Targeted inhibition of p38 MAPK promotes hypertrophic cardiomyopathy through upregulation of calcineurin-NFAT signaling.
暂无分享,去创建一个
Timothy E Hewett | T. Hewett | J. Molkentin | O. Bueno | B. Wilkins | Q. Liang | Stephanie A. Parsons | Qiangrong Liang | Jeffery D Molkentin | R. Klevitsky | Julian C Braz | Orlando F Bueno | Benjamin J Wilkins | Yan-Shan Dai | Stephanie Parsons | Joseph Braunwart | Betty J Glascock | Raisa Klevitsky | Thomas F Kimball | Thomas F. Kimball | B. Glascock | Yan Dai | Julian C. Braz | Joe Braunwart | Qiangrong Liang
[1] J. Molkentin,et al. Defective T cell development and function in calcineurin Aβ-deficient mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[2] J. Molkentin,et al. Defective T cell development and function in calcineurin A beta -deficient mice. , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[3] D. Gardner,et al. Endothelin-dependent and -independent components of strain-activated brain natriuretic peptide gene transcription require extracellular signal regulated kinase and p38 mitogen-activated protein kinase. , 2000, Hypertension.
[4] G L Johnson,et al. Organization and regulation of mitogen-activated protein kinase signaling pathways. , 1999, Current opinion in cell biology.
[5] C. Long,et al. A Role for the Extracellular Signal-regulated Kinase and p38 Mitogen-activated Protein Kinases in Interleukin-1β-stimulated Delayed Signal Tranducer and Activator of Transcription 3 Activation, Atrial Natriuretic Factor Expression, and Cardiac Myocyte Morphology* , 2001, The Journal of Biological Chemistry.
[6] J. Molkentin,et al. Impaired cardiac hypertrophic response in Calcineurin Aβ-deficient mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[7] P. Douglas,et al. Transgenic expression of green fluorescence protein can cause dilated cardiomyopathy , 2000, Nature Medicine.
[8] D. Zechner,et al. A Role for the p38 Mitogen-activated Protein Kinase Pathway in Myocardial Cell Growth, Sarcomeric Organization, and Cardiac-specific Gene Expression , 1997, The Journal of cell biology.
[9] G. Dorn,et al. Cytoplasmic signaling pathways that regulate cardiac hypertrophy. , 2001, Annual review of physiology.
[10] R. Klein,et al. Essential role of p38alpha MAP kinase in placental but not embryonic cardiovascular development. , 2000, Molecular cell.
[11] D. Gardner,et al. Mechanical strain activates BNP gene transcription through a p38/NF-kappaB-dependent mechanism. , 1999, The Journal of clinical investigation.
[12] D. Levy,et al. The epidemiology of heart failure: the Framingham Study. , 1993, Journal of the American College of Cardiology.
[13] A. Clerk,et al. Stimulation of the p38 Mitogen-activated Protein Kinase Pathway in Neonatal Rat Ventricular Myocytes by the G Protein–coupled Receptor Agonists, Endothelin-1 and Phenylephrine: A Role in Cardiac Myocyte Hypertrophy? , 1998, The Journal of cell biology.
[14] A. Lin,et al. Opposing Effects of Jun Kinase and p38 Mitogen-Activated Protein Kinases on Cardiomyocyte Hypertrophy , 1998, Molecular and Cellular Biology.
[15] A. Clerk,et al. "Stress-responsive" mitogen-activated protein kinases (c-Jun N-terminal kinases and p38 mitogen-activated protein kinases) in the myocardium. , 1998, Circulation research.
[16] D. Levy,et al. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. , 1990, The New England journal of medicine.
[17] J. Molkentin,et al. Targeted Disruption of NFATc3, but Not NFATc4, Reveals an Intrinsic Defect in Calcineurin-Mediated Cardiac Hypertrophic Growth , 2002, Molecular and Cellular Biology.
[18] R. Davis,et al. MKK3- and MKK6-regulated gene expression is mediated by the p38 mitogen-activated protein kinase signal transduction pathway , 1996, Molecular and cellular biology.
[19] N. Clipstone,et al. Identification of Amino Acid Residues and Protein Kinases Involved in the Regulation of NFATc Subcellular Localization* , 2000, The Journal of Biological Chemistry.
[20] Juan Miguel Redondo,et al. A Role for the p38 MAP Kinase Pathway in the Nuclear Shuttling of NFATp* , 2000, The Journal of Biological Chemistry.
[21] J C Lee,et al. Novel homologues of CSBP/p38 MAP kinase: activation, substrate specificity and sensitivity to inhibition by pyridinyl imidazoles. , 1997, Biochemical and biophysical research communications.
[22] J. Woodgett,et al. Mammalian Mitogen-activated Protein Kinase Pathways Are Regulated through Formation of Specific Kinase-Activator Complexes* , 1996, The Journal of Biological Chemistry.
[23] Roger J. Davis,et al. Phosphorylation of NFATc4 by p38 Mitogen-Activated Protein Kinases , 2002, Molecular and Cellular Biology.
[24] J. Molkentin,et al. Targeted inhibition of calcineurin prevents agonist-induced cardiomyocyte hypertrophy. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[25] B. Lorell,et al. Left ventricular hypertrophy: pathogenesis, detection, and prognosis. , 2000, Circulation.
[26] A. Lin,et al. Activation of NF-κB is required for hypertrophic growth of primary rat neonatal ventricular cardiomyocytes , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[27] R. Marchase,et al. Capacitative Calcium Entry Contributes to Nuclear Factor of Activated T-cells Nuclear Translocation and Hypertrophy in Cardiomyocytes* , 2002, The Journal of Biological Chemistry.
[28] T. Hewett,et al. Transgenic remodeling of the regulatory myosin light chains in the mammalian heart. , 1997, Circulation research.
[29] Roger J. Davis,et al. Selective Activation of p38 Mitogen-activated Protein (MAP) Kinase Isoforms by the MAP Kinase Kinases MKK3 and MKK6* , 1998, The Journal of Biological Chemistry.
[30] P. A. Zwieten. The influence of antihypertensive drug treatment on the prevention and regression of left ventricular hypertrophy , 2000 .
[31] E. Olson,et al. Activated glycogen synthase-3β suppresses cardiac hypertrophy in vivo , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[32] Yewei Liu,et al. Activity-dependent nuclear translocation and intranuclear distribution of NFATc in adult skeletal muscle fibers , 2001, The Journal of cell biology.
[33] T. Hewett,et al. Ablation of the murine alpha myosin heavy chain gene leads to dosage effects and functional deficits in the heart. , 1996, The Journal of clinical investigation.
[34] C. D. dos Remedios,et al. Cardiac expression and subcellular localization of the p38 mitogen-activated protein kinase member, stress-activated protein kinase-3 (SAPK3). , 2002, Journal of molecular and cellular cardiology.
[35] J. Molkentin,et al. Calcineurin expression, activation, and function in cardiac pressure-overload hypertrophy. , 2000, Circulation.
[36] Jeffrey Robbins,et al. A Calcineurin-Dependent Transcriptional Pathway for Cardiac Hypertrophy , 1998, Cell.
[37] Paul A. Overbeek,et al. TAK1 is activated in the myocardium after pressure overload and is sufficient to provoke heart failure in transgenic mice , 2000, Nature Medicine.
[38] J. Molkentin,et al. Calcineurin Promotes Protein Kinase C and c-Jun NH2-terminal Kinase Activation in the Heart , 2000, The Journal of Biological Chemistry.
[39] J Ross,et al. Cardiac Muscle Cell Hypertrophy and Apoptosis Induced by Distinct Members of the p38 Mitogen-activated Protein Kinase Family* , 1998, The Journal of Biological Chemistry.
[40] G. Sandusky,et al. Decreased p38 MAPK activity in end-stage failing human myocardium: p38 MAPK alpha is the predominant isoform expressed in human heart. , 2001, Journal of molecular and cellular cardiology.
[41] Zhijian J. Chen,et al. TAK1 is a ubiquitin-dependent kinase of MKK and IKK , 2001, Nature.
[42] D. Kass,et al. The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[43] J. Molkentin,et al. The Dual-Specificity Phosphatase MKP-1 Limits the Cardiac Hypertrophic Response In Vitro and In Vivo , 2001, Circulation research.
[44] J. Mudgett,et al. Essential role for p38alpha mitogen-activated protein kinase in placental angiogenesis. , 2000, Proceedings of the National Academy of Sciences of the United States of America.
[45] E. Olson,et al. Activated glycogen synthase-3 beta suppresses cardiac hypertrophy in vivo. , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[46] R. Hajjar,et al. Role of the stress-activated protein kinases in endothelin-induced cardiomyocyte hypertrophy. , 1998, The Journal of clinical investigation.