Bromodomain Inhibitors Correct Bioenergetic Deficiency Caused by Mitochondrial Disease Complex I Mutations.

[1]  R. Rodenburg,et al.  Mitochondrial disorders in children: toward development of small‐molecule treatment strategies , 2016, EMBO molecular medicine.

[2]  James E. Bradner,et al.  Response and resistance to BET bromodomain inhibitors in triple negative breast cancer , 2015, Nature.

[3]  Meagan E. Sullender,et al.  Optimized sgRNA design to maximize activity and minimize off-target effects of CRISPR-Cas9 , 2015, Nature Biotechnology.

[4]  Rameen Beroukhim,et al.  Sound credit scores and financial decisions despite cognitive aging , 2014, Proceedings of the National Academy of Sciences.

[5]  William B. Smith,et al.  Genome-wide localization of small molecules , 2013, Nature Biotechnology.

[6]  M. Rosenfeld,et al.  Brd4 and JMJD6-Associated Anti-Pause Enhancers in Regulation of Transcriptional Pause Release , 2013, Cell.

[7]  Hanfei Sun,et al.  Target analysis by integration of transcriptome and ChIP-seq data with BETA , 2013, Nature Protocols.

[8]  Ming-Ming Zhou,et al.  Structure-guided design of potent diazobenzene inhibitors for the BET bromodomains. , 2013, Journal of medicinal chemistry.

[9]  Eric Verdin,et al.  The nexus of chromatin regulation and intermediary metabolism , 2013, Nature.

[10]  Wang Wang,et al.  Mitochondrial complex I deficiency increases protein acetylation and accelerates heart failure. , 2013, Cell metabolism.

[11]  V. Mootha,et al.  New treatments for mitochondrial disease—no time to drop our standards , 2013, Nature Reviews Neurology.

[12]  J. Houštěk,et al.  The function and the role of the mitochondrial glycerol-3-phosphate dehydrogenase in mammalian tissues. , 2013, Biochimica et biophysica acta.

[13]  Vamsi K. Mootha,et al.  Mitochondrial disorders as windows into an ancient organelle , 2012, Nature.

[14]  M. Sharpley,et al.  Mouse mtDNA mutant model of Leber hereditary optic neuropathy , 2012, Proceedings of the National Academy of Sciences.

[15]  Michael Snyder,et al.  A highly integrated and complex PPARGC1A transcription factor binding network in HepG2 cells , 2012, Genome research.

[16]  T. Prolla,et al.  Increased mitochondrial biogenesis in muscle improves aging phenotypes in the mtDNA mutator mouse. , 2012, Human molecular genetics.

[17]  Werner J H Koopman,et al.  Monogenic mitochondrial disorders. , 2012, The New England journal of medicine.

[18]  J. Nunnari,et al.  Mitochondria: In Sickness and in Health , 2012, Cell.

[19]  R. McPherson,et al.  Galactose Enhances Oxidative Metabolism and Reveals Mitochondrial Dysfunction in Human Primary Muscle Cells , 2011, PloS one.

[20]  S. Robson,et al.  Inhibition of BET recruitment to chromatin as an effective treatment for MLL-fusion leukaemia , 2011, Nature.

[21]  R. Young,et al.  BET Bromodomain Inhibition as a Therapeutic Strategy to Target c-Myc , 2011, Cell.

[22]  Michael Erb,et al.  NQO1-Dependent Redox Cycling of Idebenone: Effects on Cellular Redox Potential and Energy Levels , 2011, PloS one.

[23]  Robert W. Taylor,et al.  Respiratory chain complex I deficiency caused by mitochondrial DNA mutations , 2011, European Journal of Human Genetics.

[24]  C. Rice,et al.  Suppression of inflammation by a synthetic histone mimic , 2010, Nature.

[25]  William B. Smith,et al.  Selective inhibition of BET bromodomains , 2010, Nature.

[26]  H. Pelicano,et al.  Cancer metabolism: is glutamine sweeter than glucose? , 2010, Cancer cell.

[27]  Rutger O. Vogel,et al.  Acyl-CoA dehydrogenase 9 is required for the biogenesis of oxidative phosphorylation complex I. , 2010, Cell metabolism.

[28]  S. Srivastava,et al.  PGC-1alpha/beta induced expression partially compensates for respiratory chain defects in cells from patients with mitochondrial disorders. , 2009, Human molecular genetics.

[29]  Ming-Ming Zhou,et al.  Brd4 Coactivates Transcriptional Activation of NF-κB via Specific Binding to Acetylated RelA , 2008, Molecular and Cellular Biology.

[30]  Clifford A. Meyer,et al.  Model-based Analysis of ChIP-Seq (MACS) , 2008, Genome Biology.

[31]  S. Srivastava,et al.  PGC-1α/β upregulation is associated with improved oxidative phosphorylation in cells harboring nonsense mtDNA mutations , 2007 .

[32]  Jiandie D. Lin,et al.  Suppression of Reactive Oxygen Species and Neurodegeneration by the PGC-1 Transcriptional Coactivators , 2006, Cell.

[33]  Shwu‐Yuan Wu,et al.  Brd4 links chromatin targeting to HPV transcriptional silencing. , 2006, Genes & development.

[34]  J. Brady,et al.  The bromodomain protein Brd4 is a positive regulatory component of P-TEFb and stimulates RNA polymerase II-dependent transcription. , 2005, Molecular cell.

[35]  B. Spiegelman,et al.  Coordination of p300-mediated chromatin remodeling and TRAP/mediator function through coactivator PGC-1alpha. , 2003, Molecular cell.

[36]  J. Jankovic,et al.  A heteroplasmic mitochondrial complex I gene mutation in adult-onset dystonia , 2003, Neurogenetics.

[37]  A. Matsuno-Yagi,et al.  Lack of Complex I Activity in Human Cells Carrying a Mutation in MtDNA-encoded ND4 Subunit Is Corrected by theSaccharomyces cerevisiae NADH-Quinone Oxidoreductase (NDI1) Gene* , 2001, The Journal of Biological Chemistry.

[38]  V. Mootha,et al.  Mechanisms Controlling Mitochondrial Biogenesis and Respiration through the Thermogenic Coactivator PGC-1 , 1999, Cell.

[39]  Lei Zeng,et al.  Structure and ligand of a histone acetyltransferase bromodomain , 1999, Nature.

[40]  P. Puigserver,et al.  A Cold-Inducible Coactivator of Nuclear Receptors Linked to Adaptive Thermogenesis , 1998, Cell.

[41]  T. Tomizaki,et al.  The Whole Structure of the 13-Subunit Oxidized Cytochrome c Oxidase at 2.8 Å , 1996, Science.

[42]  D. Wallace,et al.  A mitochondrial DNA mutation at nucleotide pair 14459 of the NADH dehydrogenase subunit 6 gene associated with maternally inherited Leber hereditary optic neuropathy and dystonia. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[43]  D. Wallace,et al.  Nonviability of cells with oxidative defects in galactose medium: a screening test for affected patient fibroblasts. , 1992, Biochemical medicine and metabolic biology.

[44]  L. Reitzer,et al.  Evidence that glutamine, not sugar, is the major energy source for cultured HeLa cells. , 1979, The Journal of biological chemistry.