Yi Ban

TL;DR: It is shown that dexrazoxane specifically abolished the DNA damage signal gamma-H2AX induced by doxorubicin, but not camptothecin or hydrogen peroxide, in H9C2 cardiomyocytes, and this results suggest that dex Razoxane antagonizesDoxorubsicin-induced DNA damage through its interference with Top2beta, which could implicate Top2 beta indoxorUBicin cardiotoxicity.

TL;DR: Results support a model in which Top1 cleavage complexes arrest transcription and activate a ubiquitin-proteasome pathway leading to the degradation of Top1 Cleavage complexes.

TL;DR: It is shown that the formation of replication-dependent DSBs requires the ubiquitin-proteasome pathway in CPT-treated cells, and results support a replication fork collision model in which Top1 cleavage complexes at the arrested replication forks are degraded by proteasome prior to replication fork runoff on the leading strand to generate D SBs.

TL;DR: Markowitz et al. as mentioned in this paper showed that deletion of pyruvate kinase muscle 2 (PKM2) results in elevated pentose phosphate pathway activity, leading to generation of an altered differentiation state responsive to PD-1 blockade.

TL;DR: Siddiqui et al. as discussed by the authors showed that deletion of pyruvate kinase muscle 2 (PKM2) results in elevated pentose phosphate pathway activity, leading to generation of an altered differentiation state responsive to checkpoint blockade.