Fig 1: Changes in ATR in AD. Scatterplots show the levels of (a) ATR, a marker of ssDNA damage, (b) T1989-phosphorylated ATR, and (c) ratio of p-ATR to total ATR. No significant changes are evident in temporal lobe of AD patients. Measured by ELISA. This was confirmed by Western blots (Fig. S02).
Fig 2: Role of p53 in DNA repair pathway. The DNA damage repair pathway involves activation of ATR for ssDNA breaks and ATM for dsDNA breaks. These kinases act on CHK1 and CHK2 to phosphorylate p53. Dephosphorylated p53 is ubiquitinated by MDM2 and rapidly degraded at the proteasome. Phosphorylation of p53 at S15 inhibits interaction with MDM2. p53 induces MDM2 transcription, ensuring that the lifetime of p53 is short. Phosphorylation and oligomerization state determine p53’s effect so that p53 acts as a switch to control the cell’s response to DNA damage. The tetramerized form most strongly binds DNA. Many other post-translational modifications of p53 have been described.
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