Hypertrophic agonists induce the binding of c-Fos to an AP-1 site in cardiac myocytes: implications for the expression of GLUT1.

[1]  S. Goswami,et al.  Modulation of MLC-2v gene expression by AP-1: Complex regulatory role of Jun in cardiac myocytes , 2004, Molecular and Cellular Biochemistry.

[2]  S. G. Finn,et al.  Chronic activation of extracellular-signal-regulated protein kinases by phenylephrine is required to elicit a hypertrophic response in cardiac myocytes. , 2003, Biochemical Journal.

[3]  J. G. Harrison,et al.  Up-regulation of c-jun mRNA in cardiac myocytes requires the extracellular signal-regulated kinase cascade, but c-Jun N-terminal kinases are required for efficient up-regulation of c-Jun protein. , 2002, The Biochemical journal.

[4]  Mohit M. Jain,et al.  Cardiac-Specific Overexpression of GLUT1 Prevents the Development of Heart Failure Attributable to Pressure Overload in Mice , 2002, Circulation.

[5]  Rey-Huei Chen,et al.  Molecular interpretation of ERK signal duration by immediate early gene products , 2002, Nature Cell Biology.

[6]  John J. Andreucci,et al.  Composition and Function of AP-1 Transcription Complexes during Muscle Cell Differentiation* , 2002, The Journal of Biological Chemistry.

[7]  O. Frazier,et al.  Metabolic Gene Expression in Fetal and Failing Human Heart , 2001, Circulation.

[8]  M. Yacoub,et al.  A novel functional co-operation between MyoD, MEF2 and TRalpha1 is sufficient for the induction of GLUT4 gene transcription. , 2001, Journal of molecular biology.

[9]  C. Acquaviva,et al.  Identification of a C-terminal tripeptide motif involved in the control of rapid proteasomal degradation of c-Fos proto-oncoprotein during the G0-to-S phase transition , 2001, Oncogene.

[10]  B. Kaina,et al.  Effect of ultraviolet light, methyl methanesulfonate and ionizing radiation on the genotoxic response and apoptosis of mouse fibroblasts lacking c-Fos, p53 or both. , 2001, Mutagenesis.

[11]  P. Barton,et al.  Identification of novel, cardiac-restricted transcription factors binding to a CACC-box within the human cardiac troponin I promoter. , 2001, Cardiovascular research.

[12]  J. Pearson,et al.  Fibroblast matrix gene expression and connective tissue remodeling: role of endothelin-1. , 2001, The Journal of investigative dermatology.

[13]  John C. Lee,et al.  Extracellular Signal-regulated Kinase Plays an Essential Role in Hypertrophic Agonists, Endothelin-1 and Phenylephrine-induced Cardiomyocyte Hypertrophy* , 2000, The Journal of Biological Chemistry.

[14]  Mark A Sussman,et al.  Phosphorylation of elk-1 by MEK/ERK pathway is necessary for c-fos gene activation during cardiac myocyte hypertrophy. , 2000, Journal of molecular and cellular cardiology.

[15]  M. Gaestel,et al.  Stress-induced Stimulation of Early Growth Response Gene-1 by p38/Stress-activated Protein Kinase 2 Is Mediated by a cAMP-responsive Promoter Element in a MAPKAP Kinase 2-independent Manner* , 1999, The Journal of Biological Chemistry.

[16]  K. Boheler,et al.  Factors Involved in GLUT-1 Glucose Transporter Gene Transcription in Cardiac Muscle* , 1999, The Journal of Biological Chemistry.

[17]  P. Sugden,et al.  Signaling in myocardial hypertrophy: life after calcineurin? , 1999, Circulation research.

[18]  A. Thorburn,et al.  Transcriptional Activation of the Glucose Transporter GLUT1 in Ventricular Cardiac Myocytes by Hypertrophic Agonists* , 1999, The Journal of Biological Chemistry.

[19]  M. Nemer,et al.  The C-Terminal Domain of c-fos Is Required for Activation of an AP-1 Site Specific forjun-fos Heterodimers , 1998, Molecular and Cellular Biology.

[20]  N. Tonks,et al.  Mitogen-activated protein kinase phosphatase 1 inhibits the stimulation of gene expression by hypertrophic agonists in cardiac myocytes. , 1997, The Biochemical journal.

[21]  E. Zandi,et al.  AP-1 function and regulation. , 1997, Current opinion in cell biology.

[22]  J. Olefsky,et al.  Negative Feedback Regulation and Desensitization of Insulin- and Epidermal Growth Factor-stimulated p21ras Activation (*) , 1995, The Journal of Biological Chemistry.

[23]  A. From,et al.  Effect of left ventricular hypertrophy secondary to chronic pressure overload on transmural myocardial 2-deoxyglucose uptake. A 31P NMR spectroscopic study. , 1995, Circulation.

[24]  K. Chien,et al.  Expression cloning of cardiotrophin 1, a cytokine that induces cardiac myocyte hypertrophy. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[25]  M. Yaniv,et al.  Mouse JunD negatively regulates fibroblast growth and antagonizes transformation by ras , 1994, Cell.

[26]  M. Karin,et al.  Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain. , 1993, Genes & development.

[27]  W. Schaper,et al.  Expression of nuclear proto-oncogenes in isoproterenol-induced cardiac hypertrophy. , 1993, Journal of molecular and cellular cardiology.

[28]  R. Bravo,et al.  Existence of different Fos/Jun complexes during the G0-to-G1 transition and during exponential growth in mouse fibroblasts: differential role of Fos proteins , 1992, Molecular and cellular biology.

[29]  Y. Ebina,et al.  Identification of two enhancer elements in the gene encoding the type 1 glucose transporter from the mouse which are responsive to serum, growth factor, and oncogenes. , 1992, The Journal of biological chemistry.

[30]  K. Chien,et al.  Transcriptional activation of the cardiac myosin light chain 2 and atrial natriuretic factor genes by protein kinase C in neonatal rat ventricular myocytes. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[31]  R. Bravo,et al.  Expression of different Jun and Fos proteins during the G0-to-G1 transition in mouse fibroblasts: in vitro and in vivo associations , 1991, Molecular and cellular biology.

[32]  Tsonwin Hai,et al.  Cross-family dimerization of transcription factors Fos/Jun and ATF/CREB alters DNA binding specificity. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[33]  V. Sukhatme,et al.  Alpha- and beta-adrenergic stimulation induces distinct patterns of immediate early gene expression in neonatal rat myocardial cells. fos/jun expression is associated with sarcomere assembly; Egr-1 induction is primarily an alpha 1-mediated response. , 1990, The Journal of biological chemistry.

[34]  M. Karin,et al.  Jun-B differs in its biological properties from, and is a negative regulator of, c-Jun , 1989, Cell.

[35]  M. Karin,et al.  Different requirements for formation of Jun: Jun and Jun: Fos complexes. , 1989, Genes & development.

[36]  J. Flier,et al.  Overproduction of the beta 1 form of protein kinase C enhances phorbol ester induction of glucose transporter mRNA. , 1989, Molecular endocrinology.

[37]  H. Lehväslaiho,et al.  Activation of the neu tyrosine kinase induces the fos/jun transcription factor complex, the glucose transporter and ornithine decarboxylase , 1989, The Journal of cell biology.

[38]  T. Kouzarides,et al.  Leucine zippers of fos, jun and GCN4 dictate dimerization specificity and thereby control DNA binding , 1989, Nature.

[39]  M. Greenberg,et al.  The c-fos transcript is targeted for rapid decay by two distinct mRNA degradation pathways. , 1989, Genes & development.

[40]  B. Rollins,et al.  Platelet-derived growth factor regulates glucose transporter expression. , 1988, The Journal of biological chemistry.

[41]  M. Birnbaum,et al.  Growth factors rapidly induce expression of the glucose transporter gene. , 1988, The Journal of biological chemistry.

[42]  M. Karin,et al.  Phorbol ester-inducible genes contain a common cis element recognized by a TPA-modulated trans-acting factor , 1987, Cell.

[43]  T. Curran,et al.  Induction of c-fos gene and protein by growth factors precedes activation of c-myc , 1984, Nature.

[44]  J. Sambrook,et al.  Molecular Cloning: A Laboratory Manual , 2001 .