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Content archived on 2024-04-30

Bypass the g2/m checkpoint in cancer therapy - inhibition of the interaction between cdc25 phosphatases and 14.3.3 proteins


Research objectives and content In order to increase the cytotoxic effect of drugs that are currently being used in cancer therapy we propose to bypass the G2/M checkpoint that is activated in response to DNA damages. Thus, the cells will enter a programmed cell death program, an effect that will increase the cytotoxicity. In this aim we propose to screen peptide library using the two hybrids and the phage display strategies, in order to identify peptides dissociator of the interaction between the cdc25 and 14.3.3 proteins, which is responsible of the cell cycle arrest in G2/M checkpoint after DNA damage. Training content (objective, benefit and expected impact) This training will be a good opportunity for me to acquire experimental experience in an international laboratory and to follow up my training about the regulatories mechanism of the cell cycle and of the cell proliferation. The identification of peptides with a dissociatory effect on the cdc25/ 14.3.3 complex formation could led, through a molecular modelling approach in association with 'drug design' strategies, to propose new peptidomimetics that could be use in future cancer therapy. Links with industry / industrial relevance (22)

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Via Ripamonti 435
20141 MILANO

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