RICHARD JOPE

Summary

Affiliation: University of Alabama at Birmingham
Country: USA

Publications

  1. ncbi Inhibition of glycogen synthase kinase-3 protects cells from intrinsic but not extrinsic oxidative stress
    Taj D King
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, AL 35294 0017, USA
    Neuroreport 16:597-601. 2005
  2. pmc GSK3 beta N-terminus binding to p53 promotes its acetylation
    Tae Yeon Eom
    Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
    Mol Cancer 8:14. 2009
  3. pmc Lipopolysaccharide-induced interleukin-6 production is controlled by glycogen synthase kinase-3 and STAT3 in the brain
    Eleonore Beurel
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    J Neuroinflammation 6:9. 2009
  4. pmc Lithium facilitates apoptotic signaling induced by activation of the Fas death domain-containing receptor
    Ling Song
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    BMC Neurosci 5:20. 2004
  5. ncbi AP-1 and NF-kappaB stimulated by carbachol in human neuroblastoma SH-SY5Y cells are differentially sensitive to inhibition by lithium
    R S Jope
    Department of Psychiatry and Behavioral Neurobiology, Sparks Center, University of Alabama at Birmingham, 35294 0017, USA
    Brain Res Mol Brain Res 50:171-80. 1997
  6. pmc Glycogen synthase kinase-3 (GSK3) in psychiatric diseases and therapeutic interventions
    Richard S Jope
    Department of Psychiatry and Behavioral Neurobiology, Sparks Center 1057, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Curr Drug Targets 7:1421-34. 2006
  7. ncbi The glamour and gloom of glycogen synthase kinase-3
    Richard S Jope
    Department of Psychiatry and Behavioral Neurobiology, Sparks Center 1057, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Trends Biochem Sci 29:95-102. 2004
  8. pmc Glycogen synthase kinase-3 (GSK3): inflammation, diseases, and therapeutics
    Richard S Jope
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Sparks Center 1057, 1720 Seventh Avenue South, Birmingham, AL 35294 0017, USA
    Neurochem Res 32:577-95. 2007
  9. ncbi Lithium and GSK-3: one inhibitor, two inhibitory actions, multiple outcomes
    Richard S Jope
    Department of Psychiatry and Behavioral Neurobiology, 1720 7th Ave South, Sparks Center 1057, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Trends Pharmacol Sci 24:441-3. 2003
  10. ncbi Anti-bipolar therapy: mechanism of action of lithium
    R S Jope
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 35294 0017, USA
    Mol Psychiatry 4:117-28. 1999

Research Grants

  1. NEURONAL SIGNALING--OXIDANTS AND ALZHEIMERS DISEASE
    RICHARD JOPE; Fiscal Year: 2002
  2. EFFECTS OF LITHIUM ON CHOLINERGIC ACTIVITY
    RICHARD JOPE; Fiscal Year: 2004
  3. Neuronal signaling : Oxidants & Alzheimers disease
    RICHARD JOPE; Fiscal Year: 2007
  4. GSK3beta: Signaling and apoptosis
    RICHARD JOPE; Fiscal Year: 2007
  5. Effects of lithium on cellular signaling
    RICHARD JOPE; Fiscal Year: 2009
  6. Effects of lithium on cellular signaling
    Richard S Jope; Fiscal Year: 2010
  7. Effects of lithium on cellular signaling
    RICHARD JOPE; Fiscal Year: 2007
  8. EFFECTS OF LITHIUM ON CHOLINERGIC ACTIVITY
    RICHARD JOPE; Fiscal Year: 1999
  9. EFFECTS OF LITHIUM ON CHOLINERGIC ACTIVITY
    RICHARD JOPE; Fiscal Year: 1993
  10. EFFECTS OF LITHIUM ON CHOLINERGIC ACTIVITY
    RICHARD JOPE; Fiscal Year: 1990

Collaborators

Detail Information

Publications52

  1. ncbi Inhibition of glycogen synthase kinase-3 protects cells from intrinsic but not extrinsic oxidative stress
    Taj D King
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, AL 35294 0017, USA
    Neuroreport 16:597-601. 2005
    ....
  2. pmc GSK3 beta N-terminus binding to p53 promotes its acetylation
    Tae Yeon Eom
    Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
    Mol Cancer 8:14. 2009
    ..These results indicate that the N-terminal region of GSK3 beta binds p53, this association promotes the acetylation of p53, and subsequently acetylated p53 dissociates from GSK3...
  3. pmc Lipopolysaccharide-induced interleukin-6 production is controlled by glycogen synthase kinase-3 and STAT3 in the brain
    Eleonore Beurel
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    J Neuroinflammation 6:9. 2009
    ..To identify potential targets to control brain IL-6, we tested if IL-6 produced by glia is regulated by signal transducer and activator of transcription-3 (STAT3) and glycogen synthase kinase-3 (GSK3)...
  4. pmc Lithium facilitates apoptotic signaling induced by activation of the Fas death domain-containing receptor
    Ling Song
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    BMC Neurosci 5:20. 2004
    ..The present investigation examined if the neuroprotection provided by lithium included apoptosis induced by stimulation of the death domain-containing receptor Fas...
  5. ncbi AP-1 and NF-kappaB stimulated by carbachol in human neuroblastoma SH-SY5Y cells are differentially sensitive to inhibition by lithium
    R S Jope
    Department of Psychiatry and Behavioral Neurobiology, Sparks Center, University of Alabama at Birmingham, 35294 0017, USA
    Brain Res Mol Brain Res 50:171-80. 1997
    ..These findings demonstrate that one mechanism by which lithium can influence the expression of specific genes is through the selective modulation of signaling processes which emanate from cholinergic receptor stimulation...
  6. pmc Glycogen synthase kinase-3 (GSK3) in psychiatric diseases and therapeutic interventions
    Richard S Jope
    Department of Psychiatry and Behavioral Neurobiology, Sparks Center 1057, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Curr Drug Targets 7:1421-34. 2006
    ..In part because of these key actions of GSK3 and its associations with mood disorders and schizophrenia, much research is currently being devoted to identifying new selective inhibitors of GSK3...
  7. ncbi The glamour and gloom of glycogen synthase kinase-3
    Richard S Jope
    Department of Psychiatry and Behavioral Neurobiology, Sparks Center 1057, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Trends Biochem Sci 29:95-102. 2004
    ..Therefore, much effort is currently directed towards understanding the functions and control of GSK3, and identifying methods capable of diminishing the deleterious impact of GSK3 in pathological conditions...
  8. pmc Glycogen synthase kinase-3 (GSK3): inflammation, diseases, and therapeutics
    Richard S Jope
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Sparks Center 1057, 1720 Seventh Avenue South, Birmingham, AL 35294 0017, USA
    Neurochem Res 32:577-95. 2007
    ..Thus, GSK3 may contribute not only to primary pathologies in these diseases, but also to the associated inflammation, suggesting that GSK3 inhibitors may have multiple effects influencing these conditions...
  9. ncbi Lithium and GSK-3: one inhibitor, two inhibitory actions, multiple outcomes
    Richard S Jope
    Department of Psychiatry and Behavioral Neurobiology, 1720 7th Ave South, Sparks Center 1057, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Trends Pharmacol Sci 24:441-3. 2003
    ..These dual effects can act in concert to magnify the influence of lithium on crucial GSK-3-regulated functions (gene expression, cell structure and survival)...
  10. ncbi Anti-bipolar therapy: mechanism of action of lithium
    R S Jope
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 35294 0017, USA
    Mol Psychiatry 4:117-28. 1999
    ....
  11. ncbi Mood stabilizers, glycogen synthase kinase-3beta and cell survival
    R S Jope
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Mol Psychiatry 7:S35-45. 2002
    ..Thus, signaling systems determining cell fate appear to be important targets of mood stabilizers, and these may include signaling pathways encompassing GSK3beta, including transcription factors regulated by GSK3beta...
  12. ncbi Oxidative stress oppositely modulates protein tyrosine phosphorylation stimulated by muscarinic G protein-coupled and epidermal growth factor receptors
    R S Jope
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 35294 0017, USA
    J Neurosci Res 55:329-40. 1999
    ..Thus, oxidative stress can oppositely modulate protein tyrosine phosphorylation induced by activation of G protein-coupled and growth factor receptors in the same cells...
  13. ncbi A bimodal model of the mechanism of action of lithium
    R S Jope
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 35294 0017, USA
    Mol Psychiatry 4:21-5. 1999
    ..Diverse sites of action of lithium are proposed to ultimately converge on the regulation of gene expression to contribute to mood stabilization...
  14. pmc HSP105 interacts with GRP78 and GSK3 and promotes ER stress-induced caspase-3 activation
    Gordon P Meares
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Cell Signal 20:347-58. 2008
    ..Thus, HSP105 appears to chaperone the responses to ER stress through its interactions with GRP78 and GSK3, and without HSP105 cell death following ER stress proceeds by a non-caspase-3-dependent process...
  15. pmc XIAP associates with GSK3 and inhibits the promotion of intrinsic apoptotic signaling by GSK3
    Mianen Sun
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
    Cell Signal 21:1857-65. 2009
    ....
  16. pmc Evidence of reactive astrocytes but not peripheral immune system activation in a mouse model of Fragile X syndrome
    Christopher J Yuskaitis
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Biochim Biophys Acta 1802:1006-12. 2010
    ..These results provide further evidence of the involvement of dysregulated GSK3 in FXS, and demonstrate that lithium administration reduces macroorchidism and reactive astrocytes in Fmr1 knockout mice...
  17. pmc Neural precursor cells are protected from apoptosis induced by trophic factor withdrawal or genotoxic stress by inhibitors of glycogen synthase kinase 3
    Tae Yeon Eom
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Biol Chem 282:22856-64. 2007
    ..Thus, NPCs are sensitive to loss of trophic factors and genotoxic stress, and inhibitors of GSK3 are capable of enhancing NPC survival...
  18. ncbi Central role of glycogen synthase kinase-3beta in endoplasmic reticulum stress-induced caspase-3 activation
    Ling Song
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Biol Chem 277:44701-8. 2002
    ..Thus, ER stress activates GSK3beta through dephosphorylation of phospho-Ser-9, a prerequisite for caspase-3 activation, and this process is amenable to pharmacological intervention...
  19. pmc Physiological and pathological changes in glucose regulate brain Akt and glycogen synthase kinase-3
    Buffie Clodfelder-Miller
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Biol Chem 280:39723-31. 2005
    ..Thus, the Akt-GSK3 signaling pathway is regulated in mouse brain in vivo in response to physiological and pathological changes in insulin and glucose...
  20. ncbi BDNF-mediated signal transduction is modulated by GSK3beta and mood stabilizing agents
    Lian Mai
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 1075 Sparks Center, 1720 7th Avenue South, Birmingham, AL 35294 00017, USA
    J Neurochem 82:75-83. 2002
    ..Therefore, increased GSK3beta selectively attenuates BDNF-induced CREB phosphorylation, and lithium and carbamazepine can facilitate activation of CREB...
  21. pmc Blocked inhibitory serine-phosphorylation of glycogen synthase kinase-3alpha/beta impairs in vivo neural precursor cell proliferation
    Tae Yeon Eom
    Department of Psychiatry, Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    Biol Psychiatry 66:494-502. 2009
    ..Because these diseases might be associated with inadequately controlled glycogen synthase kinase-3 (GSK3), we tested whether blocked inhibitory serine-phosphorylation of GSK3 impairs neurogenesis...
  22. pmc Differential regulation of STAT family members by glycogen synthase kinase-3
    Eleonore Beurel
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama, Birmingham, Alabama 35294 0017, USA
    J Biol Chem 283:21934-44. 2008
    ..Thus, inhibitors of GSK3 reduce the activation of STAT3 and STAT5, providing a mechanism to differentially regulate STATs to modulate the inflammatory response...
  23. ncbi Glycogen synthase kinase-3 beta is highly activated in nuclei and mitochondria
    Gautam N Bijur
    Department of Psychiatry and Behavioral Neurology, University of Alabama at Birmingham, 35294 0017, USA
    Neuroreport 14:2415-9. 2003
    ..Thus, the nuclei and mitochondria contain disproportionately high levels of active GSK3 beta, which is selectively further activated by some apoptotic stimuli...
  24. pmc Lithium prevents and ameliorates experimental autoimmune encephalomyelitis
    Patrizia De Sarno
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama, Birmingham, AL 35294, USA
    J Immunol 181:338-45. 2008
    ....
  25. pmc Forkhead box, class O transcription factors in brain: regulation and behavioral manifestation
    Abigail Polter
    Department of Psychiatry, University of Alabama at Birmingham, 1075 Sparks Center, 1720 7th Avenue South, Birmingham, AL35294 0017, USA
    Biol Psychiatry 65:150-9. 2009
    ..Here, we investigated whether brain FoxO1 and FoxO3a can be regulated by serotonin and antidepressant treatment and whether their genetic deletion affects behaviors...
  26. pmc Lithium ameliorates altered glycogen synthase kinase-3 and behavior in a mouse model of fragile X syndrome
    Christopher J Yuskaitis
    Department of Psychiatry and Behavioral Neurobiology, 1720 7th Ave South, Sparks Center 1057, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Biochem Pharmacol 79:632-46. 2010
    ..These findings support the hypothesis that impaired inhibition of GSK3 contributes to the pathogenesis of FXS and support GSK3 as a potential therapeutic target...
  27. pmc Deficiency in the inhibitory serine-phosphorylation of glycogen synthase kinase-3 increases sensitivity to mood disturbances
    Abigail Polter
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Neuropsychopharmacology 35:1761-74. 2010
    ....
  28. pmc Glycogen synthase kinase-3 regulates microglial migration, inflammation, and inflammation-induced neurotoxicity
    Christopher J Yuskaitis
    Department of Psychiatry and Behavioral Neurobiology, 1720 Seventh Avenue South, Sparks Center 1057, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Cell Signal 21:264-73. 2009
    ..These findings demonstrate that GSK3 promotes microglial responses to inflammation and that the utilization of GSK3 inhibitors provides a means to limit the inflammatory actions of microglia...
  29. pmc Is glycogen synthase kinase-3 a central modulator in mood regulation?
    Xiaohua Li
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    Neuropsychopharmacology 35:2143-54. 2010
    ....
  30. pmc Direct, activating interaction between glycogen synthase kinase-3beta and p53 after DNA damage
    Piyajit Watcharasit
    Departments of Psychiatry and Behavioral Neurobiology and Cell Biology, University of Alabama, Birmingham, AL 35294 0017, USA
    Proc Natl Acad Sci U S A 99:7951-5. 2002
    ..Thus, after DNA damage there is a direct interaction between p53 and GSK3beta, and these proteins act in concert to regulate cellular responses to DNA damage...
  31. ncbi Hypoxia activates glycogen synthase kinase-3 in mouse brain in vivo: protection by mood stabilizers and imipramine
    Myoung Sun Roh
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    Biol Psychiatry 57:278-86. 2005
    ....
  32. pmc Toll-like receptor-mediated cytokine production is differentially regulated by glycogen synthase kinase 3
    Michael Martin
    Department of Oral Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294 2170, USA
    Nat Immunol 6:777-84. 2005
    ..These findings demonstrate a regulatory function for GSK3 in modulating the inflammatory response...
  33. pmc Tau is hyperphosphorylated at multiple sites in mouse brain in vivo after streptozotocin-induced insulin deficiency
    Buffie J Clodfelder-Miller
    Department of Psychiatry and Behavioral Neurobiology, 1720 Seventh Ave South, Sparks Center 1057, University of Alabama, Birmingham, AL 35294 0017, USA
    Diabetes 55:3320-5. 2006
    ....
  34. pmc In vivo regulation of glycogen synthase kinase-3beta (GSK3beta) by serotonergic activity in mouse brain
    Xiaohua Li
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Neuropsychopharmacology 29:1426-31. 2004
    ..These results raise the possibility that impaired inhibitory control of GSK3beta may occur in conditions where serotonergic activity is dysregulated, such as in mood disorders...
  35. pmc Rapid accumulation of Akt in mitochondria following phosphatidylinositol 3-kinase activation
    Gautam N Bijur
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
    J Neurochem 87:1427-35. 2003
    ..These results demonstrate that signals emanating from plasma membrane receptors or generated by stress rapidly modulate Akt and glycogen synthase kinase-3beta in mitochondria...
  36. pmc Glycogen synthase kinase-3beta (GSK3beta) binds to and promotes the actions of p53
    Piyajit Watcharasit
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Biol Chem 278:48872-9. 2003
    ..Thus, GSK3beta interacts with p53 in both the nucleus and mitochondria and promotes its actions at both sites...
  37. ncbi Regulation of Akt and glycogen synthase kinase-3 beta phosphorylation by sodium valproate and lithium
    Patrizia De Sarno
    Department of Psychiatry and Behavioral Neurobiology, Sparks Center 1057, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Neuropharmacology 43:1158-64. 2002
    ....
  38. pmc Lithium regulates glycogen synthase kinase-3beta in human peripheral blood mononuclear cells: implication in the treatment of bipolar disorder
    Xiaohua Li
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Biol Psychiatry 61:216-22. 2007
    ..We tested whether lithium modified GSK3beta in vivo or in vitro in peripheral blood mononuclear cells (PBMCs) from healthy control and bipolar disorder subjects...
  39. pmc In vivo regulation of GSK3 phosphorylation by cholinergic and NMDA receptors
    Patrizia De Sarno
    Department of Psychiatry and Behavioral Neurobiology, 1720 Seventh Ave South, Sparks Center 1057, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Neurobiol Aging 27:413-22. 2006
    ..Thus, drugs in each class of therapeutic agents used for AD have the common property of increasing the regulatory serine-phosphorylation of GSK3 within common pools of the enzyme...
  40. pmc Nuclear accumulation of glycogen synthase kinase-3 during replicative senescence of human fibroblasts
    Jaroslaw W Zmijewski
    Department of Psychiatry and Behavioural Neurobiology, Sparks Center 1057, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Aging Cell 3:309-17. 2004
    ....
  41. pmc Glycogen synthase kinase-3 promotes the synergistic action of interferon-gamma on lipopolysaccharide-induced IL-6 production in RAW264.7 cells
    Eleonore Beurel
    Department of Psychiatry and Behavioral Neurobiology, 1720 Seventh Avenue South, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Cell Signal 21:978-85. 2009
    ..These results demonstrate the dependency of macrophage priming by IFN-gamma on STAT3 and GSK3, providing novel targets for intervention...
  42. pmc Anesthesia and post-mortem interval profoundly influence the regulatory serine phosphorylation of glycogen synthase kinase-3 in mouse brain
    Xiaohua Li
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 1720 7th Avenue South, Birmingham, AL 35294 0017, USA
    J Neurochem 92:701-4. 2005
    ....
  43. pmc AMP-activated protein kinase (AMPK) activating agents cause dephosphorylation of Akt and glycogen synthase kinase-3
    Taj D King
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Biochem Pharmacol 71:1637-47. 2006
    ....
  44. pmc Resolution of the nuclear localization mechanism of glycogen synthase kinase-3: functional effects in apoptosis
    Gordon P Meares
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Biol Chem 282:16989-7001. 2007
    ..Identification of a GSK3beta NLS allows new strategies to decipher and manipulate its subcellular actions regulating gene expression and apoptosis and its involvement in diseases...
  45. pmc GSK3 influences social preference and anxiety-related behaviors during social interaction in a mouse model of fragile X syndrome and autism
    Marjelo A Mines
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America
    PLoS ONE 5:e9706. 2010
    ..This used two mouse models with disrupted regulation of GSK3, Fmr1 knockout mice and GSK3 knockin mice, in which inhibitory serines of the two isoforms of GSK3, GSK3alpha and GSK3beta, are mutated to alanines, leaving GSK3 fully active...
  46. pmc Innate and adaptive immune responses regulated by glycogen synthase kinase-3 (GSK3)
    Eleonore Beurel
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Trends Immunol 31:24-31. 2010
    ..These discoveries led to the rapid application of GSK3 inhibitors to animal models of sepsis, arthritis, colitis, multiple sclerosis and others, demonstrating their potential for therapeutic intervention...
  47. pmc The paradoxical pro- and anti-apoptotic actions of GSK3 in the intrinsic and extrinsic apoptosis signaling pathways
    Eleonore Beurel
    Department of Psychiatry and Behavioral Neurobiology, Sparks Center 1057, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Prog Neurobiol 79:173-89. 2006
    ....
  48. pmc Mitochondrial-targeted active Akt protects SH-SY5Y neuroblastoma cells from staurosporine-induced apoptotic cell death
    Paramita Mookherjee
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
    J Cell Biochem 102:196-210. 2007
    ..These findings demonstrate that intramitochondrial active Akt results in efficient protection against apoptotic signaling...
  49. pmc Heat shock protein-90 dampens and directs signaling stimulated by insulin-like growth factor-1 and insulin
    Gordon P Meares
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Sparks Center 1057, 1720 7th Ave South, Birmingham, AL 35294 0017, USA
    FEBS Lett 574:181-6. 2004
    ..Thus, Hsp90 not only buffers the cellular effects of mutations and stresses, but also buffers the magnitude and duration of activation of proliferative and survival-promoting signaling responses...
  50. ncbi Anti-apoptotic effects of muscarinic receptor activation are mediated by Rho kinase
    Patrizia De Sarno
    Department of Psychiatry and Behavioral Neurobiology, 1720 Seventh Avenue South, Sparks Center 1057, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Brain Res 1041:112-5. 2005
    ..These results demonstrate that the anti-apoptotic effect provided by muscarinic receptor stimulation is dependent on the activity of Rho kinase...
  51. pmc Cellular stress increases RGS2 mRNA and decreases RGS4 mRNA levels in SH-SY5Y cells
    Ling Song
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Sparks Center 1057, Birmingham, AL 35294 0017, USA
    Neurosci Lett 402:205-9. 2006
    ..Overall, these results indicate that cell cycle arrest regulates the expression of RGS2 and RGS4, and that the expression of these two RGS family members is oppositely regulated by stress that causes cell cycle arrest...
  52. pmc Glycogen synthase kinase-3beta, mood stabilizers, and neuroprotection
    Xiaohua Li
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 35294 0017, USA
    Bipolar Disord 4:137-44. 2002
    ....

Research Grants42

  1. NEURONAL SIGNALING--OXIDANTS AND ALZHEIMERS DISEASE
    RICHARD JOPE; Fiscal Year: 2002
    ..Specific Aim 5 will terst the hypothesis that oxidative agents modulate transcription factor activation, including those activated by muscarinic receptor stimulation. ..
  2. EFFECTS OF LITHIUM ON CHOLINERGIC ACTIVITY
    RICHARD JOPE; Fiscal Year: 2004
    ....
  3. Neuronal signaling : Oxidants & Alzheimers disease
    RICHARD JOPE; Fiscal Year: 2007
    ..abstract_text> ..
  4. GSK3beta: Signaling and apoptosis
    RICHARD JOPE; Fiscal Year: 2007
    ..Overall, these experiments will clarify mechanisms regulating GSK3b and its effects on neural plasticity and survival. ..
  5. Effects of lithium on cellular signaling
    RICHARD JOPE; Fiscal Year: 2009
    ..Overall, this project will continue to provide leading-edge insight into mechanisms that may underlie the pathology of mood disorders and the actions of mood stabilizers. ..
  6. Effects of lithium on cellular signaling
    Richard S Jope; Fiscal Year: 2010
    ..Overall, this project will continue to provide leading-edge insight into mechanisms that may underlie the pathology of mood disorders and the actions of mood stabilizers. ..
  7. Effects of lithium on cellular signaling
    RICHARD JOPE; Fiscal Year: 2007
    ..Overall, this project will continue to provide leading-edge insight into mechanisms that may underlie the pathology of mood disorders and the actions of mood stabilizers. ..
  8. EFFECTS OF LITHIUM ON CHOLINERGIC ACTIVITY
    RICHARD JOPE; Fiscal Year: 1999
    ..These studies based on previous results, will clarify the effect of lithium on PKC and associated gene expression. ..
  9. EFFECTS OF LITHIUM ON CHOLINERGIC ACTIVITY
    RICHARD JOPE; Fiscal Year: 1993
    ....
  10. EFFECTS OF LITHIUM ON CHOLINERGIC ACTIVITY
    RICHARD JOPE; Fiscal Year: 1990
    ..Attainment of these goals will increase our understanding of the effects of lithium that may be related to its therapeutic effect in mania and may generate hypotheses as to the underlying causes of bipolar affective disorders...