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. 2016 Dec 7;8(2):2916–2935. doi: 10.18632/oncotarget.13807

Figure 10. HIC1 SUMOylation is dispensable for DNA repair but essential for the transcriptional response to non-repairable DSBs.

Figure 10

(A) Upon induction of repairable DSBS, HIC1 participates in the early steps of the repair process [8] by a mechanism that still remains to be deciphered. However, this is independent of HIC1 SUMOylation but could be due to other post-translational modifications. (B) Upon induction of non-repairable DSBs, the activated ATM kinase increases HIC1 SUMOylation which in turn enhances the binding of HIC1 to its responsive elements (HiRE) in the promoters of target genes (e.g. SIRT1) as well as the interaction of HIC1 with the MTA1 or MTA3 co-repressors to increase the transcriptional repression of direct target genes.