Dysregulation of AKT
The protein AKT/PKB is af essential cellular critical regulator oprocesses, and dysregulation of AKT has been implicated in many diseases, including cancer. In the present study, we wanted to test if levels of protein AKT changed in in EGF-stimulated epithelial, human breast cancer cell line when treated with varying concentrations of a drug Chondramide (ChB;or) for different lengths of time ( 1 or).
Cellular lysate was prepared for each experimental condition, and an equal concentration of protein was loaded into a single lane of the SDS-polyacrylamide gel for each sample.
We used western blot to measure the total levels of AKT and the fraction of Akt that is phosphorylated on the serine residue at position 473 (p-AktS473) using a phosphorylation specific antibody. GAPDH was used a loading control. Why do you think the researchers included GAPDH in the figure? a) Control for cell condition
b) Control for unwanted proteins c) Positive control for Antibody for AKT d) Fontrol for amount of protein loaded Indicate for the following statements is they are supported/not supported by the data in the figure. Statement 1. Phosphorylation of AKT (S473) increases upon EGF stimulation Statement 2.
The total amount of AKT in the cell reduces upon EGF stimulation Statement 3. ChB treatment (both concentration and length of time) increases the amount of phosphorylated AKT.
