00e9tapes de canc\u00e9rogen\u00e8se est mal connu. Ces recherches sont r\u00e9alis\u00e9es par notre \u00e9quipe.<\/p>\n
Les r\u00f4les des PI3K de classe II et III dans le cancer sont tr\u00e8s peu \u00e9tudi\u00e9s. Nous avons entrepris de les comprendre.<\/p>\n
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Signalisation oncog\u00e9nique<\/p>\n
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PI3K<\/p>\n
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th\u00e9rapies cibl\u00e9es<\/p>\n
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r\u00e9sistance<\/p>\n
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niche tumorale<\/p>\n
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initiation du cancer<\/p>\n
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m\u00e9canobiologie<\/p>\n
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compression<\/p>\n
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souris g\u00e9n\u00e9tiquement modifi\u00e9es<\/p>\n
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imagerie des tumeurs<\/p>\n
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cancer du pancr\u00e9as<\/p>\n
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cancer de l\u2019ovaire<\/p>\n
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