Skip to main content
. Author manuscript; available in PMC: 2021 Jul 19.
Published in final edited form as: Nature. 2019 Mar 20;567(7749):545–549. doi: 10.1038/s41586-019-1030-9

Figure 4. MYCN, USP11 and BRCA1 stabilize each other on chromatin.

Figure 4

a: Immunoblot of α-MYCN immunoprecipitates from MYCN-amplified (IMR32) neuroblastoma cells. Where indicated, EtBr (1 mg/ml) was added to the lysate to disrupt DNA-mediated interactions. The input corresponds to 1 % (n=3).

b: (Left) ChIP of BRCA1 in SH-EP MYCNER cells expressing either shSCR or shUSP11 upon 4-OHT treatment (5 h). Shown is the mean and error bars indicate SD of technical triplicates (n =2). (Right) Immunoblot of cells described above. Actin is loading control (n=2).

c: Immunoblots of indicated proteins after knockdown of USP11 in MYCN-amplified neuroblastoma cells. Asterisk denotes an unspecific band. Tubulin is loading control (n=3).

d: Immunoblots of α-USP11 immunoprecipitates from control cells or cells expressing constitutive MYCN. CDK2 is loading control. The input corresponds to 2 % (n=2).

e: Density plot of MYCN occupancy after 4-OHT treatment (3 h) in control (top) or BRCA1-depleted (bottom) cells with shBRCA1#2 around transcriptional start sites (TSS).

f: Immunoblots of α-USP11 and α-MYCN immunoprecipitates from SH-EP cells stably expressing wildtype (“wt”) MYCN or T58AS62AMYCN (“mut”) as indicated. CDK2 is loading control. The input corresponds to 1 % (n=3).