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Receptor tyrosine kinase activation of RhoA is mediated by AKT phosphorylation of DLC1.

Tripathi BK, Grant T, Qian X, et al. Receptor tyrosine kinase activation of RhoA is mediated by AKT phosphorylation of DLC1. J Cell Biol. 2017;216(12):4255-4270. doi:10.1083/jcb.201703105

Development-inspired reprogramming of the mammalian central nervous system.

Amamoto R, Arlotta P. Development-inspired reprogramming of the mammalian central nervous system. Science. 2014;343(6170):1239882. doi:10.1126/science.1239882

Biallelic C1QBP Mutations Cause Severe Neonatal-, Childhood-, or Later-Onset Cardiomyopathy Associated with Combined Respiratory-Chain Deficiencies.

Feichtinger RG, Oláhová M, Kishita Y, et al. Biallelic C1QBP Mutations Cause Severe Neonatal-, Childhood-, or Later-Onset Cardiomyopathy Associated with Combined Respiratory-Chain Deficiencies. Am J Hum Genet. 2017;101(4):525-538. doi:10.1016/j.ajhg.2017.08.015

p53 regulates enhancer accessibility and activity in response to DNA damage.

Younger ST, Rinn JL. p53 regulates enhancer accessibility and activity in response to DNA damage. Nucleic Acids Res. 2017;45(17):9889-9900. doi:10.1093/nar/gkx577

TOP2 synergizes with BAF chromatin remodeling for both resolution and formation of facultative heterochromatin.

Miller EL, Hargreaves DC, Kadoch C, et al. TOP2 synergizes with BAF chromatin remodeling for both resolution and formation of facultative heterochromatin. Nat Struct Mol Biol. 2017;24(4):344-352. doi:10.1038/nsmb.3384

Overlapping and Divergent Actions of Structurally Distinct Histone Deacetylase Inhibitors in Cardiac Fibroblasts.

Schuetze KB, Stratton MS, Blakeslee WW, et al. Overlapping and Divergent Actions of Structurally Distinct Histone Deacetylase Inhibitors in Cardiac Fibroblasts. J Pharmacol Exp Ther. 2017;361(1):140-150. doi:10.1124/jpet.116.237701

Fas signal transduction triggers either proliferation or apoptosis in human fibroblasts.

Freiberg RA, Spencer DM, Choate KA, et al. Fas signal transduction triggers either proliferation or apoptosis in human fibroblasts. J Invest Dermatol. 1997;108(2):215-9.

Overexpression of a kinase-inactive ATR protein causes sensitivity to DNA-damaging agents and defects in cell cycle checkpoints.

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

Reduced histone biosynthesis and chromatin changes arising from a damage signal at telomeres.

O’Sullivan RJ, Kubicek S, Schreiber SL, Karlseder J. Reduced histone biosynthesis and chromatin changes arising from a damage signal at telomeres. Nat Struct Mol Biol. 2010;17(10):1218-25. doi:10.1038/nsmb.1897

Depudecin induces morphological reversion of transformed fibroblasts via the inhibition of histone deacetylase.

Kwon HJ, Owa T, Hassig CA, Shimada J, Schreiber SL. Depudecin induces morphological reversion of transformed fibroblasts via the inhibition of histone deacetylase. Proc Natl Acad Sci U S A. 1998;95(7):3356-61.