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. 2010 Feb 18;285(17):13223–13232. doi: 10.1074/jbc.M110.102574

FIGURE 2.

FIGURE 2.

DYRK1A and DYRK3 activate the deacetylase activity of SIRT1. A, DYRK1A and DYRK3, but not DYRK2, promote deacetylation of p53 in HEK293T cells. Control HEK293T and HEK293T T1RNAi cells were transfected with either vector (lane V) or HA-tagged DYRK1A (lane 1A), DYRK2 (lane 2), or DYRK3 (lane 3). The cells were then treated with MG-132/etoposide as described under “Experimental Procedures.” B, DYRK1A and DYRK3, but not DYRK2, increase cell survival after genotoxic stress in a SIRT1-dependent manner. Control and SIRT1 RNAi HEK293T cells were transfected with indicated expressing vectors and treated with etoposide. Cell viability was analyzed as described under “Experimental Procedures” (n = 4; *, p < 0.01). C, DYRK1A and DYRK3, but not DYRK2, promote the deacetylation of endogenous p53 in a SIRT1-dependent manner in U2OS cells. U2OS cells were transfected with either vector (lane V) or HA-tagged DYRK1A (lane 1A), DYRK2 (lane 2), or DYRK3 (lane 3) together with wild type (WT) or H355Y mutant (HY) of SIRT1. The cells were then treated with MG132/etoposide as described under “Experimental Procedures.” D, DYRK1A and DYRK3, but not DYRK2, promote cell survival upon genotoxic stress in U2OS cells. U2OS cells expressing indicated proteins were treated with etoposide and analyzed as described under “Experimental Procedures” (n = 4; *, p < 0.01). E, DYRK1A and DYRK3 promote deacetylation of H3K9 and H4K16 in a SIRT1-dependent manner in HEK293T cells. HEK293T and HEK293T T1RNAi cells were transfected and treated as in A.