The inhibitor protein IF1 binds to, and blocks ATP synthase during ATP hydrolysis. Interestingly, IF1 is overexpressed in glioma, colon, lung and breast cancers. Evidence exists to suggest that IF1 causes a shift to Warburg metabolism during neoplastic growth. We hypothesize the existence of a second, hitherto unidentified binding site on ATP synthase. The most plausible candidate is the OSCP subunit, a key modulator site of the PTP that was shown to interact with IF1 in vitro. Our working hypothesis is that IF1 binding to OSCP subunit promotes tumorigenesis by inhibiting PTP opening and therefore desensitising cell to death stimuli. The Reasearch Project will aim at (i) identifying the (novel) binding site where IF1 is bound in tumors; (ii) clarifying the role of IF1 in the modulation of the PTP and tumorigenic growth; (iii) identifying new molecules able to displace IF1 from its binding site and therefore promoting apoptosis in cancer cell lines.
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