Schmidt DR, Schreiber SL. Molecular association between ATR and two components of the nucleosome remodeling and deacetylating complex, HDAC2 and CHD4. Biochemistry. 1999;38(44):14711-7.
Brown EJ, Schreiber SL. A signaling pathway to translational control. Cell. 1996;86(4):517-20.
Cimprich KA, Shin TB, Keith CT, Schreiber SL. cDNA cloning and gene mapping of a candidate human cell cycle checkpoint protein. Proc Natl Acad Sci U S A. 1996;93(7):2850-5.
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
Cliby WA, Roberts CJ, Cimprich KA, et al. Overexpression of a kinase-inactive ATR protein causes sensitivity to DNA-damaging agents and defects in cell cycle checkpoints. EMBO J. 1998;17(1):159-69. doi:10.1093/emboj/17.1.159
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
Rao SSP, Huang SC, St Hilaire BG, et al. Cohesin Loss Eliminates All Loop Domains. Cell. 2017;171(2):305-320.e24. doi:10.1016/j.cell.2017.09.026
Evrony GD, Cordero DR, Shen J, et al. Integrated genome and transcriptome sequencing identifies a noncoding mutation in the genome replication factor as the cause of microcephaly-micromelia syndrome. Genome Res. 2017;27(8):1323-1335. doi:10.1101/gr.219899.116
Ng SY, Yoshida N, Christie AL, et al. Targetable vulnerabilities in T- and NK-cell lymphomas identified through preclinical models. Nat Commun. 2018;9(1):2024. doi:10.1038/s41467-018-04356-9