While it has been demonstrated the involvement of caveolae during endocytic processes, it is yet to be clarified whether Cav-1 and PTRF/Cavin could play a role to regulate Sarafloxacin HCl IGF-IR surface levels following IGF1 treatment. We investigated whether PTRF/Cavin, could physically interact with IGF-IR during IGF-IR activation. HaCat cells were stimulated with IGF1 and lysed. We performed reciprocal co-immunoprecipitations between IGF-IR, Cav-1 and PTRF. The time course of IGF-IR and Cav-1 co-immunoprecipitation showed a maximum at 5 min, while PTRF/Cavin and IGFIR co-immunoprecipitation increased till 15 min and was associated with IGF-IR tyrosine phosphorylation. The graphs represent quantification of co-immunoprecipitation experiments following densitometric analysis of bands. Subcellular localization of IGF-IR with PTRF/Cavin and Cav-1 was studied by confocal microscopy. Consistently with previous reports in basal condition both Cav-1 and PTRF/Cavin colocalized in plasma membrane showing a distribution typical of caveolae staining-pattern. IGF1 induced Cav-1 and PTRF/Cavin Ganoderenic-acid-D Internalization as shown by the punctuate staining of the two proteins in the cytoplasm. IGF-IR showed a cell surface staining which co-localized with Cav-1 and PTRF/Cavin. IGF1induced cytoplasmatic co-localization of IGF-IR with Cav-1 and PTRF/Cavin suggesting that IGF1treatment resulted in Cav-1 and PTRF/Cavin redistribution from plasma membrane to intracellular compartment. Internalization is a mechanism by which RTKs leave the plasma membrane, traveling inside the cell to specific signaling sites. The fine turning of these processes can be altered in cancer cells favouring tumor growth. RTK internalization can follow mainly two pathways: via Clathrin-coated pits and via caveolae. IGF-IR internalization could be Clathrin dependent but some observations have shown a significant role of caveolae in this process. The caveolar mechanisms that regulate internalization and recovery of IGF-IR on plasma membrane remain to be clarified.In basal condition, we observed that Cav-1 and PTRF/ Cavin down regulation did not change the total as well as the surface expression of IGF-IR compared with control cells suggesting that these two proteins are not involved in the post transductional processes that allow IGF-IR traveling to cell surface.