Advances in revealing the molecular targets downstream of oxidative stress-induced proapoptotic kinase signaling in diabetic embryopathy.
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[1] S. Fang,et al. Ask1 Gene Deletion Blocks Maternal Diabetes–Induced Endoplasmic Reticulum Stress in the Developing Embryo by Disrupting the Unfolded Protein Response Signalosome , 2014, Diabetes.
[2] D. Wishart,et al. Metabolomic prediction of fetal congenital heart defect in the first trimester. , 2014, American journal of obstetrics and gynecology.
[3] D. Graves,et al. FOXO Transcription Factors: Their Clinical Significance and Regulation , 2014, BioMed research international.
[4] F. Wang,et al. Superoxide dismutase 1 overexpression in mice abolishes maternal diabetes-induced endoplasmic reticulum stress in diabetic embryopathy. , 2013, American journal of obstetrics and gynecology.
[5] G. MacLennan,et al. Deregulation of FoxO3a accelerates prostate cancer progression in TRAMP mice , 2013, The Prostate.
[6] F. Wang,et al. Trehalose prevents neural tube defects by correcting maternal diabetes-suppressed autophagy and neurogenesis. , 2013, American journal of physiology. Endocrinology and metabolism.
[7] M. Werler,et al. The impact of folic acid intake on the association among diabetes mellitus, obesity, and spina bifida. , 2013, American journal of obstetrics and gynecology.
[8] H. R. Zielke,et al. Maternal Hyperglycemia Activates an ASK1–FoxO3a–Caspase 8 Pathway That Leads to Embryonic Neural Tube Defects , 2013, Science Signaling.
[9] D. Wishart,et al. Metabolomic analysis for first-trimester trisomy 18 detection. , 2013, American journal of obstetrics and gynecology.
[10] D. Wishart,et al. Metabolomic analysis for first-trimester Down syndrome prediction. , 2013, American journal of obstetrics and gynecology.
[11] Jan Koster,et al. FOXO3a is a major target of inactivation by PI3K/AKT signaling in aggressive neuroblastoma. , 2013, Cancer research.
[12] Peixin Yang,et al. c-Jun NH2-Terminal Kinase 1/2 and Endoplasmic Reticulum Stress as Interdependent and Reciprocal Causation in Diabetic Embryopathy , 2013, Diabetes.
[13] E. A. Reece,et al. Oxidative Stress–Induced JNK1/2 Activation Triggers Proapoptotic Signaling and Apoptosis That Leads to Diabetic Embryopathy , 2012, Diabetes.
[14] Xue Zhou,et al. A novel bridge between oxidative stress and immunity: the interaction between hydrogen peroxide and human leukocyte antigen G in placental trophoblasts during preeclampsia. , 2012, American journal of obstetrics and gynecology.
[15] E. A. Reece,et al. SOD1 suppresses maternal hyperglycemia-increased iNOS expression and consequent nitrosative stress in diabetic embryopathy. , 2012, American journal of obstetrics and gynecology.
[16] G. Oakley. Failing to prevent birth defects caused by maternal diabetes mellitus. , 2012, American journal of obstetrics and gynecology.
[17] Lorenzo D Botto,et al. Lack of periconceptional vitamins or supplements that contain folic acid and diabetes mellitus-associated birth defects. , 2012, American journal of obstetrics and gynecology.
[18] E. A. Reece,et al. SOD1 overexpression in vivo blocks hyperglycemia-induced specific PKC isoforms: substrate activation and consequent lipid peroxidation in diabetic embryopathy. , 2011, American journal of obstetrics and gynecology.
[19] E. A. Reece,et al. Role of HIF-1α in maternal hyperglycemia-induced embryonic vasculopathy. , 2011, American journal of obstetrics and gynecology.
[20] Peixin Yang,et al. Hyperglycemia induces inducible nitric oxide synthase gene expression and consequent nitrosative stress via c-Jun N-terminal kinase activation. , 2010, American journal of obstetrics and gynecology.
[21] Peixin Yang,et al. Epigallocatechin-3-gallate ameliorates hyperglycemia-induced embryonic vasculopathy and malformation by inhibition of Foxo3a activation. , 2010, American journal of obstetrics and gynecology.
[22] Katsuhiko Yano,et al. FOXO3A genotype is strongly associated with human longevity , 2008, Proceedings of the National Academy of Sciences.
[23] E. A. Reece,et al. Demonstration of the Essential Role of Protein Kinase C Isoforms in Hyperglycemia-Induced Embryonic Malformations , 2008, Reproductive Sciences.
[24] E. A. Reece,et al. Involvement of c-Jun N-terminal kinases activation in diabetic embryopathy. , 2007, Biochemical and biophysical research communications.
[25] E. Lam,et al. FOXO transcription factors: key regulators of cell fate. , 2006, Biochemical Society transactions.
[26] E. Lam,et al. Differential expression of FOXO1 and FOXO3a confers resistance to oxidative cell death upon endometrial decidualization. , 2006, Molecular endocrinology.
[27] Toshio Ogihara,et al. Apoptosis Signal-Regulating Kinase 1 Mediates Cellular Senescence Induced by High Glucose in Endothelial Cells , 2006, Diabetes.
[28] Zheng‐gang Liu,et al. JNK signaling pathway is a key modulator in cell death mediated by reactive oxygen and nitrogen species. , 2006, Free radical biology & medicine.
[29] E. Reece,et al. Dietary vitamin and lipid therapy rescues aberrant signaling and apoptosis and prevents hyperglycemia-induced diabetic embryopathy in rats. , 2006, American journal of obstetrics and gynecology.
[30] E. Greer,et al. FOXO transcription factors at the interface between longevity and tumor suppression , 2005, Oncogene.
[31] A. Jawerbaum,et al. Peroxynitrites and impaired modulation of nitric oxide concentrations in embryos from diabetic rats during early organogenesis. , 2005, Reproduction.
[32] W. Aird,et al. Forkhead Transcription Factors Inhibit Vascular Smooth Muscle Cell Proliferation and Neointimal Hyperplasia*[boxs] , 2005, Journal of Biological Chemistry.
[33] M. Hori,et al. Apoptosis signal-regulating kinase 1 is involved not only in apoptosis but also in non-apoptotic cardiomyocyte death. , 2005, Biochemical and biophysical research communications.
[34] Fuminori Tsuruta,et al. JNK antagonizes Akt-mediated survival signals by phosphorylating 14-3-3 , 2005, The Journal of cell biology.
[35] M. Loeken,et al. Hypoxic stress in diabetic pregnancy contributes to impaired embryo gene expression and defective development by inducing oxidative stress. , 2005, American journal of physiology. Endocrinology and metabolism.
[36] H. Jasper,et al. JNK Extends Life Span and Limits Growth by Antagonizing Cellular and Organism-Wide Responses to Insulin Signaling , 2005, Cell.
[37] A. Jawerbaum,et al. The role of alterations in arachidonic acid metabolism and nitric oxide homeostasis in rat models of diabetes during early pregnancy. , 2005, Current pharmaceutical design.
[38] E. Reece,et al. Aberrant patterns of cellular communication in diabetes-induced embryopathy in rats: II, apoptotic pathways. , 2005, American journal of obstetrics and gynecology.
[39] K. Eguchi,et al. Apoptosis and its pathway in early post-implantation embryos of diabetic rats. , 2005, Diabetes research and clinical practice.
[40] K. Maiese,et al. Oxidative stress in the brain: Novel cellular targets that govern survival during neurodegenerative disease , 2005, Progress in Neurobiology.
[41] J. Bos,et al. FOXO transcription factor activation by oxidative stress mediated by the small GTPase Ral and JNK , 2004, The EMBO journal.
[42] L. Glimcher,et al. Endoplasmic Reticulum Stress Links Obesity, Insulin Action, and Type 2 Diabetes , 2004, Science.
[43] M. Loeken,et al. Activation of the hexosamine pathway causes oxidative stress and abnormal embryo gene expression: involvement in diabetic teratogenesis. , 2004, Birth defects research. Part A, Clinical and molecular teratology.
[44] D. Jhon,et al. Involvement of ROS and JNK1 in selenite-induced a poptosisin Chang liver cells , 2004, Experimental & Molecular Medicine.
[45] Teiji Wada,et al. Mitogen-activated protein kinases in apoptosis regulation , 2004, Oncogene.
[46] Steven P. Gygi,et al. Stress-Dependent Regulation of FOXO Transcription Factors by the SIRT1 Deacetylase , 2004, Science.
[47] Jau-Song Yu,et al. Curcumin inhibits UV irradiation‐induced oxidative stress and apoptotic biochemical changes in human epidermoid carcinoma A431 cells , 2003, Journal of cellular biochemistry.
[48] P. Coffer,et al. FOXO transcription factors directly activate bim gene expression and promote apoptosis in sympathetic neurons , 2003, The Journal of cell biology.
[49] M. Weil,et al. Nitric oxide is involved in establishing the balance between cell cycle progression and cell death in the developing neural tube. , 2003, Experimental cell research.
[50] Y. Arita,et al. Inhibition of c-Jun N-terminal kinase pathway improves cell viability in response to oxidant injury. , 2003, American journal of respiratory cell and molecular biology.
[51] C. Szabó. Multiple pathways of peroxynitrite cytotoxicity. , 2003, Toxicology letters.
[52] M. Loeken,et al. Oxidant regulation of gene expression and neural tube development: Insights gained from diabetic pregnancy on molecular causes of neural tube defects , 2003, Diabetologia.
[53] A. Kessler,et al. High glucose promotes mesangial cell apoptosis by oxidant-dependent mechanism. , 2003, American journal of physiology. Renal physiology.
[54] M. Haneda,et al. Progression of diabetic nephropathy. , 2003, American journal of kidney diseases : the official journal of the National Kidney Foundation.
[55] Quan-guang Zhang,et al. Biphasic activation of apoptosis signal-regulating kinase 1-stress-activated protein kinase 1-c-Jun N-terminal protein kinase pathway is selectively mediated by Ca2+-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors involving oxidative stress following brain ischemia in rat hi , 2003, Neuroscience Letters.
[56] A. Lin. Activation of the JNK signaling pathway: Breaking the brake on apoptosis , 2003, BioEssays : news and reviews in molecular, cellular and developmental biology.
[57] Rakesh Nagarajan,et al. FOXO Proteins Regulate Tumor Necrosis Factor-related Apoptosis Inducing Ligand Expression , 2002, The Journal of Biological Chemistry.
[58] Yusuke Nakamura,et al. Involvement of FKHR-Dependent TRADD Expression in Chemotherapeutic Drug-Induced Apoptosis , 2002, Molecular and Cellular Biology.
[59] A. Lin,et al. The true face of JNK activation in apoptosis , 2002, Aging cell.
[60] G. Soltész,et al. Polyunsaturated fatty acids in plasma and erythrocyte membrane lipids of diabetic children. , 2002, Prostaglandins, leukotrienes, and essential fatty acids.
[61] Geert J. P. L. Kops,et al. Forkhead transcription factor FOXO3a protects quiescent cells from oxidative stress , 2002, Nature.
[62] M. Loeken,et al. Diacylglycerol production and protein kinase C activity are increased in a mouse model of diabetic embryopathy. , 2002, Diabetes.
[63] Sang-Oh Yoon,et al. Sustained Production of H2O2Activates Pro-matrix Metalloproteinase-2 through Receptor Tyrosine Kinases/Phosphatidylinositol 3-Kinase/NF-κB Pathway* , 2002, The Journal of Biological Chemistry.
[64] T. Peng,et al. Development of Heart Failure and Congenital Septal Defects in Mice Lacking Endothelial Nitric Oxide Synthase , 2002, Circulation.
[65] Y. Fujita,et al. Ebselen attenuates oxidative stress‐induced apoptosis via the inhibition of the c‐Jun N‐terminal kinase and activator protein‐1 signalling pathway in PC12 cells , 2002, British journal of pharmacology.
[66] M. Ueno,et al. Redox control of cell death. , 2002, Antioxidants & redox signaling.
[67] D. Feig,et al. Type 2 diabetes in pregnancy: a growing concern , 2002, The Lancet.
[68] Xianglin Shi,et al. Differential role of hydrogen peroxide in UV-induced signal transduction , 2002, Molecular and Cellular Biochemistry.
[69] S. R. Datta,et al. DNA Repair Pathway Stimulated by the Forkhead Transcription Factor FOXO3a Through the Gadd45 Protein , 2002, Science.
[70] H. Ichijo,et al. Activation of apoptosis signal‐regulating kinase 1 by the stress‐induced activating phosphorylation of pre‐formed oligomer , 2002, Journal of cellular physiology.
[71] A. Bode,et al. Deficiency of c-Jun-NH(2)-terminal kinase-1 in mice enhances skin tumor development by 12-O-tetradecanoylphorbol-13-acetate. , 2002, Cancer research.
[72] L. Kirshenbaum,et al. Suppression of Akt Signaling Induces Fas Ligand Expression: Involvement of Caspase and Jun Kinase Activation in Akt-Mediated Fas Ligand Regulation , 2002, Molecular and Cellular Biology.
[73] E. Reece,et al. Aberrant patterns of cellular communication in diabetes-induced embryopathy I. Membrane signalling , 2002, The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians.
[74] A. Ornoy,et al. Vitamins C and E improve rat embryonic antioxidant defense mechanism in diabetic culture medium. , 2001, Teratology.
[75] F. McCormick,et al. Transcriptional activation of TRADD mediates p53-independent radiation-induced apoptosis of glioma cells , 2001, Oncogene.
[76] M. Jung,et al. Role of ATM in Oxidative Stress-mediated c-Jun Phosphorylation in Response to Ionizing Radiation and CdCl2 * , 2001, The Journal of Biological Chemistry.
[77] J. Avruch,et al. Mammalian mitogen-activated protein kinase signal transduction pathways activated by stress and inflammation. , 2001, Physiological reviews.
[78] T Takahashi,et al. ASK1 is required for sustained activations of JNK/p38 MAP kinases and apoptosis , 2001, EMBO reports.
[79] K. Moley. Hyperglycemia and apoptosis: mechanisms for congenital malformations and pregnancy loss in diabetic women , 2001, Trends in Endocrinology & Metabolism.
[80] A. Jawerbaum,et al. Modulation of PGE2 generation in the diabetic embryo: effect of nitric oxide and superoxide dismutase. , 2001, Prostaglandins, leukotrienes, and essential fatty acids.
[81] James E. Ferrell,et al. c-Jun N-terminal Kinase Activation in Xenopus laevis Eggs and Embryos , 2001, The Journal of Biological Chemistry.
[82] R. Davis,et al. Signal Transduction by the JNK Group of MAP Kinases , 2000, Cell.
[83] P A Insel,et al. Protein kinase C isozymes and the regulation of diverse cell responses. , 2000, American journal of physiology. Lung cellular and molecular physiology.
[84] T. Finkel. Redox‐dependent signal transduction , 2000, FEBS letters.
[85] R. Flavell,et al. JNK is required for effector T-cell function but not for T-cell activation , 2000, Nature.
[86] F. Urano,et al. Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1. , 2000, Science.
[87] U. Eriksson,et al. Pathogenesis of Diabetes-Induced Congenital Malformations , 2000, Upsala journal of medical sciences.
[88] M. Loeken,et al. Evidence that elevated glucose causes altered gene expression, apoptosis, and neural tube defects in a mouse model of diabetic pregnancy. , 1999, Diabetes.
[89] R. Kohen,et al. Role of reactive oxygen species (ROS) in the diabetes-induced anomalies in rat embryos in vitro: reduction in antioxidant enzymes and low-molecular-weight antioxidants (LMWA) may be the causative factor for increased anomalies. , 1999, Teratology.
[90] S. Nagataki,et al. Significance of glutathione-dependent antioxidant system in diabetes-induced embryonic malformations. , 1999, Diabetes.
[91] P. Rakic,et al. The Jnk1 and Jnk2 Protein Kinases Are Required for Regional Specific Apoptosis during Early Brain Development , 1999, Neuron.
[92] N. Welsh,et al. Developmental damage, increased lipid peroxidation, diminished cyclooxygenase-2 gene expression, and lowered prostaglandin E2 levels in rat embryos exposed to a diabetic environment. , 1999, Diabetes.
[93] M. Greenberg,et al. Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor , 1999, Cell.
[94] Paul J Thornalley,et al. Teratogenicity of 3-deoxyglucosone and diabetic embryopathy. , 1998, Diabetes.
[95] K. Miyazono,et al. ASK1 is essential for JNK/SAPK activation by TRAF2. , 1998, Molecular cell.
[96] N. Welsh,et al. Apoptosis in embryos of diabetic rats. , 1998, Pharmacology & toxicology.
[97] Kohei Miyazono,et al. Mammalian thioredoxin is a direct inhibitor of apoptosis signal‐regulating kinase (ASK) 1 , 1998, The EMBO journal.
[98] G. Wolf,et al. Distribution of the endothelial constitutive nitric oxide synthase in the developing rat brain: an immunohistochemical study , 1998, Brain Research.
[99] W. Cavenee,et al. Cloning and characterization of three human forkhead genes that comprise an FKHR-like gene subfamily. , 1998, Genomics.
[100] U. Eriksson,et al. Decreased catalase activity in malformation-prone embryos of diabetic rats. , 1997, Teratology.
[101] M. Loeken,et al. Neural Tube Defects in Embryos of Diabetic Mice: Role of the Pax-3 Gene and Apoptosis , 1997, Diabetes.
[102] E. Reece,et al. Prevention of diabetic embryopathy in offspring of diabetic rats with use of a cocktail of deficient substrates and an antioxidant. , 1997, American journal of obstetrics and gynecology.
[103] E. Reece,et al. Dietary polyunsaturated fatty acid prevents malformations in offspring of diabetic rats. , 1996, American journal of obstetrics and gynecology.
[104] A. Chinnaiyan,et al. FADD/MORT1 Is a Common Mediator of CD95 (Fas/APO-1) and Tumor Necrosis Factor Receptor-induced Apoptosis (*) , 1996, The Journal of Biological Chemistry.
[105] Hong-Bing Shu,et al. TRADD–TRAF2 and TRADD–FADD Interactions Define Two Distinct TNF Receptor 1 Signal Transduction Pathways , 1996, Cell.
[106] E. Reece,et al. Prevention of diabetes-associated embryopathy by overexpression of the free radical scavenger copper zinc superoxide dismutase in transgenic mouse embryos. , 1995, American journal of obstetrics and gynecology.
[107] S. Nagataki,et al. Significance of Glutathione Depletion and Oxidative Stress in Early Embryogenesis in Glucose-Induced Rat Embryo Culture , 1995, Diabetes.
[108] D. Betteridge,et al. Plasma 8‐epi‐PGF2α levels are elevated in individuals with non‐insulin dependent diabetes mellitus , 1995, FEBS letters.
[109] D. Goeddel,et al. The TNF receptor 1-associated protein TRADD signals cell death and NF-κB activation , 1995, Cell.
[110] J. Camonis,et al. A Novel Protein That Interacts with the Death Domain of Fas/APO1 Contains a Sequence Motif Related to the Death Domain (*) , 1995, The Journal of Biological Chemistry.
[111] M. Juchau,et al. Dysmorphogenic effects of nitric oxide (NO) and NO-synthase inhibition: studies with intra-amniotic injections of sodium nitroprusside and NG-monomethyl-L-arginine. , 1994, Teratology.
[112] S. Moncada,et al. Nitric oxide: physiology, pathophysiology, and pharmacology. , 1991, Pharmacological reviews.
[113] J. Morrow,et al. A series of prostaglandin F2-like compounds are produced in vivo in humans by a non-cyclooxygenase, free radical-catalyzed mechanism. , 1990, Proceedings of the National Academy of Sciences of the United States of America.
[114] E. A. Reece,et al. 45: Role of HIF-1alpha in maternal hyperglycemia-induced embryonic vasculopathy , 2011 .
[115] F. Urano,et al. Amyloid β induces neuronal cell death through ROS-mediated ASK1 activation , 2005, Cell Death and Differentiation.
[116] S. Kyosseva. Mitogen-activated protein kinase signaling. , 2004, International review of neurobiology.
[117] H. Forman,et al. Redox signaling and the MAP kinase pathways , 2003, BioFactors.
[118] M. Torres. Mitogen-activated protein kinase pathways in redox signaling. , 2003, Frontiers in bioscience : a journal and virtual library.
[119] C. McMaster,et al. Phospholipid synthesis, diacylglycerol compartmentation, and apoptosis. , 2002, Biological research.
[120] A. Srivastava. High glucose-induced activation of protein kinase signaling pathways in vascular smooth muscle cells: a potential role in the pathogenesis of vascular dysfunction in diabetes (review). , 2002, International journal of molecular medicine.
[121] C. Widmann,et al. Mitogen-activated protein kinase: conservation of a three-kinase module from yeast to human. , 1999, Physiological reviews.
[122] A. Jawerbaum,et al. Increased prostaglandin E generation and enhanced nitric oxide synthase activity in the non-insulin-dependent diabetic embryo during organogenesis. , 1998, Reproduction, fertility, and development.
[123] D. Häussinger,et al. Menadione induces both necrosis and apoptosis in rat pancreatic acinar AR4-2J cells. , 1997, Free radical biology & medicine.
[124] S. Gangolli,et al. Malformations induced in cultured rat embryos by enzymically generated active oxygen species. , 1986, Teratogenesis, carcinogenesis, and mutagenesis.