Final answer:
FAK and SRC initiate a signaling cascade in integrins, leading to cell adhesion and signaling. FAK directly interacts with p53, affecting its stability and activity. Abnormally high levels of FAK are associated with tumor cell lines.
Step-by-step explanation:
Integrins are cell surface receptors that play a crucial role in cell adhesion and signaling. When FAK (focal adhesion kinase) and SRC (non-receptor tyrosine kinase) are activated, they initiate a signaling cascade in integrins. Integrin-mediated signal transduction involves the binding of integrins to extracellular matrix proteins, such as fibronectin. This binding leads to the activation of FAK, which regulates cell-cell and cell-ECM adhesion at focal adhesion points. One of the functions of FAK is to bind directly to inactive p53 and increase p53-Mdm2 binding. This interaction affects the stability and activity of p53, a tumor suppressor protein. Abnormally high levels of FAK have been found in various tumor cell lines.