Figure 7
Figure 7. Proposed model. SIRT6 binds DNA damage sites, recruits and blocks MAPK signaling, including RSK2. As a result, Chk1 is phosphorylated at Ser317 and maintains genome integrity by repairing DNA injuries. In contrast, inhibiting SIRT6 activity results in hyperactivation of MEK/ERK signaling (by H3K9 acetylation and ELK1-mediated activity), which in turn results in RSK2-mediated Chk1 blockade (which is phosphorylated at Ser280) and ATR/CHK1 signaling impairment. In such a scenario of SIRT6 depletion, G2 DNA damage checkpoint impairment results in enhanced lethality of genotoxic stress.

Proposed model. SIRT6 binds DNA damage sites, recruits and blocks MAPK signaling, including RSK2. As a result, Chk1 is phosphorylated at Ser317 and maintains genome integrity by repairing DNA injuries. In contrast, inhibiting SIRT6 activity results in hyperactivation of MEK/ERK signaling (by H3K9 acetylation and ELK1-mediated activity), which in turn results in RSK2-mediated Chk1 blockade (which is phosphorylated at Ser280) and ATR/CHK1 signaling impairment. In such a scenario of SIRT6 depletion, G2 DNA damage checkpoint impairment results in enhanced lethality of genotoxic stress.

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