Metabolic Dysfunction Consistent With Premature Aging Results From Deletion of Pim Kinases
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Mark A Sussman | Å. Gustafsson | M. Völkers | A. Kraft | H. Toko | D. Kelly | Mirko Völkers | Daniel P Kelly | A. de la Torre | Andrew S Kraft | M. Konstandin | Asa B Gustafsson | Haruhiro Toko | Shabana Din | Mathias H Konstandin | Bevan Johnson | Jacqueline Emathinger | Brett Collins | Lucy Ormachea | Kaitlen Samse | Dieter A Kubli | Andrea De La Torre | B. Collins | S. Din | D. Kubli | L. Ormachea | Kaitlen Samse | B. Johnson | Jacqueline M. Emathinger | Dieter A. Kubli
[1] C. Bearzi,et al. Activation of Cardiac Progenitor Cells Reverses the Failing Heart Senescent Phenotype and Prolongs Lifespan , 2008, Circulation research.
[2] S. Houser,et al. Pim-1 kinase antagonizes aspects of myocardial hypertrophy and compensation to pathological pressure overload , 2008, Proceedings of the National Academy of Sciences.
[3] Z. Darżynkiewicz,et al. Telomere shortening is an in vivo marker of myocyte replication and aging. , 2000, The American journal of pathology.
[4] C. Zechner,et al. Transcriptional coactivators PGC-1alpha and PGC-lbeta control overlapping programs required for perinatal maturation of the heart. , 2008, Genes & development.
[5] N. Magnuson,et al. Pim-1 Kinase-Dependent Phosphorylation of p21Cip1/WAF1 Regulates Its Stability and Cellular Localization in H1299 Cells , 2007, Molecular Cancer Research.
[6] Torsten Doenst,et al. PGC-1&bgr; Deficiency Accelerates the Transition to Heart Failure in Pressure Overload Hypertrophy , 2011, Circulation research.
[7] D. Kelly,et al. Transcriptional control of cardiac fuel metabolism and mitochondrial function. , 2011, Cold Spring Harbor symposia on quantitative biology.
[8] Kathryn A. O’Donnell,et al. Myc Stimulates Nuclearly Encoded Mitochondrial Genes and Mitochondrial Biogenesis , 2005, Molecular and Cellular Biology.
[9] P. D. del Nido,et al. Impaired Mitochondrial Biogenesis Precedes Heart Failure in Right Ventricular Hypertrophy in Congenital Heart Disease , 2011, Circulation. Heart failure.
[10] Mark A Sussman,et al. Pim-1 preserves mitochondrial morphology by inhibiting dynamin-related protein 1 translocation , 2013, Proceedings of the National Academy of Sciences.
[11] Joshua M. Finkelstein,et al. Metabolism and disease , 2012, Nature.
[12] Mark A Sussman. Mitochondrial integrity: preservation through Akt/Pim-1 kinase signaling in the cardiomyocyte , 2009, Expert review of cardiovascular therapy.
[13] Mark A Sussman,et al. Fibronectin contributes to pathological cardiac hypertrophy but not physiological growth , 2013, Basic Research in Cardiology.
[14] Xiaoxue Zhang,et al. Parkin Protein Deficiency Exacerbates Cardiac Injury and Reduces Survival following Myocardial Infarction*♦ , 2012, The Journal of Biological Chemistry.
[15] Richard M. Cawthon,et al. Telomere length measurement by a novel monochrome multiplex quantitative PCR method , 2009, Nucleic acids research.
[16] E. Frohlich,et al. The aging hypertensive heart: a brief update , 2008, Nature Clinical Practice Cardiovascular Medicine.
[17] Yau-Huei Wei,et al. Mitochondria and aging. , 2012, Advances in experimental medicine and biology.
[18] A. Kraft,et al. The Pim protein kinases regulate energy metabolism and cell growth , 2010, Proceedings of the National Academy of Sciences.
[19] R. Scarpulla,et al. Transcriptional regulatory circuits controlling mitochondrial biogenesis and function. , 2004, Genes & development.
[20] Mark A Sussman,et al. Fibronectin Is Essential for Reparative Cardiac Progenitor Cell Response After Myocardial Infarction , 2013, Circulation research.
[21] Z. Wang,et al. Pim kinase-dependent inhibition of c-Myc degradation , 2008, Oncogene.
[22] T. Wenz. Regulation of mitochondrial biogenesis and PGC-1α under cellular stress. , 2013, Mitochondrion.
[23] P. Anversa,et al. Myocyte mitotic division in the aging mammalian rat heart. , 1991, Circulation research.
[24] J. Saffitz,et al. Peroxisome proliferator-activated receptor gamma coactivator-1 promotes cardiac mitochondrial biogenesis. , 2000, The Journal of clinical investigation.
[25] M. Matsuda,et al. Aging-induced decrease in the PPAR-α level in hearts is improved by exercise training , 2002 .
[26] Yibin Wang,et al. Myc controls transcriptional regulation of cardiac metabolism and mitochondrial biogenesis in response to pathological stress in mice. , 2010, The Journal of clinical investigation.
[27] Lauren E. Neidig,et al. Increased Mitotic Rate Coincident with Transient Telomere Lengthening Resulting from Pim-1 Overexpression in Cardiac Progenitor Cells , 2012, Stem cells.
[28] L. Chin,et al. Telomere dysfunction induces metabolic and mitochondrial compromise , 2011, Nature.
[29] J. Loscalzo,et al. Cardiomyogenesis in the Aging and Failing Human Heart , 2012, Circulation.
[30] Rick B. Vega,et al. Perturbations in the gene regulatory pathways controlling mitochondrial energy production in the failing heart. , 2013, Biochimica et biophysica acta.
[31] T. Tsuruo,et al. Pim kinases promote cell cycle progression by phosphorylating and down-regulating p27Kip1 at the transcriptional and posttranscriptional levels. , 2008, Cancer research.
[32] Jos Jonkers,et al. Mice Deficient for All PIM Kinases Display Reduced Body Size and Impaired Responses to Hematopoietic Growth Factors , 2004, Molecular and Cellular Biology.
[33] K. Noguchi,et al. Physical and Functional Interactions between Pim-1 Kinase and Cdc25A Phosphatase , 1999, The Journal of Biological Chemistry.
[34] Marcello Rota,et al. Myocyte Turnover in the Aging Human Heart , 2010, Circulation research.
[35] Mark A Sussman,et al. Pim-1 Kinase Protects Mitochondrial Integrity in Cardiomyocytes , 2010, Circulation research.
[36] Jiandie D. Lin,et al. Transcriptional coactivator PGC-1 alpha controls the energy state and contractile function of cardiac muscle. , 2005, Cell metabolism.
[37] D. Chan. Fusion and fission: interlinked processes critical for mitochondrial health. , 2012, Annual review of genetics.
[38] C. Thompson,et al. The survival kinases Akt and Pim as potential pharmacological targets. , 2005, The Journal of clinical investigation.
[39] Barbara Cannon,et al. Ablation of PGC-1β Results in Defective Mitochondrial Activity, Thermogenesis, Hepatic Function, and Cardiac Performance , 2006, PLoS biology.
[40] L. Marchionni,et al. Effects of age and heart failure on human cardiac stem cell function. , 2011, The American journal of pathology.
[41] S. Houser,et al. Pim-1 regulates cardiomyocyte survival downstream of Akt , 2006, Nature Medicine.
[42] G. Semenza,et al. HIF-1 inhibits mitochondrial biogenesis and cellular respiration in VHL-deficient renal cell carcinoma by repression of C-MYC activity. , 2007, Cancer cell.
[43] Mark A Sussman,et al. Pim-1 kinase inhibits pathological injury by promoting cardioprotective signaling. , 2011, Journal of molecular and cellular cardiology.
[44] Jun Ren,et al. AMP‐activated protein kinase deficiency exacerbates aging‐induced myocardial contractile dysfunction , 2010, Aging cell.
[45] D. Kelly,et al. Transcriptional Activation Of Energy Metabolic Switches In The Developing And Hypertrophied Heart , 2002, Clinical and experimental pharmacology & physiology.
[46] D. Kelly,et al. Insulin-Resistant Heart Exhibits a Mitochondrial Biogenic Response Driven by the Peroxisome Proliferator-Activated Receptor-&agr;/PGC-1&agr; Gene Regulatory Pathway , 2007, Circulation.
[47] S. Sihag,et al. PGC-1alpha and ERRalpha target gene downregulation is a signature of the failing human heart. , 2009, Journal of molecular and cellular cardiology.
[48] J. Callés-Escandon,et al. Prolonged AMPK Activation Increases the Expression of Fatty Acid Transporters in Cardiac Myocytes and Perfused Hearts , 2006, Molecular and Cellular Biochemistry.
[49] Manuel Serrano,et al. The Hallmarks of Aging , 2013, Cell.
[50] Mark A Sussman,et al. Rejuvenation of Human Cardiac Progenitor Cells With Pim-1 Kinase , 2013, Circulation research.
[51] M. Matsuda,et al. Aging-induced decrease in the PPAR-alpha level in hearts is improved by exercise training. , 2002, American journal of physiology. Heart and circulatory physiology.