Fig. 6: CRL4ADTL is recruited to DSB sites and degrades DNA-PKcs in the nucleus. | Oncogene

Fig. 6: CRL4ADTL is recruited to DSB sites and degrades DNA-PKcs in the nucleus.

From: CRL4ADTL degrades DNA-PKcs to modulate NHEJ repair and induce genomic instability and subsequent malignant transformation

Fig. 6

(A) Nuclear and cytoplasmic protein fractionation assays showed the intracellular localization of CUL4A and DTL after DSB induction in HPDE6-C7 cells. (B, C) Immunofluorescence experiments showed the colocalization of CUL4A and DTL with γ-H2AX after DSB induction in HPDE6-C7 cells. (D, E) Immunofluorescence experiments showed the colocalization of CUL4A and DTL with DNA-PKcs after DSB induction in HPDE6-C7 cells. (F) Nuclear and cytoplasmic protein fractionation assays and coimmunoprecipitation showed the intracellular binding sites of CUL4A and DNA-PKcs. (G) Nuclear protein fractionation assays and coimmunoprecipitation showed that CUL4A ubiquitinated DNA-PKcs in the nucleus after DSB induction (H, I) A chromatin fractionation assay was performed to show the changes in CUL4A, DTL, and DNA-PKcs in chromatin after DSB induction in HPDE6-C7 cells. * p < 0.05, ** p < 0.01, *** p < 0.001 based on Student’s t-test. The data are presented as the means ± SDs of five (A) or three (D, E, H, and I) independent experiments. The scale bars indicate 2 μm in B and C, and 5 μm in D and E.

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