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Cytotoxic drugs stimulate the processing of WT1 by HtrA2. HtrA2 (H) is present in the mitochondria and nucleus. Upon exposure to apoptotic agents, HtrA2 cleaves WT1 (W), resulting in its loss from gene promoters, with concomitant changes in the expression of these genes. Those genes that were subject to repression or activation by WT1 would be upregulated and downregulated respectively. The HtrA2-dependent proteolysis of WT1 acts to drive apoptosis.
