Liver‐specific deletion of histone deacetylase 3 disrupts metabolic transcriptional networks

[1]  D. Cortez,et al.  Deletion of histone deacetylase 3 reveals critical roles in S phase progression and DNA damage control. , 2008, Molecular cell.

[2]  G. Perdomo,et al.  The mammalian target of rapamycin regulates lipid metabolism in primary cultures of rat hepatocytes. , 2007, Metabolism: clinical and experimental.

[3]  U. Koch,et al.  Unraveling the hidden catalytic activity of vertebrate class IIa histone deacetylases , 2007, Proceedings of the National Academy of Sciences.

[4]  P. Iynedjian,et al.  Activation of mammalian target of rapamycin complex 1 and insulin resistance induced by palmitate in hepatocytes. , 2007, Biochemical and biophysical research communications.

[5]  V. Santini,et al.  Histone deacetylase inhibitors: molecular and biological activity as a premise to clinical application. , 2007, Current drug metabolism.

[6]  J. Clapham,et al.  Thermogenic and metabolic antiobesity drugs: rationale and opportunities , 2007, Diabetes, obesity & metabolism.

[7]  Michele Pallaoro,et al.  HDACs, histone deacetylation and gene transcription: from molecular biology to cancer therapeutics , 2007, Cell Research.

[8]  Nan Guo,et al.  PANTHER version 6: protein sequence and function evolution data with expanded representation of biological pathways , 2006, Nucleic Acids Res..

[9]  Wolfgang Wurst,et al.  Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3 beta activity. , 2007, Nature medicine.

[10]  Minghong Xu,et al.  Histone Deacetylase 3 Interacts with and Deacetylates Myocyte Enhancer Factor 2 , 2006, Molecular and Cellular Biology.

[11]  M. Graham,et al.  Aberrant Hepatic Expression of PPARγ2 Stimulates Hepatic Lipogenesis in a Mouse Model of Obesity, Insulin Resistance, Dyslipidemia, and Hepatic Steatosis* , 2006, Journal of Biological Chemistry.

[12]  K. Nakayama,et al.  Regulation of SV40 large T-antigen stability by reversible acetylation , 2006, Oncogene.

[13]  B. Garcia,et al.  A novel histone deacetylase pathway regulates mitosis by modulating Aurora B kinase activity. , 2006, Genes & development.

[14]  S. Akira,et al.  Compensatory recovery of liver mass by Akt-mediated hepatocellular hypertrophy in liver-specific STAT3-deficient mice. , 2005, Journal of hepatology.

[15]  Jonathan C. Cohen,et al.  Dual roles for cholesterol in mammalian cells. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[16]  M. Linton,et al.  Physiological relevance of apolipoprotein E recycling: studies in primary mouse hepatocytes. , 2005, Metabolism: clinical and experimental.

[17]  M. Lazar,et al.  The histone‐binding code of nuclear receptor co‐repressors matches the substrate specificity of histone deacetylase 3 , 2005, EMBO reports.

[18]  M. Lazar,et al.  Corepressors selectively control the transcriptional activity of PPARgamma in adipocytes. , 2005, Genes & development.

[19]  A. Sanyal.  Mechanisms of Disease: pathogenesis of nonalcoholic fatty liver disease , 2005, Nature Clinical Practice Gastroenterology &Hepatology.

[20]  R. Loewith,et al.  Mammalian TOR complex 2 controls the actin cytoskeleton and is rapamycin insensitive , 2004, Nature Cell Biology.

[21]  N. Sonenberg,et al.  Upstream and downstream of mTOR. , 2004, Genes & development.

[22]  Namjin Chung,et al.  Sirt1 promotes fat mobilization in white adipocytes by repressing PPAR-γ , 2004, Nature.

[23]  J. Blenis,et al.  Target of rapamycin (TOR): an integrator of nutrient and growth factor signals and coordinator of cell growth and cell cycle progression , 2004, Oncogene.

[24]  T. Asano,et al.  Hepatic Akt activation induces marked hypoglycemia, hepatomegaly, and hypertriglyceridemia with sterol regulatory element binding protein involvement. , 2003, Diabetes.

[25]  K. Glaser,et al.  Role of class I and class II histone deacetylases in carcinoma cells using siRNA. , 2003, Biochemical and biophysical research communications.

[26]  T. Vanhaecke,et al.  Trichostatin A induces differential cell cycle arrests but does not induce apoptosis in primary cultures of mitogen-stimulated rat hepatocytes. , 2003, Journal of hepatology.

[27]  M. Campbell,et al.  PANTHER: a library of protein families and subfamilies indexed by function. , 2003, Genome research.

[28]  Jun Qin,et al.  Purification and functional characterization of the human N‐CoR complex: the roles of HDAC3, TBL1 and TBLR1 , 2003, The EMBO journal.

[29]  A. V. van Kuilenburg,et al.  Histone deacetylases (HDACs): characterization of the classical HDAC family. , 2003, The Biochemical journal.

[30]  F. Gonzalez,et al.  Adipocyte-specific Gene Expression and Adipogenic Steatosis in the Mouse Liver Due to Peroxisome Proliferator-activated Receptor γ1 (PPARγ1) Overexpression* , 2003, The Journal of Biological Chemistry.

[31]  J. Reddy,et al.  Adipocyte-specific gene expression and adipogenic steatosis in the mouse liver due to peroxisome proliferator-activated receptor gamma1 (PPARgamma1) overexpression. , 2003, The Journal of biological chemistry.

[32]  D. Rozman,et al.  Many facets of mammalian lanosterol 14alpha-demethylase from the evolutionarily conserved cytochrome P450 family CYP51. , 2003, Archives of biochemistry and biophysics.

[33]  K. Kristiansen,et al.  The retinoblastoma-histone deacetylase 3 complex inhibits PPARgamma and adipocyte differentiation. , 2002, Developmental cell.

[34]  J. Crespo,et al.  Two TOR complexes, only one of which is rapamycin sensitive, have distinct roles in cell growth control. , 2002, Molecular cell.

[35]  D. O’Carroll,et al.  Essential function of histone deacetylase 1 in proliferation control and CDK inhibitor repression , 2002, The EMBO journal.

[36]  Xiao-Fan Wang,et al.  HDAC6 is a microtubule-associated deacetylase , 2002, Nature.

[37]  F. Dequiedt,et al.  Enzymatic activity associated with class II HDACs is dependent on a multiprotein complex containing HDAC3 and SMRT/N-CoR. , 2002, Molecular cell.

[38]  A. Wolffe,et al.  PPARγ knockdown by engineered transcription factors: exogenous PPARγ2 but not PPARγ1 reactivates adipogenesis , 2002 .

[39]  A. Wolffe,et al.  PPARgamma knockdown by engineered transcription factors: exogenous PPARgamma2 but not PPARgamma1 reactivates adipogenesis. , 2002, Genes & development.

[40]  V. Richon,et al.  Histone deacetylase inhibitors as new cancer drugs , 2001, Current opinion in oncology.

[41]  Sandy D. Westerheide,et al.  The p65 (RelA) Subunit of NF-κB Interacts with the Histone Deacetylase (HDAC) Corepressors HDAC1 and HDAC2 To Negatively Regulate Gene Expression , 2001, Molecular and Cellular Biology.

[42]  James R. Downing,et al.  ETO, a Target of t(8;21) in Acute Leukemia, Makes Distinct Contacts with Multiple Histone Deacetylases and Binds mSin3A through Its Oligomerization Domain , 2001, Molecular and Cellular Biology.

[43]  M. Guenther,et al.  The SMRT and N-CoR Corepressors Are Activating Cofactors for Histone Deacetylase 3 , 2001, Molecular and Cellular Biology.

[44]  S. Hiebert,et al.  TEL contacts multiple co-repressors and specifically associates with histone deacetylase-3 , 2001, Oncogene.

[45]  M. Lorenzo,et al.  Akt mediates insulin induction of glucose uptake and up‐regulation of GLUT4 gene expression in brown adipocytes , 2001, FEBS letters.

[46]  Delin Chen,et al.  Deacetylation of p53 modulates its effect on cell growth and apoptosis , 2000, Nature.

[47]  M. Greaves,et al.  Recruitment of the nuclear receptor corepressor N-CoR by the TEL moiety of the childhood leukemia-associated TEL-AML1 oncoprotein. , 2000, Blood.

[48]  J. Qin,et al.  Both corepressor proteins SMRT and N‐CoR exist in large protein complexes containing HDAC3 , 2000, The EMBO journal.

[49]  L. Matrisian,et al.  TEL, a Putative Tumor Suppressor, Modulates Cell Growth and Cell Morphology of Ras-Transformed Cells While Repressing the Transcription of stromelysin-1 , 2000, Molecular and Cellular Biology.

[50]  Wen‐Ming Yang,et al.  Histone Deacetylases Specifically Down-regulate p53-dependent Gene Activation* , 2000, The Journal of Biological Chemistry.

[51]  T. Nakayama,et al.  N-terminal Region, C-terminal Region, Nuclear Export Signal, and Deacetylation Activity of Histone Deacetylase-3 Are Essential for the Viability of the DT40 Chicken B Cell Line* , 2000, The Journal of Biological Chemistry.

[52]  M. Gartenberg.  The Sir proteins of Saccharomyces cerevisiae: mediators of transcriptional silencing and much more. , 2000, Current opinion in microbiology.

[53]  L. Guarente,et al.  Transcriptional silencing and longevity protein Sir2 is an NAD-dependent histone deacetylase , 2000, Nature.

[54]  M. Magnuson,et al.  DNA excision in liver by an albumin‐Cre transgene occurs progressively with age , 2000, Genesis.

[55]  G. Nucifora,et al.  The leukemia-associated gene TEL encodes a transcription repressor which associates with SMRT and mSin3A. , 1999, Biochemical and biophysical research communications.

[56]  J. Downing,et al.  Both TEL and AML-1 Contribute Repression Domains to the t(12;21) Fusion Protein , 1999, Molecular and Cellular Biology.

[57]  M. Magnuson,et al.  Dual Roles for Glucokinase in Glucose Homeostasis as Determined by Liver and Pancreatic β Cell-specific Gene Knock-outs Using Cre Recombinase* , 1999, The Journal of Biological Chemistry.

[58]  A. Zelent,et al.  Reduced retinoic acid-sensitivities of nuclear receptor corepressor binding to PML- and PLZF-RARalpha underlie molecular pathogenesis and treatment of acute promyelocytic leukemia. , 1998, Blood.

[59]  S. Inoue,et al.  Role of the histone deacetylase complex in acute promyelocytic leukaemia , 1998, Nature.

[60]  S. Minucci,et al.  Fusion proteins of the retinoic acid receptor-α recruit histone deacetylase in promyelocytic leukaemia , 1998, Nature.

[61]  C. Tribioli,et al.  Distinct interactions of PML-RARα and PLZF-RARα with co-repressors determine differential responses to RA in APL , 1998, Nature Genetics.

[62]  C. Tribioli,et al.  Distinct interactions of PML-RARalpha and PLZF-RARalpha with co-repressors determine differential responses to RA in APL. , 1998, Nature genetics.

[63]  J. Flier,et al.  Ligand-independent activation domain in the N terminus of peroxisome proliferator-activated receptor gamma (PPARgamma). Differential activity of PPARgamma1 and -2 isoforms and influence of insulin. , 1997, The Journal of biological chemistry.

[64]  K. Kim,et al.  Identification of a second human acetyl-CoA carboxylase gene. , 1996, The Biochemical journal.

[65]  K. Moulder,et al.  Sulfated Glycans Stimulate Endocytosis of the Cellular Isoform of the Prion Protein, PrPC, in Cultured Cells (*) , 1995, The Journal of Biological Chemistry.

[66]  M Aguet,et al.  Inducible gene targeting in mice , 1995, Science.

[67]  J. Lehmann,et al.  An Antidiabetic Thiazolidinedione Is a High Affinity Ligand for Peroxisome Proliferator-activated Receptor γ (PPARγ) (*) , 1995, The Journal of Biological Chemistry.

[68]  J. Lehmann,et al.  An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferator-activated receptor gamma (PPAR gamma). , 1995, The Journal of biological chemistry.

[69]  B. Spiegelman,et al.  Stimulation of adipogenesis in fibroblasts by PPARγ2, a lipid-activated transcription factor , 1994, Cell.

[70]  B. Spiegelman,et al.  Stimulation of adipogenesis in fibroblasts by PPAR gamma 2, a lipid-activated transcription factor. , 1994, Cell.

[71]  M. Rao,et al.  Cloning of a new member of the peroxisome proliferator-activated receptor gene family from mouse liver. , 1993, The Journal of biological chemistry.

[72]  P. Pandolfi,et al.  Translocation breakpoint of acute promyelocytic leukemia lies within the retinoic acid receptor alpha locus. , 1991, Proceedings of the National Academy of Sciences of the United States of America.