• Arizona State University

• BIO 181

Cell Biology Final Assignment Background More than one in ten women develop breast cancer during life, but death rates have declined steadily because of earlier detection and new treatments. As with other forms of cancer, breast cancer results from mutations in DNA. When enough mutations accumulate, a cell can be more readily triggered to reproduce by division and ignore signals that trigger death by apoptosis. This rapidly dividing cell forms a tumor, which differs in structure and function from normal tissue. Ultimately, some of these cells leave the tumor and enter the bloodstream. Death results when these cells circulate to vital organs and interfere with their functions. Scientists have identified a signaling pathway called the GPR/TRPV signaling pathway that regulates reproduction and death of cells in breast tissue (Figure 1). In the absence of the signaling molecule S1 (Figure 1, left panel), the receptor GPR is in its inactive form. The subsequent structures: G-complex, Erk1, and p38, are also in their inactive form, thus cell division does not occur. Similarly, TRPV is in its inactive form in the absence of S1. Consequently, the concentration of calcium ions (Ca2+) does not increase and the structures ATM and p53 are in their inactive form, thus cell death does not occur. When S1 is present (Figure 1, right panel), the following steps occur: GPR signaling pathway 1. A signal called S1 binds to the receptor GPR, inducing a conformational change. 2. The active form of GPR binds and phosphorylates the G-complex. 3. The active form of the G-complex binds and phosphorylates a kinase called Erk1. 4. The activation of Erk1 leads to the activation of a kinase called p38 by phosphorylation. 5. The activation of p38 leads to an increase in cell division. TRPV signaling pathway 1. A signal called S1 binds to the receptor TRPV, preventing a conformational change. 2. The inactive form of TRPV does NOT open a channel to allow Ca2+ to move into the cell. 3. Since Ca2+ levels in the cell do NOT increase, a kinase called ATM can NOT become activated by phosphorylation. 4. Since ATM is NOT activated, this does NOT lead to the activation of p53 by phosphorylation. 5. Since p53 is NOT activated, this does not lead to