Research Topics
Genomes and Genes
| John M KyriakisSummaryAffiliation: Harvard University Country: USA Publications
| Collaborators
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Detail Information
Publications
Activation of the AP-1 transcription factor by inflammatory cytokines of the TNF familyJ M Kyriakis
Massachusetts General Hospital and Department of Medicine, Harvard Medical School, Charlestown, USA
Gene Expr 7:217-31. 1999....- Mammalian mitogen-activated protein kinase signal transduction pathways activated by stress and inflammationJ M Kyriakis
Diabetes Research Laboratory, Medical Services, Massachusetts General Hospital, Boston, Massachusetts 02129, USA
Physiol Rev 81:807-69. 2001..The nuclear factor-kappa B pathway, a second stress signaling paradigm, has been the subject of several excellent recent reviews (258, 260)... - MAP kinases and the regulation of nuclear receptorsJ M Kyriakis
Diabetes Research Laboratory, Massachusetts General Hospital East, Charlestown, MA, USA
Sci STKE 2000:pe1. 2000..Kyriakis discusses how cross talk between MAPK signaling and nuclear receptor signaling occurs and the effect this cross talk has on nuclear receptor function... 
Helix-loop-helix protein p8, a transcriptional regulator required for cardiomyocyte hypertrophy and cardiac fibroblast matrix metalloprotease inductionSandro Goruppi
Molecular Cardiology Research Institute, Tufts New England Medical Center, 750 Washington Street, Box 8486, Boston, MA 02111, USA
Mol Cell Biol 27:993-1006. 2007..Our results identify an unexpectedly broad involvement for p8 in key cellular events linked to cardiomyocyte hypertrophy and cardiac fibroblast MMP production, both of which occur in heart failure...- Deficiency of the transcriptional regulator p8 results in increased autophagy and apoptosis, and causes impaired heart functionDerek K Kong
Molecular Cardiology Research Institute, Tufts Medical Center and Department of Medicine, Tufts University School of Medicine, Boston, MA 02111, USA
Mol Biol Cell 21:1335-49. 2010..Our studies provide evidence of a p8-dependent mechanism regulating autophagy by acting as FoxO3 corepressor, which may be relevant for diseases associated with dysregulated autophagy, as cardiovascular pathologies and cancer... - Gene 33/RALT is induced by hypoxia in cardiomyocytes, where it promotes cell death by suppressing phosphatidylinositol 3-kinase and extracellular signal-regulated kinase survival signalingDazhong Xu
Molecular Cardiology Research Institute, Tufts-New England Medical Center, 750 Washington Street, Box 8486, Boston, MA 02111, USA
Mol Cell Biol 26:5043-54. 2006..Gene 33 levels are also strikingly increased in myocardial ischemic injury and infarction. Our results identify a new role for Gene 33 as a component in the molecular pathophysiology of ischemic injury... - Mammalian Ste20-like kinase (Mst2) indirectly supports Raf-1/ERK pathway activity via maintenance of protein phosphatase-2A catalytic subunit levels and consequent suppression of inhibitory Raf-1 phosphorylationGeoffrey K Kilili
Molecular Cardiology Research Institute, Tufts Medical Center, Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, Massachusetts 02111, USA
J Biol Chem 285:15076-87. 2010..Our studies reveal a more complex role for Mst2 than previously thought. The Mst2 --> LATS1/2 pathway, by maintaining PP2A-C levels, may, in some situations, positively affect mitogenic signaling... - The pro-hypertrophic basic helix-loop-helix protein p8 is degraded by the ubiquitin/proteasome system in a protein kinase B/Akt- and glycogen synthase kinase-3-dependent manner, whereas endothelin induction of p8 mRNA and renal mesangial cell hypertrophy Sandro Goruppi
Molecular Cardiology Research Institute, Tufts New England Medical Center and the Department of Medicine, Tufts University School of Medicine, 750 Washington Street, Boston, MA 02111, USA
J Biol Chem 279:20950-8. 2004..Thus, p8 levels in the cell are likely maintained by a balance between signal-dependent transcriptional induction and proteolysis... - Mixed-lineage kinase 3 regulates B-Raf through maintenance of the B-Raf/Raf-1 complex and inhibition by the NF2 tumor suppressor proteinDeborah N Chadee
Molecular Cardiology Research Institute, Tufts New England Medical Center, Tufts University School of Medicine, 750 Washington Street, Boston, MA 02111, USA
Proc Natl Acad Sci U S A 103:4463-8. 2006..Thus, MLK3 is part of a multiprotein complex and is required for ERK activation. The levels of this complex may be negatively regulated by merlin... - GCK is essential to systemic inflammation and pattern recognition receptor signaling to JNK and p38Jian Zhong
The Molecular Cardiology Research Institute, and Department of Medicine, Tufts University School of Medicine, Boston, MA 02111, USA
Proc Natl Acad Sci U S A 106:4372-7. 2009..Extracellular signal-regulated kinase (ERK) and nuclear factor-kappaB (NF-kappaB) activation are largely unaffected. Thus, GCK is an essential PAMP effector coupling JNK and p38, but not ERK or NF-kappaB to systemic inflammation... - Decreased metalloprotease 9 induction, cardiac fibrosis, and higher autophagy after pressure overload in mice lacking the transcriptional regulator p8Serban P Georgescu
Molecular Cardiology Research Institute, Tufts Medical Center, Department of Medicine, Tufts University School of Medicine, Boston, MA 02111, USA
Am J Physiol Cell Physiol 301:C1046-56. 2011..These findings suggest a role for p8 in regulating in vivo key signaling pathways involved in the pathogenesis of heart failure... - Germinal center kinase is required for optimal Jun N-terminal kinase activation by Toll-like receptor agonists and is regulated by the ubiquitin proteasome system and agonist-induced, TRAF6-dependent stabilizationJian Zhong
Molecular Cardiology Research Institute Tufts New England Medical Center, 750 Washington St, Box 8486, Boston, MA 02111, USA
Mol Cell Biol 24:9165-75. 2004..Our results identify a physiologic function and unexpected mode of regulation for GCK... - Activation of SAPKs/JNKs and p38s in vitroJohn M Kyriakis
Molecular Cardiology Research Institute, Tufts-New England Medical Center, Boston, MA, USA
Methods Mol Biol 250:61-88. 2004 - MLK3 is required for mitogen activation of B-Raf, ERK and cell proliferationDeborah N Chadee
The Molecular Cardiology Research Institute, Department of Medicine, Tufts New England Medical Center and the Department of Medicine, Tufts University School of Medicine, 750 Washington Street, Box 8486, Boston, MA 02111, USA
Nat Cell Biol 6:770-6. 2004..The proliferation of tumour cells containing activating B-raf or raf-1 mutations was unaffected by silencing mlk3. Our results define an unexpected role for MLK3 in mitogen regulation of B-Raf, ERK and cell proliferation... - Gene 33 is an endogenous inhibitor of epidermal growth factor (EGF) receptor signaling and mediates dexamethasone-induced suppression of EGF functionDazhong Xu
Molecular Cardiology Research Institute, Tufts New England Medical Center and Department of Medicine, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
J Biol Chem 280:2924-33. 2005..Our results also indicate a role for Gene 33 in the suppression, by Dex, of EGF signaling pathways. We propose that Gene 33 may function in the cross-talk between EGF signaling and other mitogenic and/or stress signaling pathways... - Inhibitors of protein kinase signaling pathways: emerging therapies for cardiovascular diseaseThomas Force
Molecular Cardiology Research Institute, Tufts New England Medical Center and Tufts University School of Medicine, Boston, Mass 02111, USA
Circulation 109:1196-205. 2004..We will specifically focus on disease states for which drug development has proceeded to the point of clinical or advanced preclinical studies... - Phosphatidylinositol 3'-kinase-dependent activation of renal mesangial cell Ki-Ras and ERK by advanced glycation end productsDazhong Xu
Molecular Cardiology Research Institute, New England Medical Center and the Department of Medicine, Tufts University School of Medicine, Boston, Massachusetts 02111, USA
J Biol Chem 278:39349-55. 2003..Thus, AGEs signal to Ki-Ras and ERK through reactive oxygen species-dependent activation of PI3K... - The integration of signaling by multiprotein complexes containing Raf kinasesJohn M Kyriakis
The Molecular Cardiology Research Institute, Tufts New England Medical Center and the Department of Medicine, Tufts University School of Medicine, 750 Washington Street, Boston, MA 02111, USA
Biochim Biophys Acta 1773:1238-47. 2007..This review will focus on two signal integrating multiprotein complexes that involve Raf family kinases: the MLK3-B-Raf-Raf-1 complex and the Raf-1-Mst-2 complex... 
Mammalian MAPK signal transduction pathways activated by stress and inflammation: a 10-year updateJohn M Kyriakis
Molecular Cardiology Research Institute, Tufts Medical Center, 800 Washington St, Box 8486, Boston, MA 02111, USA
Physiol Rev 92:689-737. 2012..Herein we first summarize the molecular components of the mammalian stress-regulated MAPK pathways and their regulation as described thus far. We then review some of the in vivo functions of these pathways...- Phosphorylation of threonine 276 in Smad4 is involved in transforming growth factor-beta-induced nuclear accumulationBernard A J Roelen
Program in Membrane Biology and Renal Unit, Massachusetts General Hospital, and Department of Medicine, Harvard Medical School, Charlestown, MA 02129, USA
Am J Physiol Cell Physiol 285:C823-30. 2003..Our results suggest that MAP kinase can phosphorylate Thr276 of Smad4 and that phosphorylation can lead to enhanced TGF-beta-induced nuclear accumulation and, as a consequence, enhanced transcriptional activity of Smad4... - A novel role for mixed lineage kinase 3 (MLK3) in B-Raf activation and cell proliferationDeborah N Chadee
The Molecular Cardiology Research Institute, Tufts New England Medical Center, Boston, Massachusetts 02111, USA
Cell Cycle 3:1227-9. 2004..Accordingly, targeting MLK3 could be beneficial to the treatment of tumors with activated receptor tyrosine kinase or ras mutations, and to the treatment of NF1 or NF2 tumors... - Signaling pathways and late-onset gene induction associated with renal mesangial cell hypertrophySandro Goruppi
Diabetes Research Laboratory, Department of Medicine, Massachusetts General Hospital, Charlestown, MA 02129, USA
EMBO J 21:5427-36. 2002..Small interfering RNA (siRNA)-mediated RNA interference indicates that p8 is required for endothelin-induced hypertrophy. Thus, p8 is a novel marker for diabetic renal hypertrophy...