Figure 3
Figure 3. DDR-compromised Myc lymphomas share checkpoint defects with Atm-deficient lymphomas. (A) Immunoblot analysis of Myc, Atm, Atm-P-S1987, p53, p53-P-S18, and tubulin as a loading control in immunobead-isolated normal B cells and 12 randomly selected control lymphomas. (B) Immunoblot analysis of Atm, Atm-P-S1987, p53, p53-P-S18, cleaved caspase-3, and tubulin as a loading control in Atm−/− and representative control lymphomas with detectable versus undetectable basal p53-P-S18 levels (compare with panel A); basal (−) and induced (+) levels 5 hours after ADR in vitro, aligned with the relative (ADR/no ADR [ut indicates untreated]) S-phase fraction of the same lymphoma samples, now stably expressing Bcl2, 48 hours after ADR or left untreated. Shown are representative examples of the entirety of lymphomas presented in panel A.

DDR-compromised Myc lymphomas share checkpoint defects with Atm-deficient lymphomas. (A) Immunoblot analysis of Myc, Atm, Atm-P-S1987, p53, p53-P-S18, and tubulin as a loading control in immunobead-isolated normal B cells and 12 randomly selected control lymphomas. (B) Immunoblot analysis of Atm, Atm-P-S1987, p53, p53-P-S18, cleaved caspase-3, and tubulin as a loading control in Atm−/− and representative control lymphomas with detectable versus undetectable basal p53-P-S18 levels (compare with panel A); basal (−) and induced (+) levels 5 hours after ADR in vitro, aligned with the relative (ADR/no ADR [ut indicates untreated]) S-phase fraction of the same lymphoma samples, now stably expressing Bcl2, 48 hours after ADR or left untreated. Shown are representative examples of the entirety of lymphomas presented in panel A.

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