How chronic myeloid leukaemia inhibitors influence Bcr-Abl interactions with its partner protein CrkII

Diplôme Master How chronic myeloid leukaemia inhibitors influence Bcr-Abl interactions with its partner protein CrkII eng 2011 author Nayak Jeremie 657780 director Kranjc Pietrucci Agata 712787 director Scapozza Leonardo 600318 The pathology of chronic myeloid leukaemia (CML) is tightly connected with the Bcr-Abl fusion protein and its molecular network [1]. Its network has been recently solved [2] and opened a possibility for new approach to drug discovery, where drug targets are studied in the context of molecular pathways. In the work proposed here we will study how CML inhibitors influence interactions between the Bcr-Abl and Crk-II proteins. Crk adaptor proteins regulates transcription and cytoskeletal reorganization during cell growth, motility, proliferation, adhesion, differentiation and apoptosis by acting as an adaptor to link tyrosine kinases and small G-proteins [3]. Crk is responsible for the malignant features of various human cancers. [3]. Based on structure analysis of the CrkII SH2 domain in a complex with the Bcr-Abl SH3 domain [4] it seems that CrkII protein keeps the Bcr-Abl tyrosine kinase (TyrK) in its active state. We will study if the CML inhibitors however influence the Bcr-Abl-CrkII interactions and consequently help that Bcr-Abl returns to its inactive conformation. Chronic myeloid leukaemia Bcr-Abl fusion protein Crk adaptor proteins Chronic myeloid leukaemia inhibitors Protein-protein interactions The interactome Dewey 615 Maitrise Universitaire en Pharmacie 31 Section des sciences pharmaceutiques 17 false 4cc9f773-f445-48fe-9f99-4febed27c7b9 Master thesis Restricted TPR_Nayak_Jérémie.pdf 29735338 application/pdf restrictedAccess Faculté des sciences / Section des sciences pharmaceutiques

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Nayak, Jeremie