Figure 7.
HEATR3 loss does not affect levels of p53, uL5, or uL18. (A) Western blots of LCLs exposed to either 100 nM camptothecin (CPT) for 4 hours, or 10 µM MG-132 for 6 hours, or the vehicle control, dimethyl sulfoxide (DMSO). Blots shown are probed with antibodies against p53. HEATR3 variants do not lead to p53 stabilization on their own but they do, as expected, in combination with CPT or MG-132 treatments. (B) Quantification of panel A from 3 independent experimental replicates. Results shown are the relative levels of p53/actin. (C) Western blots of LCLs exposed to 100 nM CPT for 4 hours, or the vehicle control, DMSO. Blots shown are probed with antibodies against HEATR3, p53, uL5, and uL18. (D) Quantification of panel C from 3 independent experimental replicates. Results shown are the relative levels of uL5/actin or uL18/actin.

HEATR3 loss does not affect levels of p53, uL5, or uL18. (A) Western blots of LCLs exposed to either 100 nM camptothecin (CPT) for 4 hours, or 10 µM MG-132 for 6 hours, or the vehicle control, dimethyl sulfoxide (DMSO). Blots shown are probed with antibodies against p53. HEATR3 variants do not lead to p53 stabilization on their own but they do, as expected, in combination with CPT or MG-132 treatments. (B) Quantification of panel A from 3 independent experimental replicates. Results shown are the relative levels of p53/actin. (C) Western blots of LCLs exposed to 100 nM CPT for 4 hours, or the vehicle control, DMSO. Blots shown are probed with antibodies against HEATR3, p53, uL5, and uL18. (D) Quantification of panel C from 3 independent experimental replicates. Results shown are the relative levels of uL5/actin or uL18/actin.

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