Neuroprotection by PGE2 receptor EP1 inhibition involves the PTEN/AKT pathway

[1]  Lewis C. Cantley,et al.  AKT/PKB Signaling: Navigating Downstream , 2007, Cell.

[2]  J. Gidday,et al.  Oxygen Sensing : Life and Death of a Cell Hypoxic preconditioning protects human brain endothelium from ischemic apoptosis by Akt-dependent survivin activation , 2007 .

[3]  C. Iadecola,et al.  Cyclooxygenase-2 Does Not Contribute to Postischemic Production of Reactive Oxygen Species , 2007, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[4]  P. Chan,et al.  Bad as a Converging Signaling Molecule between Survival PI3-K/Akt and Death JNK in Neurons after Transient Focal Cerebral Ischemia in Rats , 2007, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[5]  Klaus Heese,et al.  The Bad Guy Cooperates with Good Cop p53: Bad Is Transcriptionally Up-Regulated by p53 and Forms a Bad/p53 Complex at the Mitochondria To Induce Apoptosis , 2006, Molecular and Cellular Biology.

[6]  Gang Wang,et al.  Prostaglandin E2 EP1 receptors: downstream effectors of COX-2 neurotoxicity , 2006, Nature Medicine.

[7]  R. Sapolsky,et al.  Akt Contributes to Neuroprotection by Hypothermia against Cerebral Ischemia in Rats , 2005, The Journal of Neuroscience.

[8]  Seung-Rock Lee,et al.  The major target of the endogenously generated reactive oxygen species in response to insulin stimulation is phosphatase and tensin homolog and not phosphoinositide-3 kinase (PI-3 kinase) in the PI-3 kinase/Akt pathway. , 2004, Molecular biology of the cell.

[9]  M. Ross,et al.  Prostanoids, not reactive oxygen species, mediate COX‐2–dependent neurotoxicity , 2004, Annals of neurology.

[10]  T. James,et al.  PI3K inhibition in neonatal rat brain slices during and after hypoxia reduces phospho-Akt and increases cytosolic cytochrome c and apoptosis. , 2004, Brain research. Molecular brain research.

[11]  E. Nagata,et al.  Akt as a mediator of cell death , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[12]  M. J. Fry,et al.  The phosphoinositide (PI) 3-kinase family , 2003, Journal of Cell Science.

[13]  H. Okano,et al.  Implication of cyclooxygenase‐2 on enhanced proliferation of neural progenitor cells in the adult mouse hippocampus after ischemia , 2003, Journal of neuroscience research.

[14]  R. Simon,et al.  Activation of Bcl-2-Associated Death Protein and Counter-Response of Akt within Cell Populations during Seizure-Induced Neuronal Death , 2002, The Journal of Neuroscience.

[15]  M. Ross,et al.  Reduced susceptibility to ischemic brain injury and N-methyl-D-aspartate-mediated neurotoxicity in cyclooxygenase-2-deficient mice. , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[16]  S R Datta,et al.  14-3-3 proteins and survival kinases cooperate to inactivate BAD by BH3 domain phosphorylation. , 2000, Molecular cell.

[17]  Tomohiko Maehama,et al.  The Tumor Suppressor, PTEN/MMAC1, Dephosphorylates the Lipid Second Messenger, Phosphatidylinositol 3,4,5-Trisphosphate* , 1998, The Journal of Biological Chemistry.

[18]  S. R. Datta,et al.  Akt Phosphorylation of BAD Couples Survival Signals to the Cell-Intrinsic Death Machinery , 1997, Cell.

[19]  T. Hökfelt,et al.  Spreading depression and focal brain ischemia induce cyclooxygenase-2 in cortical neurons through N-methyl-D-aspartic acid-receptors and phospholipase A2. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[20]  M. Ross,et al.  Cyclo-Oxygenase-2 Gene Expression in Neurons Contributes to Ischemic Brain Damage , 1997, The Journal of Neuroscience.

[21]  Elizabeth Yang,et al.  Serine Phosphorylation of Death Agonist BAD in Response to Survival Factor Results in Binding to 14-3-3 Not BCL-XL , 1996, Cell.

[22]  M. Harrison,et al.  Cyclo-oxygenase-2 Messenger RNA Induction in Focal Cerebral Ischemia , 1996, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[23]  S. Korsmeyer,et al.  Bad, a heterodimeric partner for Bcl-xL and Bcl-2, displaces bax and promotes cell death , 1995, Cell.

[24]  Arleen Richardson,et al.  Protocols for Neural Cell Culture , 1992, Humana Press.

[25]  N. Carlson Neuroprotection of cultured cortical neurons mediated by the cyclooxygenase‐2 inhibitor APHS can be reversed by a prostanoid , 2003, Journal of neuroscience research.

[26]  R. DuBois,et al.  Cyclooxygenase-2: a therapeutic target. , 2002, Annual review of medicine.

[27]  R. Breyer,et al.  Prostanoid receptors: subtypes and signaling. , 2001, Annual review of pharmacology and toxicology.

[28]  N. Toni,et al.  Interface Organotypic Hippocampal Slice Cultures , 2001 .