Functional interactions among members of the MAX and MLX transcriptional network during oncogenesis.
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[1] J. Yokota,et al. MAX inactivation in small cell lung cancer disrupts MYC-SWI/SNF programs and is synthetic lethal with BRG1. , 2014, Cancer discovery.
[2] Yuhua Sun,et al. Extraembryonic signals under the control of MGA, Max, and Smad4 are required for dorsoventral patterning. , 2014, Developmental cell.
[3] Bruno Amati,et al. Genome recognition by MYC. , 2014, Cold Spring Harbor perspectives in medicine.
[4] Medical Faculty,et al. High-Resolution Genomic Profiling of Chronic Lymphocytic Leukemia Reveals New Recurrent Genomic Alterations , 2014 .
[5] P. Hellman,et al. MAX mutations status in Swedish patients with pheochromocytoma and paraganglioma tumours , 2014, Familial Cancer.
[6] S. Dalton,et al. Roles for MYC in the establishment and maintenance of pluripotency. , 2013, Cold Spring Harbor perspectives in medicine.
[7] P. Leoni,et al. Telomere length, c-myc and mad-1 expression could represent prognosis markers of myelodysplastic syndrome. , 2013, Leukemia research.
[8] P. Gallant. Myc function in Drosophila. , 2013, Cold Spring Harbor perspectives in medicine.
[9] D. Ayer,et al. Coordination of nutrient availability and utilization by MAX- and MLX-centered transcription networks. , 2013, Cold Spring Harbor perspectives in medicine.
[10] C. Dang. MYC, metabolism, cell growth, and tumorigenesis. , 2013, Cold Spring Harbor perspectives in medicine.
[11] D. Ayer,et al. MondoA senses adenine nucleotides: transcriptional induction of thioredoxin-interacting protein. , 2013, The Biochemical journal.
[12] Chung-Hyun Cho,et al. Mad1 mediates hypoxia-induced doxorubicin resistance in colon cancer cells by inhibiting mitochondrial function. , 2013, Free radical biology & medicine.
[13] Francesco Bertoni,et al. MGA, a suppressor of MYC, is recurrently inactivated in high risk chronic lymphocytic leukemia , 2013, Leukemia & lymphoma.
[14] P. Auvinen,et al. Mondo/ChREBP-Mlx-Regulated Transcriptional Network Is Essential for Dietary Sugar Tolerance in Drosophila , 2013, PLoS genetics.
[15] Ezekiel J. Maier,et al. Role of Fat Body Lipogenesis in Protection against the Effects of Caloric Overload in Drosophila* , 2013, The Journal of Biological Chemistry.
[16] P. Hurlin,et al. MYC needs MNT , 2013, Cell cycle.
[17] C. Dang,et al. Unlocking the mysterious mechanisms of Myc , 2013, Nature Medicine.
[18] J. Maris,et al. ATF4 regulates MYC-mediated neuroblastoma cell death upon glutamine deprivation. , 2012, Cancer cell.
[19] Colin J. Daniel,et al. A critical role for Mnt in Myc-driven T-cell proliferation and oncogenesis , 2012, Proceedings of the National Academy of Sciences.
[20] N. McCarthy. Tumorigenesis: Megaphone MYC , 2012, Nature Reviews Cancer.
[21] D. Green,et al. c-Myc Is a Universal Amplifier of Expressed Genes in Lymphocytes and Embryonic Stem Cells , 2012, Cell.
[22] G. Evan,et al. All Things to All People , 2012, Cell.
[23] Charles Y. Lin,et al. Transcriptional Amplification in Tumor Cells with Elevated c-Myc , 2012, Cell.
[24] S. Burdach,et al. MondoA is highly overexpressed in acute lymphoblastic leukemia cells and modulates their metabolism, differentiation and survival. , 2012, Leukemia research.
[25] V. Hietakangas,et al. Glucose sensing by ChREBP/MondoA-Mlx transcription factors. , 2012, Seminars in cell & developmental biology.
[26] A. F. Stewart,et al. ChREBP Mediates Glucose-Stimulated Pancreatic β-Cell Proliferation , 2012, Diabetes.
[27] W. Atchley,et al. A Novel N-Terminal Domain May Dictate the Glucose Response of Mondo Proteins , 2012, PloS one.
[28] M. Urioste,et al. MAX Mutations Cause Hereditary and Sporadic Pheochromocytoma and Paraganglioma , 2012, Clinical Cancer Research.
[29] P. Saha,et al. Carbohydrate response element-binding protein (ChREBP) plays a pivotal role in beta cell glucotoxicity , 2012, Diabetologia.
[30] T. Fan,et al. The metabolic profile of tumors depends on both the responsible genetic lesion and tissue type. , 2012, Cell metabolism.
[31] D. Green,et al. The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation. , 2011, Immunity.
[32] S. Lowe,et al. RNAi screen identifies Brd4 as a therapeutic target in acute myeloid leukaemia , 2011, Nature.
[33] W. Atchley,et al. Evolution of the Max and Mlx Networks in Animals , 2011, Genome biology and evolution.
[34] Sung‐Min Ahn,et al. Integrated Expression Profiling and Genome-Wide Analysis of ChREBP Targets Reveals the Dual Role for ChREBP in Glucose-Regulated Gene Expression , 2011, PloS one.
[35] Y. Okazaki,et al. Indefinite self-renewal of ESCs through Myc/Max transcriptional complex-independent mechanisms. , 2011, Cell stem cell.
[36] Peder E. Z. Larson,et al. 13C-pyruvate imaging reveals alterations in glycolysis that precede c-Myc-induced tumor formation and regression. , 2011, Cell metabolism.
[37] J. Benítez,et al. Exome sequencing identifies MAX mutations as a cause of hereditary pheochromocytoma , 2011, Nature Genetics.
[38] D. Ayer,et al. An extended Myc network contributes to glucose homeostasis in cancer and diabetes. , 2011, Frontiers in bioscience.
[39] Susan L Young,et al. Premetazoan ancestry of the Myc-Max network. , 2011, Molecular biology and evolution.
[40] N. Vasilevsky,et al. OX40 engagement stabilizes Mxd4 and Mnt protein levels in antigen‐stimulated T cells leading to an increase in cell survival , 2011, European journal of immunology.
[41] C. Dang,et al. Therapeutic targeting of Myc-reprogrammed cancer cell metabolism. , 2011, Cold Spring Harbor symposia on quantitative biology.
[42] Stuart H. Orkin,et al. A Myc Network Accounts for Similarities between Embryonic Stem and Cancer Cell Transcription Programs , 2010, Cell.
[43] H. Towle,et al. Activation and repression of glucose-stimulated ChREBP requires the concerted action of multiple domains within the MondoA conserved region. , 2010, American journal of physiology. Endocrinology and metabolism.
[44] Fionnuala Morrish,et al. Myc-dependent Mitochondrial Generation of Acetyl-CoA Contributes to Fatty Acid Biosynthesis and Histone Acetylation during Cell Cycle Entry* , 2010, The Journal of Biological Chemistry.
[45] Daniel Merl,et al. Lactic Acidosis Triggers Starvation Response with Paradoxical Induction of TXNIP through MondoA , 2010, PLoS genetics.
[46] D. Ayer,et al. Coordination of glucose and glutamine utilization by an expanded Myc network , 2010, Transcription.
[47] D. Ayer,et al. Myc, mondo, and metabolism. , 2010, Genes & cancer.
[48] E. Prochownik,et al. c-Myc is required for the CHREBP-dependent activation of glucose-responsive genes. , 2010, Molecular endocrinology.
[49] D. Ayer,et al. Glucose Controls Nuclear Accumulation, Promoter Binding, and Transcriptional Activity of the MondoA-Mlx Heterodimer , 2010, Molecular and Cellular Biology.
[50] D. Felsher,et al. MYC as a regulator of ribosome biogenesis and protein synthesis , 2010, Nature Reviews Cancer.
[51] Christopher B. Burge,et al. c-Myc Regulates Transcriptional Pause Release , 2010, Cell.
[52] C. Liu,et al. Chromatin remodeling: recruitment of histone demethylase RBP2 by Madl for transcriptional repression of a Myc target gene, telomerase reverse transcriptase , 2010, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[53] Chi V Dang,et al. Rethinking the Warburg effect with Myc micromanaging glutamine metabolism. , 2010, Cancer research.
[54] G. Semenza,et al. Inhibition of lactate dehydrogenase A induces oxidative stress and inhibits tumor progression , 2010, Proceedings of the National Academy of Sciences.
[55] C. Thompson,et al. The glucose-responsive transcription factor ChREBP contributes to glucose-dependent anabolic synthesis and cell proliferation , 2009, Proceedings of the National Academy of Sciences.
[56] P. Gallant,et al. Myc’s secret life without Max , 2009, Cell cycle.
[57] Hisashi Tanaka,et al. Gene Regulation and Epigenetic Remodeling in Murine Embryonic Stem Cells by c-Myc , 2009, PloS one.
[58] C. Dang,et al. MYC-Induced Cancer Cell Energy Metabolism and Therapeutic Opportunities , 2009, Clinical Cancer Research.
[59] K. Jones,et al. SKIP interacts with c-Myc and Menin to promote HIV-1 Tat transactivation. , 2009, Molecular cell.
[60] D. Ayer,et al. Glutamine-dependent anapleurosis dictates glucose uptake and cell growth by regulating MondoA transcriptional activity , 2009, Proceedings of the National Academy of Sciences.
[61] Xudong Dai,et al. MicroRNA miR-210 modulates cellular response to hypoxia through the MYC antagonist MNT , 2009, Cell cycle.
[62] Stephen Dalton,et al. The cell cycle and Myc intersect with mechanisms that regulate pluripotency and reprogramming. , 2009, Cell stem cell.
[63] A. Shalev,et al. Glucose-stimulated Expression of Txnip Is Mediated by Carbohydrate Response Element-binding Protein, p300, and Histone H4 Acetylation in Pancreatic Beta Cells* , 2009, The Journal of Biological Chemistry.
[64] J. León,et al. Inhibition of cell differentiation: A critical mechanism for MYC-mediated carcinogenesis? , 2009, Cell cycle.
[65] Tsung-Cheng Chang,et al. c-Myc suppression of miR-23 enhances mitochondrial glutaminase and glutamine metabolism , 2009, Nature.
[66] Anthony Mancuso,et al. Myc regulates a transcriptional program that stimulates mitochondrial glutaminolysis and leads to glutamine addiction , 2008, Proceedings of the National Academy of Sciences.
[67] E. Guccione,et al. Analysis of Myc-Induced Histone Modifications on Target Chromatin , 2008, PloS one.
[68] W. Kaelin. The von Hippel–Lindau tumour suppressor protein: O2 sensing and cancer , 2008, Nature Reviews Cancer.
[69] R. Eisenman,et al. Myc's broad reach. , 2008, Genes & development.
[70] J. Sedivy,et al. Myc Inhibits p27-Induced Erythroid Differentiation of Leukemia Cells by Repressing Erythroid Master Genes without Reversing p27-Mediated Cell Cycle Arrest , 2008, Molecular and Cellular Biology.
[71] Bin Tean Teh,et al. Inhibition of Mxi1 suppresses HIF-2α-dependent renal cancer tumorigenesis , 2008 .
[72] M.-H. Lee,et al. Roles of p53, Myc and HIF-1 in Regulating Glycolysis — the Seventh Hallmark of Cancer , 2008, Cellular and Molecular Life Sciences.
[73] P. Gallant,et al. Max-independent functions of Myc in Drosophila melanogaster , 2008, Nature Genetics.
[74] H. Towle,et al. Glucose Activates ChREBP by Increasing Its Rate of Nuclear Entry and Relieving Repression of Its Transcriptional Activity* , 2008, Journal of Biological Chemistry.
[75] R. Cencic,et al. c-Myc and eIF4F are components of a feedforward loop that links transcription and translation. , 2008, Cancer research.
[76] J. Boult,et al. Oesophageal adenocarcinoma is associated with a deregulation in the MYC/MAX/MAD network , 2008, British Journal of Cancer.
[77] Yukio Horikawa,et al. ChREBP: a glucose-activated transcription factor involved in the development of metabolic syndrome. , 2008, Endocrine journal.
[78] D. Ayer,et al. Glucose sensing by MondoA:Mlx complexes: A role for hexokinases and direct regulation of thioredoxin-interacting protein expression , 2008, Proceedings of the National Academy of Sciences.
[79] Remco Dijkman,et al. Novel and highly recurrent chromosomal alterations in Sézary syndrome. , 2008, Cancer research.
[80] B. Lüscher,et al. Inhibition of apoptosis by MAD1 is mediated by repression of the PTEN tumor suppressor gene , 2008, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[81] B Franz Lang,et al. A phylogenomic investigation into the origin of metazoa. , 2008, Molecular biology and evolution.
[82] J. Delrow,et al. Drosophila growth and development in the absence of dMyc and dMnt. , 2008, Developmental biology.
[83] Nicholas H. Putnam,et al. The genome of the choanoflagellate Monosiga brevicollis and the origin of metazoans , 2008, Nature.
[84] F. Calvo,et al. c-Myc Inhibits Ras-Mediated Differentiation of Pheochromocytoma Cells by Blocking c-Jun Up-Regulation , 2008, Molecular Cancer Research.
[85] Christopher Logothetis,et al. Inhibition of Mxi1 suppresses HIF-2alpha-dependent renal cancer tumorigenesis. , 2008, Cancer biology & therapy.
[86] J. Partanen,et al. c-Myc Blazing a Trail of Death: Coupling of the Mitochondrial and Death Receptor Apoptosis Pathways by c-Myc , 2007, Cell cycle.
[87] S. Amente,et al. P-TEFb is a Crucial Co-Factor for Myc Transactivation , 2007, Cell cycle.
[88] J. Girard,et al. ChREBP, a transcriptional regulator of glucose and lipid metabolism. , 2007, Annual review of nutrition.
[89] Nicola Zamboni,et al. Deficiency in glutamine but not glucose induces MYC-dependent apoptosis in human cells , 2007, The Journal of cell biology.
[90] J. Haycock,et al. c-Myc and ChREBP regulate glucose-mediated expression of the L-type pyruvate kinase gene in INS-1-derived 832/13 cells. , 2007, American journal of physiology. Endocrinology and metabolism.
[91] R. Eisenman,et al. The Function and Regulation of the JARID1 Family of Histone H3 Lysine 4 Demethylases: the Myc Connection , 2007, Cell cycle.
[92] R. Eisenman,et al. The Trithorax group protein Lid is a trimethyl histone H3K4 demethylase required for dMyc-induced cell growth. , 2007, Genes & development.
[93] J. Partanen,et al. c‐Myc primed mitochondria determine cellular sensitivity to TRAIL‐induced apoptosis , 2007, The EMBO journal.
[94] Xiao-ling Guo,et al. Expression and mutation analysis of genes that encode the Myc antagonists Mad1, Mxi1 and Rox in acute leukaemia , 2007, Leukemia & lymphoma.
[95] Y. Sham,et al. A critical role for the loop region of the basic helix–loop–helix/leucine zipper protein Mlx in DNA binding and glucose-regulated transcription , 2006, Nucleic acids research.
[96] H. Towle,et al. ChREBP•Mlx Is the Principal Mediator of Glucose-induced Gene Expression in the Liver* , 2006, Journal of Biological Chemistry.
[97] B. Jayaprakasam,et al. Regulation of hepatic fatty acid elongase and desaturase expression in diabetes and obesity Published, JLR Papers in Press, June 21, 2006. , 2006, Journal of Lipid Research.
[98] S. Yamanaka,et al. Induction of Pluripotent Stem Cells from Mouse Embryonic and Adult Fibroblast Cultures by Defined Factors , 2006, Cell.
[99] L. Penn,et al. The Oscar-worthy role of Myc in apoptosis. , 2006, Seminars in cancer biology.
[100] J. Repa,et al. Carbohydrate response element binding protein, ChREBP, a transcription factor coupling hepatic glucose utilization and lipid synthesis. , 2006, Cell metabolism.
[101] S. R. Hann. Role of post-translational modifications in regulating c-Myc proteolysis, transcriptional activity and biological function. , 2006, Seminars in cancer biology.
[102] D. Ayer,et al. MondoA-Mlx Heterodimers Are Candidate Sensors of Cellular Energy Status: Mitochondrial Localization and Direct Regulation of Glycolysis , 2006, Molecular and Cellular Biology.
[103] Giacomo Finocchiaro,et al. Myc-binding-site recognition in the human genome is determined by chromatin context , 2006, Nature Cell Biology.
[104] Philip R. Gafken,et al. Myc influences global chromatin structure , 2006, The EMBO journal.
[105] M. Cole,et al. A Conserved Myc Protein Domain, MBIV, Regulates DNA Binding, Apoptosis, Transformation, and G2 Arrest , 2006, Molecular and Cellular Biology.
[106] Peng-hui Zhang,et al. Mad1 suppresses bladder cancer cell proliferation by inhibiting human telomerase reverse transcriptase transcription and telomerase activity. , 2006, Urology.
[107] C. Glass,et al. Mnt-deficient mammary glands exhibit impaired involution and tumors with characteristics of myc overexpression. , 2006, Cancer research.
[108] A. Wynshaw-Boris,et al. Inflammatory Disease and Lymphomagenesis Caused by Deletion of the Myc Antagonist Mnt in T Cells , 2006, Molecular and Cellular Biology.
[109] S. McMahon,et al. Targeting of Miz-1 Is Essential for Myc-mediated Apoptosis* , 2006, Journal of Biological Chemistry.
[110] P. Gallant. Myc/Max/Mad in invertebrates: the evolution of the Max network. , 2006, Current topics in microbiology and immunology.
[111] M. Cole,et al. Transcriptional activation by the Myc oncoprotein. , 2006, Current topics in microbiology and immunology.
[112] D. Ayer,et al. The Mlx network: evidence for a parallel Max-like transcriptional network that regulates energy metabolism. , 2006, Current topics in microbiology and immunology.
[113] N. Schreiber-Agus,et al. Lessons learned from Myc/Max/Mad knockout mice. , 2006, Current topics in microbiology and immunology.
[114] C. Grandori,et al. Activation by c-Myc of transcription by RNA polymerases I, II and III. , 2006, Biochemical Society symposium.
[115] M. Henriksson,et al. Mnt transcriptional repressor is functionally regulated during cell cycle progression , 2005, Oncogene.
[116] E. Wang,et al. c‐Myc creates an activation loop by transcriptionally repressing its own functional inhibitor, hMad4, in young fibroblasts, a loop lost in replicatively senescent fibroblasts , 2005, Journal of cellular biochemistry.
[117] P. Lavigne,et al. Toward the elucidation of the structural determinants responsible for the molecular recognition between Mad1 and Max. , 2005, Biochemistry.
[118] W. El-Deiry,et al. Mxi1 is induced by hypoxia in a HIF-1–dependent manner and protects cells from c-Myc-induced apoptosis , 2005, Cancer biology & therapy.
[119] B. Edgar,et al. The Transcriptional Repressor dMnt Is a Regulator of Growth in Drosophila melanogaster , 2005, Molecular and Cellular Biology.
[120] Kathryn A. O’Donnell,et al. Myc Stimulates Nuclearly Encoded Mitochondrial Genes and Mitochondrial Biogenesis , 2005, Molecular and Cellular Biology.
[121] A. Wynshaw-Boris,et al. Mnt–Max to Myc–Max complex switching regulates cell cycle entry , 2005, The Journal of cell biology.
[122] H. Koeffler,et al. Mxi1 isoforms are expressed in hematological cell lines and normal bone marrow. , 2005, International journal of oncology.
[123] E. Kremmer,et al. Mad1 Function in Cell Proliferation and Transcriptional Repression Is Antagonized by Cyclin E/CDK2* , 2005, Journal of Biological Chemistry.
[124] H. Towle,et al. Direct Role of ChREBP·Mlx in Regulating Hepatic Glucose-responsive Genes* , 2005, Journal of Biological Chemistry.
[125] Carla Grandori,et al. c-Myc binds to human ribosomal DNA and stimulates transcription of rRNA genes by RNA polymerase I , 2005, Nature Cell Biology.
[126] S. Lowe,et al. A conserved element in Myc that negatively regulates its proapoptotic activity , 2005, EMBO reports.
[127] Katsumi Iizuka,et al. Carbohydrate response element binding protein directly promotes lipogenic enzyme gene transcription. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[128] J. Zavadil,et al. Analysis of transcripts from 17p13.3 in medulloblastoma suggests ROX/MNT as a potential tumour suppressor gene. , 2004, European journal of cancer.
[129] Bruce J. Aronow,et al. Chromatin Immunoprecipitation Assays Footprints in Glycolytic Genes by Evaluation of Myc E-box Phylogenetic Supplemental Material , 2004 .
[130] J. S. Britton,et al. dMyc is required for larval growth and endoreplication in Drosophila , 2004, Development.
[131] R. Eisenman,et al. Loss of the Max-interacting protein Mnt in mice results in decreased viability, defective embryonic growth and craniofacial defects: relevance to Miller-Dieker syndrome. , 2004, Human molecular genetics.
[132] K. Iizuka,et al. Deficiency of carbohydrate response element-binding protein (ChREBP) reduces lipogenesis as well as glycolysis. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[133] H. Towle,et al. Mlx Is the Functional Heteromeric Partner of the Carbohydrate Response Element-binding Protein in Glucose Regulation of Lipogenic Enzyme Genes* , 2004, Journal of Biological Chemistry.
[134] J. Cleveland,et al. Mnt Loss Triggers Myc Transcription Targets, Proliferation, Apoptosis, and Transformation , 2004, Molecular and Cellular Biology.
[135] John L Cleveland,et al. Myc pathways provoking cell suicide and cancer , 2003, Oncogene.
[136] A. Wynshaw-Boris,et al. Deletion of Mnt leads to disrupted cell cycle control and tumorigenesis , 2003, The EMBO journal.
[137] D. Livingston,et al. MYC recruits the TIP60 histone acetyltransferase complex to chromatin , 2003, EMBO reports.
[138] Yvonne A. Evrard,et al. c-Myc Transformation Domain Recruits the Human STAGA Complex and Requires TRRAP and GCN5 Acetylase Activity for Transcription Activation* , 2003, Journal of Biological Chemistry.
[139] D. Scott,et al. c-Myc Is Required for the Glucose-mediated Induction of Metabolic Enzyme Genes* , 2003, The Journal of Biological Chemistry.
[140] S. Wright,et al. Mad4 is regulated by a transcriptional repressor complex that contains Miz-1 and c-Myc. , 2003, The Biochemical journal.
[141] Stephen K. Burley,et al. X-Ray Structures of Myc-Max and Mad-Max Recognizing DNA Molecular Bases of Regulation by Proto-Oncogenic Transcription Factors , 2003, Cell.
[142] R. Eisenman,et al. Direct activation of RNA polymerase III transcription by c-Myc , 2003, Nature.
[143] Fionnuala Morrish,et al. c-MYC apoptotic function is mediated by NRF-1 target genes. , 2003, Genes & development.
[144] D. Ayer,et al. A Novel Heterodimerization Domain, CRM1, and 14-3-3 Control Subcellular Localization of the MondoA-Mlx Heterocomplex , 2002, Molecular and Cellular Biology.
[145] P. Farnham,et al. Myc Recruits P-TEFb to Mediate the Final Step in the Transcriptional Activation of the cad Promoter* , 2002, The Journal of Biological Chemistry.
[146] Yuko Hamada,et al. Effect of the transcriptional repressor Mad1 on proliferation of human melanoma cells , 2002, Experimental dermatology.
[147] Stuart L. Schreiber,et al. Active genes are tri-methylated at K4 of histone H3 , 2002, Nature.
[148] Carla Grandori,et al. Modulation of T‐lymphocyte development, growth and cell size by the Myc antagonist and transcriptional repressor Mad1 , 2002, The EMBO journal.
[149] R. Eisenman,et al. Myc and Mad bHLHZ domains possess identical DNA-binding specificities but only partially overlapping functions in vivo , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[150] Stuart L. Schreiber,et al. Methylation of histone H3 Lys 4 in coding regions of active genes , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[151] David M. Livingston,et al. A Complex with Chromatin Modifiers That Occupies E2F- and Myc-Responsive Genes in G0 Cells , 2002, Science.
[152] James M. Roberts,et al. MAD1 and p27KIP1 Cooperate To Promote Terminal Differentiation of Granulocytes and To Inhibit Myc Expression and Cyclin E-CDK2 Activity , 2002, Molecular and Cellular Biology.
[153] M. Eilers,et al. Contributions of Myc to tumorigenesis. , 2002, Biochimica et biophysica acta.
[154] G. Finocchiaro,et al. Mxi1 inhibits the proliferation of U87 glioma cells through down-regulation of cyclin B1 gene expression , 2002, British Journal of Cancer.
[155] M. Henriksson,et al. Repression of in vivo growth of Myc/Ras transformed tumor cells by Mad1 , 2002, Oncogene.
[156] J. Massagué,et al. Myc suppression of the p21(Cip1) Cdk inhibitor influences the outcome of the p53 response to DNA damage. , 2002, Nature.
[157] K. Uyeda,et al. Glucose and cAMP regulate the L-type pyruvate kinase gene by phosphorylation/dephosphorylation of the carbohydrate response element binding protein , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[158] S. Korsmeyer,et al. Bax Loss Impairs Myc-Induced Apoptosis and Circumvents the Selection of p53 Mutations during Myc-Mediated Lymphomagenesis , 2001, Molecular and Cellular Biology.
[159] E. J. Fox,et al. S-phase-specific expression of the Mad3 gene in proliferating and differentiating cells. , 2001, The Biochemical journal.
[160] M. Eilers,et al. Regulation of cyclin D2 gene expression by the Myc/Max/Mad network: Myc-dependent TRRAP recruitment and histone acetylation at the cyclin D2 promoter. , 2001, Genes & development.
[161] D. Kahn,et al. New members of the Drosophila Myc transcription factor subfamily revealed by a genome-wide examination for basic helix-loop-helix genes , 2001, Mechanisms of Development.
[162] D. Wechsler,et al. Mxi1, a Myc antagonist, suppresses proliferation of DU145 human prostate cells , 2001, The Prostate.
[163] J. Massagué,et al. TGFβ influences Myc, Miz-1 and Smad to control the CDK inhibitor p15INK4b , 2001, Nature Cell Biology.
[164] J. Massagué,et al. Repression of p15INK4b expression by Myc through association with Miz-1 , 2001, Nature Cell Biology.
[165] Nikita Popov,et al. Switch from Myc/Max to Mad1/Max binding and decrease in histone acetylation at the telomerase reverse transcriptase promoter during differentiation of HL60 cells , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[166] A Ballabio,et al. WBSCR14, a gene mapping to the Williams--Beuren syndrome deleted region, is a new member of the Mlx transcription factor network. , 2001, Human molecular genetics.
[167] G. Evan,et al. Expression of Mad1 in T cells leads to reduced thymic cellularity and impaired mitogen-induced proliferation , 2001, Oncogene.
[168] R. Eisenman,et al. Targeted Deletion of the S-Phase-Specific Myc Antagonist Mad3 Sensitizes Neuronal and Lymphoid Cells to Radiation-Induced Apoptosis , 2001, Molecular and Cellular Biology.
[169] U. Weidle,et al. The transcriptional program of a human B cell line in response to Myc. , 2001, Nucleic acids research.
[170] D. Ayer,et al. MondoA, a Novel Basic Helix-Loop-Helix–Leucine Zipper Transcriptional Activator That Constitutes a Positive Branch of a Max-Like Network , 2000, Molecular and Cellular Biology.
[171] R. Eisenman,et al. Solution Structure of the Interacting Domains of the Mad–Sin3 Complex Implications for Recruitment of a Chromatin-Modifying Complex , 2000, Cell.
[172] C. Asker,et al. Inhibition of cell growth and apoptosis by inducible expression of the transcriptional repressor Mad1. , 2000, Experimental cell research.
[173] C. Dang,et al. Deregulation of Glucose Transporter 1 and Glycolytic Gene Expression by c-Myc* , 2000, The Journal of Biological Chemistry.
[174] A. Reymond,et al. Mlx, a new Max-like bHLHZip family member: the center stage of a novel transcription factors regulatory pathway? , 2000, Oncogene.
[175] C. Englert,et al. Expression of the hTERT gene is regulated at the level of transcriptional initiation and repressed by Mad1. , 2000, Cancer research.
[176] Young-Hwa Song,et al. Identification of Mad as a repressor of the human telomerase (hTERT) gene , 2000, Oncogene.
[177] T. Littlewood,et al. Action of Myc in vivo - proliferation and apoptosis. , 2000, Current opinion in genetics & development.
[178] M. Cole,et al. An ATPase/helicase complex is an essential cofactor for oncogenic transformation by c-Myc. , 2000, Molecular cell.
[179] M. Cole,et al. The Essential Cofactor TRRAP Recruits the Histone Acetyltransferase hGCN5 to c-Myc , 2000, Molecular and Cellular Biology.
[180] D. Ayer,et al. Mlx, a Novel Max-like BHLHZip Protein That Interacts with the Max Network of Transcription Factors* , 1999, The Journal of Biological Chemistry.
[181] N. Jenkins,et al. Mga, a dual‐specificity transcription factor that interacts with Max and contains a T‐domain DNA‐binding motif , 1999, The EMBO journal.
[182] R. Eisenman,et al. Dwarfism and dysregulated proliferation in mice overexpressing the MYC antagonist MAD1. , 1999, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
[183] Jun Liu,et al. A 13-Amino Acid Amphipathic α-Helix Is Required for the Functional Interaction between the Transcriptional Repressor Mad1 and mSin3A* , 1999, The Journal of Biological Chemistry.
[184] M. Roussel,et al. Disruption of the ARF-Mdm2-p53 tumor suppressor pathway in Myc-induced lymphomagenesis. , 1999, Genes & development.
[185] W. Ansorge,et al. Direct induction of cyclin D2 by Myc contributes to cell cycle progression and sequestration of p27 , 1999, The EMBO journal.
[186] J. Tonn,et al. Analysis of the max‐binding protein MNT in human medulloblastomas , 1999, International journal of cancer.
[187] D. Roop,et al. Targeted expression of c-Myc in the epidermis alters normal proliferation, differentiation and UV-B induced apoptosis , 1999, Oncogene.
[188] H. Sugimura,et al. Mxi1 Mutations in Human Neurofibrosarcomas , 1999, Japanese journal of cancer research : Gann.
[189] E. Reddy,et al. The v-myc oncogene , 1999, Oncogene.
[190] M. Cole,et al. The Myc oncoprotein: a critical evaluation of transactivation and target gene regulation , 1999, Oncogene.
[191] G. Prendergast,et al. Mechanisms of apoptosis by c-Myc , 1999, Oncogene.
[192] Yong Hua Xu,et al. mad-overexpression down regulates the malignant growth and p53 mediated apoptosis in human hepatocellular carcinoma BEL-7404 cells , 1999, Cell Research.
[193] M. Eilers,et al. Control of cell proliferation by Myc family genes. , 1999, Molecules and cells.
[194] L. Chin,et al. Telomerase reverse transcriptase gene is a direct target of c-Myc but is not functionally equivalent in cellular transformation , 1999, Oncogene.
[195] Chi V. Dang,et al. c-Myc Target Genes Involved in Cell Growth, Apoptosis, and Metabolism , 1999, Molecular and Cellular Biology.
[196] D. Botstein,et al. Cluster analysis and display of genome-wide expression patterns. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[197] M. Cole,et al. The Novel ATM-Related Protein TRRAP Is an Essential Cofactor for the c-Myc and E2F Oncoproteins , 1998, Cell.
[198] J L Cleveland,et al. Myc signaling via the ARF tumor suppressor regulates p53-dependent apoptosis and immortalization. , 1998, Genes & development.
[199] E. Prochownik,et al. Commonly occurring loss and mutation of the MXI1 gene in prostate cancer , 1998, Genes, chromosomes & cancer.
[200] R. DePinho,et al. Role of Mxi1 in ageing organ systems and the regulation of normal and neoplastic growth , 1998, Nature.
[201] H. Konishi,et al. Molecular Analysis of a Myc Antagonist, ROX/Mnt, at 17p13.3 in Human Lung Cancers , 1998, Japanese journal of cancer research : Gann.
[202] R. Eisenman,et al. Sequential expression of the MAD family of transcriptional repressors during differentiation and development , 1998, Oncogene.
[203] C. Dang,et al. A unique glucose-dependent apoptotic pathway induced by c-Myc. , 1998, Proceedings of the National Academy of Sciences of the United States of America.
[204] B. Amati,et al. Myc and the cell cycle. , 1998, Frontiers in bioscience : a journal and virtual library.
[205] A. Giaccia,et al. p53 mediates apoptosis induced by c-Myc activation in hypoxic or gamma irradiated fibroblasts , 1998, Cell Death and Differentiation.
[206] R. Eisenman,et al. Targeted disruption of the MYC antagonist MAD1 inhibits cell cycle exit during granulocyte differentiation , 1998, The EMBO journal.
[207] J. Serth,et al. The MXI1 tumor suppressor gene is not mutated in primary prostate cancer. , 1998, Oncology reports.
[208] D. Wechsler,et al. MXI1, a putative tumor suppressor gene, suppresses growth of human glioblastoma cells. , 1997, Cancer research.
[209] R. Bernards,et al. Repression of c-Myc responsive genes in cycling cells causes G1 arrest through reduction of cyclin E/CDK2 kinase activity , 1997, Oncogene.
[210] L. Larsson,et al. Analysis of the DNA-binding activities of Myc/Max/Mad network complexes during induced differentiation of U-937 monoblasts and F9 teratocarcinoma cells , 1997, Oncogene.
[211] R A Jungmann,et al. c-Myc transactivation of LDH-A: implications for tumor metabolism and growth. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[212] M. Hengstschläger,et al. Cellular targets for activation by c-Myc include the DNA metabolism enzyme thymidine kinase. , 1997, DNA and cell biology.
[213] E. Kremmer,et al. Cell growth inhibition by the Mad/Max complex through recruitment of histone deacetylase activity , 1997, Current Biology.
[214] D. Ledbetter,et al. Rox, a novel bHLHZip protein expressed in quiescent cells that heterodimerizes with Max, binds a non‐canonical E box and acts as a transcriptional repressor , 1997, The EMBO journal.
[215] Wen‐Ming Yang,et al. Histone Deacetylases Associated with the mSin3 Corepressor Mediate Mad Transcriptional Repression , 1997, Cell.
[216] C. Cultraro,et al. Function of the c-Myc antagonist Mad1 during a molecular switch from proliferation to differentiation , 1997, Molecular and cellular biology.
[217] R. DePinho,et al. Drosophila Myc is oncogenic in mammalian cells and plays a role in the diminutive phenotype. , 1997, Proceedings of the National Academy of Sciences of the United States of America.
[218] R. Eisenman,et al. Mnt, a novel Max-interacting protein is coexpressed with Myc in proliferating cells and mediates repression at Myc binding sites. , 1997, Genes & development.
[219] R. Eisenman,et al. Mnt: a novel Max-interacting protein and Myc antagonist. , 1997, Current topics in microbiology and immunology.
[220] R. Eisenman,et al. Myc and Max Homologs in Drosophila , 1996, Science.
[221] R. Eisenman,et al. Mad proteins contain a dominant transcription repression domain , 1996, Molecular and cellular biology.
[222] M. Polymenis,et al. An essential E box in the promoter of the gene encoding the mRNA cap-binding protein (eukaryotic initiation factor 4E) is a target for activation by c-myc , 1996, Molecular and cellular biology.
[223] D. Beach,et al. Cdc25 cell-cycle phosphatase as a target of c-myc , 1996, Nature.
[224] M. Roussel,et al. Inhibition of cell proliferation by the Mad1 transcriptional repressor , 1996, Molecular and cellular biology.
[225] W. Ansorge,et al. Activation of cyclin‐dependent kinases by Myc mediates induction of cyclin A, but not apoptosis. , 1996, The EMBO journal.
[226] P. Goodfellow,et al. Mxi1 tumor suppressor gene is not mutated in primary pancreatic adenocarcinoma. , 1996, Cancer letters.
[227] N. Copeland,et al. Mad3 and Mad4: novel Max-interacting transcriptional repressors that suppress c-myc dependent transformation and are expressed during neural and epidermal differentiation. , 1996, The EMBO journal.
[228] N. Copeland,et al. Mad3 and Mad4: novel Max‐interacting transcriptional repressors that suppress c‐myc dependent transformation and are expressed during neural and epidermal differentiation. , 1995, The EMBO journal.
[229] M. Pagano,et al. Identification of a Myc‐dependent step during the formation of active G1 cyclin‐cdk complexes. , 1995, The EMBO journal.
[230] H. Shih,et al. Two CACGTG Motifs with Proper Spacing Dictate the Carbohydrate Regulation of Hepatic Gene Transcription (*) , 1995, The Journal of Biological Chemistry.
[231] C. Seelos,et al. Differential effects by Mad and Max on transformation by cellular and viral oncoproteins. , 1995, Oncogene.
[232] E. Ziff,et al. The nerve growth factor-responsive PC12 cell line does not express the Myc dimerization partner Max , 1995, Molecular and cellular biology.
[233] R. DePinho,et al. Effects of the MYC oncogene antagonist, MAD, on proliferation, cell cycling and the malignant phenotype of human brain tumour cells , 1995, Nature Medicine.
[234] R. Eisenman,et al. Repression of Myc-Ras cotransformation by Mad is mediated by multiple protein-protein interactions. , 1995, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.
[235] P. Farnham,et al. An E-box-mediated increase in cad transcription at the G1/S-phase boundary is suppressed by inhibitory c-Myc mutants , 1995, Molecular and cellular biology.
[236] R. Eisenman,et al. Mad-max transcriptional repression is mediated by ternary complex formation with mammalian homologs of yeast repressor Sin3 , 1995, Cell.
[237] L. Chin,et al. An amino-terminal domain of Mxi1 mediates anti-myc oncogenic activity and interacts with a homolog of the Yeast Transcriptional Repressor SIN3 , 1995, Cell.
[238] K. Alitalo,et al. Expression of the mad gene during cell differentiation in vivo and its inhibition of cell growth in vitro , 1995, The Journal of cell biology.
[239] Arthur R. Brothman,et al. Mutation of the MXI1 gene in prostate cancer , 1995, Nature Genetics.
[240] R. DePinho,et al. Erratum: Effects of the MYC oncogene antagonist, MAD, on proliferation, cell cycling and the malignant phenotype of human brain tumour cells (Nature Medicine (1995) 1 (638-643)) , 1995 .
[241] S. Mai,et al. Overexpression of c-myc precedes amplification of the gene encoding dihydrofolate reductase. , 1994, Gene.
[242] C. Ling,et al. Transfected c-myc and c-Ha-ras modulate radiation-induced apoptosis in rat embryo cells. , 1994, Radiation research.
[243] R. DePinho,et al. Suppression of Myc, but not E1a, transformation activity by Max-associated proteins, Mad and Mxi1. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[244] L. Larsson,et al. Expression of mad, mxi1, max and c-myc during induced differentiation of hematopoietic cells: opposite regulation of mad and c-myc. , 1994, Oncogene.
[245] R. Eisenman,et al. The Max transcription factor network: involvement of Mad in differentiation and an approach to identification of target genes. , 1994, Cold Spring Harbor symposia on quantitative biology.
[246] R. Eisenman,et al. A switch from Myc:Max to Mad:Max heterocomplexes accompanies monocyte/macrophage differentiation. , 1993, Genes & development.
[247] Stephen K. Burley,et al. Recognition by Max of its cognate DNA through a dimeric b/HLH/Z domain , 1993, Nature.
[248] N. Hay,et al. Myc-mediated apoptosis is blocked by ectopic expression of Bcl-2 , 1993, Molecular and cellular biology.
[249] R. Eisenman,et al. Mad: A heterodimeric partner for Max that antagonizes Myc transcriptional activity , 1993, Cell.
[250] R. Brent,et al. Mxi1, a protein that specifically interacts with Max to bind Myc-Max recognition sites , 1993, Cell.
[251] Bruno Amati,et al. Oncogenic activity of the c-Myc protein requires dimerization with Max , 1993, Cell.
[252] R. Eisenman,et al. Regulation of Myc: Max complex formation and its potential role in cell proliferation. , 1992, The Tohoku journal of experimental medicine.
[253] R. Eisenman,et al. Myc and Max proteins possess distinct transcriptional activities , 1992, Nature.
[254] R. Eisenman,et al. Myc and Max function as a nucleoprotein complex , 1992, Current Biology.
[255] M. Cole,et al. Casein kinase II inhibits the DNA-binding activity of Max homodimers but not Myc/Max heterodimers. , 1992, Genes & development.
[256] J. Cleveland,et al. c-myc transactivates the ornithine decarboxylase gene. , 1992, Current topics in microbiology and immunology.
[257] R. Eisenman,et al. Myc and Max associate in vivo. , 1992, Genes & development.
[258] C. Dang,et al. Intracellular leucine zipper interactions suggest c-Myc hetero-oligomerization , 1991, Molecular and cellular biology.
[259] G. Prendergast,et al. Methylation-sensitive sequence-specific DNA binding by the c-Myc basic region. , 1991, Science.
[260] R. Eisenman,et al. Max: a helix-loop-helix zipper protein that forms a sequence-specific DNA-binding complex with Myc. , 1991, Science.
[261] G. Inghirami,et al. Negative autoregulation of c‐myc gene expression is inactivated in transformed cells. , 1990, The EMBO journal.
[262] R. Eisenman,et al. New light on Myc and Myb. Part II. Myb. , 1990, Genes & development.
[263] H. Weintraub,et al. Sequence-specific DNA binding by the c-Myc protein. , 1990, Science.
[264] L. Penn,et al. C-MYC: evidence for multiple regulatory functions. , 1990, Seminars in cancer biology.
[265] R. Eisenman,et al. New light on Myc and Myb. Part I. Myc. , 1990, Genes & development.
[266] M. Schwab,et al. Suppression of MYC by high expression of NMYC in human neuroblastoma cells , 1989, Journal of neuroscience research.
[267] David Baltimore,et al. A new DNA binding and dimerization motif in immunoglobulin enhancer binding, daughterless, MyoD, and myc proteins , 1989, Cell.
[268] A. W. Harris,et al. N‐myc transgene promotes B lymphoid proliferation, elicits lymphomas and reveals cross‐regulation with c‐myc. , 1989, The EMBO journal.
[269] A. Ogura,et al. Sarcoma viruses carrying ras oncogenes induce differentiation-associated properties in a neuronal cell line , 1985, Nature.
[270] M. Greenberg,et al. Nerve growth factor and epidermal growth factor induce rapid transient changes in proto-oncogene transcription in PC12 cells. , 1985, The Journal of biological chemistry.
[271] J. Battey,et al. L-myc, a new myc-related gene amplified and expressed in human small cell lung cancer , 1985, Nature.
[272] D. Bar-Sagi,et al. Microinjection of the ras oncogene protein into PC12 cells induces morphological differentiation , 1985, Cell.
[273] G. Evan,et al. Metabolism of c‐myc gene products: c‐myc mRNA and protein expression in the cell cycle. , 1985, EMBO Journal.
[274] H. Varmus,et al. Amplification of N-myc in untreated human neuroblastomas correlates with advanced disease stage. , 1984, Science.
[275] F. Alt,et al. Transposition and amplification of oncogene-related sequences in human neuroblastomas , 1983, Cell.
[276] J. Trent,et al. Amplified DNA with limited homology to myc cellular oncogene is shared by human neuroblastoma cell lines and a neuroblastoma tumour , 1983, Nature.
[277] C. Croce,et al. Human c-myc onc gene is located on the region of chromosome 8 that is translocated in Burkitt lymphoma cells. , 1982, Proceedings of the National Academy of Sciences of the United States of America.
[278] P. Leder,et al. Translocation of the c-myc gene into the immunoglobulin heavy chain locus in human Burkitt lymphoma and murine plasmacytoma cells. , 1982, Proceedings of the National Academy of Sciences of the United States of America.
[279] M. Groudine,et al. Amplification of endogenous myc-related DNA sequences in a human myeloid leukaemia cell line , 1982, Nature.
[280] B. Vennstrom,et al. Isolation and characterization of c-myc, a cellular homolog of the oncogene (v-myc) of avian myelocytomatosis virus strain 29 , 1982, Journal of virology.
[281] J. Bishop,et al. DNA and RNA from Uninfected Vertebrate Cells Contain Nucleotide Sequences Related to the Putative Transforming Gene of Avian Myelocytomatosis Virus , 1979, Journal of virology.