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Image Search Results
Journal: bioRxiv
Article Title: Induction of PARP7 Creates a Vulnerability for Growth Inhibition by RBN2397 in Prostate Cancer Cells
doi: 10.1101/2022.09.02.506406
Figure Lengend Snippet: (A) Treating PC3-AR cells with si PARP7 partially reduces the growth inhibitory effect of RBN2397. PARP7 knockdown in the cell growth experiments (A-C) was confirmed by immunoblotting using TUBULIN as a loading control (upper panels). For the cell growth in A-C, each RBN2397 concentration reflects eight biological replicates, error bars show the standard deviation, and the statistical differences between cell lines at each RBN concentration are ****, p<0.0001; ***, p<0.001; **, <0.01; *, <0.05 (lower panels). (B, C) Stable knockdown of PARP7 in PC3-AR and CWR22Rv1 cells partially protects from the growth inhibitory effects of RBN2397. CWR22Rv1( shGFP ) cell growth is copied from . (D) Immunoblot detection of CDK inhibitor p21 and PARP7 in prostate cancer lines grown +R1881 and +RBN2397 for 24 hrs. (E) Treating PC3-AR cells with si-p21 (20 nM) partially reverses the growth inhibitory effect of RBN2397. The expression levels of p21 and PARP7 +R1881 and +RBN2397 were determined by immunoblotting (upper panel). (F) CRISPR knockout of CDKN1A (p21) in PC3-AR cells reduces the growth inhibitory effect of RBN2397. The knockout was confirmed by DNA sequencing (not shown) and by immunoblotting for p21 (upper panel).
Article Snippet: Commercial antibodies used were TUBULIN (1:10,000–20,000, mouse mAb TUB-1A2, Sigma T9028), HA tag (1:1,000, mouse mAb 16b12, Covance A488-101L, also used for IP),
Techniques: Western Blot, Concentration Assay, Standard Deviation, Expressing, CRISPR, Knock-Out, DNA Sequencing