Regulation of nuclear activities by HSPI3K-C2a and its possible involvement in cell cycle control

• Research unit: IRB
• Project number: 2000-MT-SLC

Key words (English)

Cancer / Cell cycle / PI 3-kinase /Signal transduction

Short description (English)

Phosphatidylinositol 3-kinases regulate intracellular signal transduction. Through the generation of 3-phosphoinositides the enzymes control vesicular transport, membrane remodeling, secretion, cell survival and gene activation. Genetic inactivation of the enzymes leads to enhanced carcinogenesis or is lethal. More distantly related family of protein kinases, which share the catalytic domain of PI 3-kinases, controls cell cycle progression in response to DNA damage, thus implement therefore a vital function in tumor formation.

Abstract (English)

Our recent investigations on the type II PI 3-kinase, HsPI3K-C2a , opened new perspectives on potential functions of the lipid kinases. The most prominent findings are the nuclear localization of HsPI3K-C2a. Exposure of cells to UV light, a well known treatment that induces stress responses and leads to tumor formation, causes phosphorylation of the enzyme. The association in the nucleus and the cytosol with macromolecular structures, which contain nucleic acids suggests that PI 3-kinases function in RNA processing. Current investigations focus on the identification of downstream targets of HsPI3K-C2a .A better understanding of the HsPI3K-C2a-dependnet signaling cascade is expected to lead to the identification of possible targets that can be used for the development of new therapeutic strategies.