KDM6A mutations promote acute cytoplasmic DNA release, DNA damage response and mitosis defects.

Thus, under which conditions and in which manner do both proteins directly or indirectly interact? Conclusion Overall, our approach combining biochemical, cellular and imaging techniques revealed that truncating KDM6A mutations lacking TPR, JmjC and/or IDR dramatically increase nuclear damage and apoptosis whereas single substitution variants with diminished demethylase activity or unknown features (T726K) show at most a weak trend towards these effects which are summarized in Fig. 6 C.

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