Objective:To investigate the role and mechanism of G-protein-coupled receptor kinase interacting protein 1(GIT1)and extracellular signal-regulated kinases 1 and 2(ERK1/2)in osteoblasts induced by durative pressure. Methods:The osteoblasts were mechanically stimulated on coverslips. The phosphorylation of ERK1/2 and GIT1 of osteobasts treated with or without the Src kinase inhibitor PP2 was measured by Western blot. The interaction between GIT1 and pERK1/2 was detected by coimmunoprecipitation. Cell area of groups treated with or without the Src kinase inhibitor PP2 was caculated by image-pro plus 5.0. Results:The phosphorylation of ERK1/2 and GIT1 and the interaction between GIT1 and pERK1/2 of osteoblasts treated with durative pressure significantly increased. The cell size increased significantly after durative pressure. Conclusion:These data suggests that 300 kPa durative pressure stimuates Src,consequently pathway induces the phosphorylation of ERK1/2 and GIT1 in osteoblasts,further increases the combination of pERK1/2 and GIT1 to migrate osteoblasts. The Src-GIT1/ERK1/2 pathway may play a important role in osteoblast migration induced by durative pressure.