Apoptotic gene which is also associated with autophagy is
High-Yield Explanation
In autophagy, senescent organelles or denatured proteins are targeted for lysosome-driven degradation by encircling them with a double membrane derived from the endoplasmic reticulum and marked by LC3 proteins (microtubule-associated protein 1A/1B-light chain 3). Gene associated with autophagy: ATG-3. Marker of autophagy: LC-3. Protein responsible for autophagy: BECLIN-1. Beclin -1 when it forms a complex with BCL-2 which inhibit apoptosis, the complex inhibits the autophagy process. Inhibition of autophagy might lead to malignancy. Exposure of cells to radiation or chemotherapeutic agents induces apoptosis by a mechanism that is initiated by DNA damage (genotoxic stress) and that involves the tumor-suppressor gene TP53. p53 protein accumulates in cells when DNA is damaged, and it arrests the cell cycle (at the G1 phase) to allow time for repair. However, if the damage is too great to be repaired successfully, p53 triggers apoptosis. When TP53 is mutated or absent (as it is in many cancers), cells with damaged DNA fail to undergo p53-mediated apoptosis and instead survive. In such cells, the DNA damage may result in mutations of various types that lead to neoplastic transformation. Thus, p53 serves as a critical "life or death" switch following genotoxic stress. Among the proteins whose production is stimulated by p53 are several pro-apoptotic members of the BCL2 family, notably BAX, BAK and some BH3-only proteins.