Sasanuma H, Tsuda M, Morimoto S, et al. BRCA1 ensures genome integrity by eliminating estrogen-induced pathological topoisomerase II-DNA complexes. Proc Natl Acad Sci U S A. 2018;115(45):E10642-E10651. doi:10.1073/pnas.1803177115.

Zheng XF, Florentino D, Chen J, Crabtree GR, Schreiber SL. TOR kinase domains are required for two distinct functions, only one of which is inhibited by rapamycin. Cell. 1995;82(1):121-30.

Brown EJ, Albers MW, Shin TB, et al. A mammalian protein targeted by G1-arresting rapamycin-receptor complex. Nature. 1994;369(6483):756-8. doi:10.1038/369756a0.

Albers MW, Brown EJ, Tanaka A, Williams RT, Hall FL, Schreiber SL. An FKBP-rapamycin-sensitive, cyclin-dependent kinase activity that correlates with the FKBP-rapamycin-induced G1 arrest point in MG-63 cells. Ann N Y Acad Sci. 1993;696:54-62.

Albers MW, Williams RT, Brown EJ, Tanaka A, Hall FL, Schreiber SL. FKBP-rapamycin inhibits a cyclin-dependent kinase activity and a cyclin D1-Cdk association in early G1 of an osteosarcoma cell line. J Biol Chem. 1993;268(30):22825-9.

DeRan M, Pulvino M, Zhao J. Assessing G1-to-S-phase progression after genotoxic stress. Methods Mol Biol. 2011;782:221-30. doi:10.1007/978-1-61779-273-1_16.

DeRan M, Pulvino M, Greene E, Su C, Zhao J. Transcriptional activation of histone genes requires NPAT-dependent recruitment of TRRAP-Tip60 complex to histone promoters during the G1/S phase transition. Mol Cell Biol. 2008;28(1):435-47. doi:10.1128/MCB.00607-07.

Solit DB, Garraway LA, Pratilas CA, et al. BRAF mutation predicts sensitivity to MEK inhibition. Nature. 2006;439(7074):358-62. doi:10.1038/nature04304.

Gong Y, Zack TI, Morris LGT, et al. Pan-cancer genetic analysis identifies PARK2 as a master regulator of G1/S cyclins. Nat Genet. 2014;46(6):588-94. doi:10.1038/ng.2981.

Naetar N, Soundarapandian V, Litovchick L, et al. PP2A-mediated regulation of Ras signaling in G2 is essential for stable quiescence and normal G1 length. Mol Cell. 2014;54(6):932-45. doi:10.1016/j.molcel.2014.04.023.