Final answer:
Upon exposure to UV or chemotherapy, ATM kinase activates and phosphorylates MDM2 and p53. This leads to DNA damage repair or apoptosis if the damage is irreparable. Proteins like p53, p21, and Bax play essential roles in maintaining cellular integrity by dictating cell cycle arrest or cell death.
Step-by-step explanation:
When cells are exposed to UV radiation or chemotherapy, a series of molecular events involving p53, ATM, MDM2, and Bax are initiated to ensure cellular integrity. p53, a crucial protein in this process, is normally bound to MDM2. Upon DNA damage, ATM kinase is activated, which phosphorylates MDM2 causing it to release p53. ATM kinase simultaneously phosphorylates p53 and another kinase, Chk2, leading to cell cycle arrest and DNA repair efforts. If DNA damage cannot be resolved, p53 upregulates the expression of pro-apoptotic genes like Bax, initiating apoptosis to prevent the propagation of damaged DNA.
Moreover, p21, another protein regulated by p53, plays a critical role in this response by inhibiting the activity of Cdk/cyclin complexes, thereby halting the cell cycle. This allows the cell more time to repair DNA before proceeding to the S phase. In summary, the levels and activity of p53 are pivotal in determining whether a cell will arrest its cycle for repair or enter apoptosis if repairs are unsuccessful. This intricate interplay of regulatory proteins ensures the maintenance of genetic stability and prevents the development of cancer.