Gail V W Johnson

Summary

Affiliation: University of Alabama at Birmingham
Country: USA

Publications

  1. pmc Transglutaminase 2 protects against ischemic insult, interacts with HIF1beta, and attenuates HIF1 signaling
    Anthony J Filiano
    Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA
    FASEB J 22:2662-75. 2008
  2. pmc Tissue transglutaminase does not contribute to the formation of mutant huntingtin aggregates
    W Chun
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 35294, USA
    J Cell Biol 153:25-34. 2001
  3. ncbi request reprint Transglutaminase activity is increased in Alzheimer's disease brain
    G V Johnson
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 35294 0017, USA
    Brain Res 751:323-9. 1997
  4. ncbi request reprint The p38 MAP kinase signaling pathway in Alzheimer's disease
    Gail V W Johnson
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Exp Neurol 183:263-8. 2003
  5. ncbi request reprint Tau, where are we now?
    Gail V W Johnson
    Department of Psychiatry, University of Alabama at Birmingham School of Medicine, 35294 0017, USA
    J Alzheimers Dis 4:375-98. 2002
  6. ncbi request reprint Immunoblot analysis reveals that isopeptide antibodies do not specifically recognize the epsilon-(gamma-glutamyl)lysine bonds formed by transglutaminase activity
    Gail V W Johnson
    Department of Psychiatry, School of Medicine 1720, University of Alabama at Birmingham, 7th Avenue South, SC1061, Birmingham, AL 35294 0017, USA
    J Neurosci Methods 134:151-8. 2004
  7. ncbi request reprint Tau phosphorylation in neuronal cell function and dysfunction
    Gail V W Johnson
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    J Cell Sci 117:5721-9. 2004
  8. ncbi request reprint Tau phosphorylation and proteolysis: insights and perspectives
    Gail V W Johnson
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    J Alzheimers Dis 9:243-50. 2006
  9. ncbi request reprint Microtubule/MAP-affinity regulating kinase (MARK) is activated by phenylarsine oxide in situ and phosphorylates tau within its microtubule-binding domain
    S M Jenkins
    Department of Psychiatry, University of Alabama at Birmingham, 35294 0017, USA
    J Neurochem 74:1463-8. 2000
  10. ncbi request reprint Type 2 transglutaminase differentially modulates striatal cell death in the presence of wild type or mutant huntingtin
    Qingmin Ruan
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Neurochem 102:25-36. 2007

Collaborators

Detail Information

Publications64

  1. pmc Transglutaminase 2 protects against ischemic insult, interacts with HIF1beta, and attenuates HIF1 signaling
    Anthony J Filiano
    Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA
    FASEB J 22:2662-75. 2008
    ..These results indicate that TG2 may play an important role in protecting against the delayed neuronal cell death in ischemia and stroke...
  2. pmc Tissue transglutaminase does not contribute to the formation of mutant huntingtin aggregates
    W Chun
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 35294, USA
    J Cell Biol 153:25-34. 2001
    ..Therefore, in HD, as well as in other polyglutamine diseases, tTG is unlikely to play a role in the formation of aggregates...
  3. ncbi request reprint Transglutaminase activity is increased in Alzheimer's disease brain
    G V Johnson
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 35294 0017, USA
    Brain Res 751:323-9. 1997
    ....
  4. ncbi request reprint The p38 MAP kinase signaling pathway in Alzheimer's disease
    Gail V W Johnson
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Exp Neurol 183:263-8. 2003
  5. ncbi request reprint Tau, where are we now?
    Gail V W Johnson
    Department of Psychiatry, University of Alabama at Birmingham School of Medicine, 35294 0017, USA
    J Alzheimers Dis 4:375-98. 2002
    ..This review highlights recent findings concerning the normal metabolism and function of tau, as well as the abnormal processing and function of tau in Alzheimer's disease and in the tauopathies, both sporadic and familial...
  6. ncbi request reprint Immunoblot analysis reveals that isopeptide antibodies do not specifically recognize the epsilon-(gamma-glutamyl)lysine bonds formed by transglutaminase activity
    Gail V W Johnson
    Department of Psychiatry, School of Medicine 1720, University of Alabama at Birmingham, 7th Avenue South, SC1061, Birmingham, AL 35294 0017, USA
    J Neurosci Methods 134:151-8. 2004
    ..In this report we demonstrate that the two most commonly used isopeptide antibodies do not specifically recognize the isopeptide bonds formed by transglutaminase when they are within or between proteins...
  7. ncbi request reprint Tau phosphorylation in neuronal cell function and dysfunction
    Gail V W Johnson
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    J Cell Sci 117:5721-9. 2004
    ....
  8. ncbi request reprint Tau phosphorylation and proteolysis: insights and perspectives
    Gail V W Johnson
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    J Alzheimers Dis 9:243-50. 2006
    ....
  9. ncbi request reprint Microtubule/MAP-affinity regulating kinase (MARK) is activated by phenylarsine oxide in situ and phosphorylates tau within its microtubule-binding domain
    S M Jenkins
    Department of Psychiatry, University of Alabama at Birmingham, 35294 0017, USA
    J Neurochem 74:1463-8. 2000
    ..Immunoblot analysis of the protein kinase bands confirmed this finding, providing the first demonstration that activation of endogenous MARK results in increased tau phosphorylation within its microtubule-binding domain in situ...
  10. ncbi request reprint Type 2 transglutaminase differentially modulates striatal cell death in the presence of wild type or mutant huntingtin
    Qingmin Ruan
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Neurochem 102:25-36. 2007
    ..These data suggest that mutant htt alters the activation of TG2 in response to certain stimuli and therefore differentially modulates how TG2 contributes to cell death processes...
  11. ncbi request reprint Split GFP complementation assay: a novel approach to quantitatively measure aggregation of tau in situ: effects of GSK3beta activation and caspase 3 cleavage
    Wanjoo Chun
    Department of Psychiatry, University of Alabama at Birmingham School of Medicine, Alabama, USA
    J Neurochem 103:2529-39. 2007
    ..These data demonstrate that split GFP complementation may be a valuable approach to determine the aggregation process in living cells...
  12. pmc Immortalized cortical neurons expressing caspase-cleaved tau are sensitized to endoplasmic reticulum stress induced cell death
    Tori A Matthews-Roberson
    Department of Cell Biology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Brain Res 1234:206-12. 2008
    ..Our results suggest that the presence of Asp421 cleaved tau may sensitize neurons to ER stressors and possibly potentiate cell death processes during AD progression...
  13. ncbi request reprint The low density lipoprotein receptor-related protein 6 interacts with glycogen synthase kinase 3 and attenuates activity
    Kaihong Mi
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Biol Chem 281:4787-94. 2006
    ..This is the first identification of a direct interaction between LRP6 and GSK3, which results in an attenuation of GSK3 activity...
  14. ncbi request reprint FRAT-2 preferentially increases glycogen synthase kinase 3 beta-mediated phosphorylation of primed sites, which results in enhanced tau phosphorylation
    William H Stoothoff
    Department of Psychiatry, University of Alabama at Birmingham, Alabama 35294 0017, USA
    J Biol Chem 280:270-6. 2005
    ..In addition, FRAT-2 is phosphorylated by GSK3 beta. This is the first demonstration of a protein differentially regulating the activity of GSK3 beta toward primed and unprimed epitopes...
  15. pmc Histone deacetylase 6 interacts with the microtubule-associated protein tau
    Huiping Ding
    Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA
    J Neurochem 106:2119-30. 2008
    ..These findings establish HDAC6 as a tau-interacting protein and as a potential modulator of tau phosphorylation and accumulation...
  16. ncbi request reprint Tissue transglutaminase differentially modulates apoptosis in a stimuli-dependent manner
    Janusz Tucholski
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 1720 7th Avenue South, SC 1061, Birmingham, AL 35294 0017, USA
    J Neurochem 81:780-91. 2002
    ....
  17. ncbi request reprint Glycogen synthase kinase 3 beta induces caspase-cleaved tau aggregation in situ
    Jae Hyeon Cho
    Department of Psychiatry, University of Alabama at Birmingham, Alabama 35294 0017, USA
    J Biol Chem 279:54716-23. 2004
    ..These data suggest that a combination of phosphorylation events and caspase activation contribute to the tau oligomerization process in Alzheimer's disease, with GSK3 beta-mediated tau phosphorylation preceding caspase cleavage...
  18. ncbi request reprint Effects of cyclin-dependent kinase-5 activity on apoptosis and tau phosphorylation in immortalized mouse brain cortical cells
    Shirley B Shelton
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294 0001, USA
    J Neurosci Res 76:110-20. 2004
    ..In summary, these results demonstrate that CDK5 does not have a significant impact on tau phosphorylation and thapsigargin-induced apoptosis in this neuronal cell model...
  19. ncbi request reprint Mitochondrial respiration and ATP production are significantly impaired in striatal cells expressing mutant huntingtin
    Tamara Milakovic
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Biol Chem 280:30773-82. 2005
    ..These findings demonstrate that the presence of mutant huntingtin impairs mitochondrial ATP production through one or more mechanisms that do not directly affect the function of the respiration complexes...
  20. ncbi request reprint Activation of glycogen synthase kinase 3beta promotes the intermolecular association of tau. The use of fluorescence resonance energy transfer microscopy
    Wanjoo Chun
    Department of Psychiatry, University of Alabama at Birmingham School of Medicine, Birmingham, Alabama 35294, USA
    J Biol Chem 282:23410-7. 2007
    ..These data imply that increased association of tau should not be regarded as a direct indicator of the formation of insoluble tau aggregates...
  21. ncbi request reprint Striatal cells from mutant huntingtin knock-in mice are selectively vulnerable to mitochondrial complex II inhibitor-induced cell death through a non-apoptotic pathway
    Qingmin Ruan
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Hum Mol Genet 13:669-81. 2004
    ..These findings suggest that impaired mitochondrial complex II function in HD may contribute to non-apoptotic neuronal cell death...
  22. ncbi request reprint Mutant (R406W) human tau is hyperphosphorylated and does not efficiently bind microtubules in a neuronal cortical cell model
    Pavan K Krishnamurthy
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
    J Biol Chem 279:7893-900. 2004
    ..Furthermore, expression of R406W tau sensitized cells to apoptotic stress, which may contribute to the neuronal cell loss that occurs in this FTDP-17 tauopathy...
  23. ncbi request reprint Site-specific phosphorylation and caspase cleavage differentially impact tau-microtubule interactions and tau aggregation
    Huiping Ding
    Department of Psychiatry, University of Alabama, Birmingham, Alabama 35294 0017, USA
    J Biol Chem 281:19107-14. 2006
    ..These results show that site-specific phosphorylation and caspase cleavage of tau differentially affect the ability of tau to bind and stabilize microtubules and facilitate tau self-association...
  24. ncbi request reprint Mutant huntingtin aggregates do not sensitize cells to apoptotic stressors
    Wanjoo Chun
    Department of Psychiatry and Behavioral Neurobiology, 1720 7th Avenue South, SC1061, University of Alabama at Birmingham, School of Medicine, Birmingham, AL 35294 0017, USA
    FEBS Lett 515:61-5. 2002
    ....
  25. ncbi request reprint Tissue transglutaminase contributes to disease progression in the R6/2 Huntington's disease mouse model via aggregate-independent mechanisms
    Craig D C Bailey
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Neurochem 92:83-92. 2005
    ..Moreover, the combined results from this study suggest that the formation of striatal huntingtin aggregates does not directly influence motor dysfunction or death in this HD mouse model...
  26. ncbi request reprint Mutant huntingtin directly increases susceptibility of mitochondria to the calcium-induced permeability transition and cytochrome c release
    Yeun Su Choo
    Department of Psychiatry, University of Alabama at Birmingham, 35294, USA
    Hum Mol Genet 13:1407-20. 2004
    ..These findings suggest that the development of specific MPT inhibitors may be an interesting therapeutic avenue to delay the onset of HD...
  27. ncbi request reprint Transient osmotic stress facilitates mutant huntingtin aggregation
    Wanjoo Chun
    Department of Psychiatry and Behavioral Neurobiology, 1720 7th Avenue South, SC1061, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Neuroreport 13:2543-6. 2002
    ..Further, treatment of cells with geldanamycin, which activates a heat shock response, significantly attenuated the hyperosmotic-induced increase in aggregate formation...
  28. pmc A caspase cleaved form of tau is preferentially degraded through the autophagy pathway
    Philip J Dolan
    Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
    J Biol Chem 285:21978-87. 2010
    ....
  29. 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...
  30. ncbi request reprint Increased glutathione levels in cortical and striatal mitochondria of the R6/2 Huntington's disease mouse model
    Yeun Su Choo
    Department of Cell Biology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Neurosci Lett 386:63-8. 2005
    ..This specific increase in the levels of glutathione in mitochondria suggests that a compensatory mechanism is induced in the R6/2 mice to protect against an increase in oxidative stress in mitochondria...
  31. ncbi request reprint Ubiquitin-proteasome system alterations in a striatal cell model of Huntington's disease
    Jesse M Hunter
    Department of Cell Biology, and Department of Psychiatry, The University of Alabama at Birmingham, Birmingham, Alabama, USA
    J Neurosci Res 85:1774-88. 2007
    ....
  32. ncbi request reprint Tissue transglutaminase overexpression in the brain potentiates calcium-induced hippocampal damage
    Janusz Tucholski
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 35294, USA
    J Neurochem 97:582-94. 2006
    ....
  33. ncbi request reprint The role of tau phosphorylation and cleavage in neuronal cell death
    Wanjoo Chun
    Department of Psychiatry, School of Medicine, University of Alabama at Birmingham, 1061 Sparks Center, 1720 7th Avenue South, Birmingham, AL 35294 0017, USA
    Front Biosci 12:733-56. 2007
    ..This review highlights recent findings concerning the normal metabolism and function of tau, as well as the abnormal processing and function of tau in AD and in the tauopathies...
  34. ncbi request reprint Cdk5 phosphorylates p53 and regulates its activity
    Jianwen Zhang
    Department of Psychiatry and Neurobiology, University of Alabama at Birmingham, 35294 0017, USA
    J Neurochem 81:307-13. 2002
    ..This is the first demonstration that p53 is a substrate of Cdk5, and that Cdk5 can modulate p53 levels and activity...
  35. ncbi request reprint Tissue transglutaminase directly regulates adenylyl cyclase resulting in enhanced cAMP-response element-binding protein (CREB) activation
    Janusz Tucholski
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Biol Chem 278:26838-43. 2003
    ..This is the first study to provide evidence of the mechanism by which tTG may contribute to neuronal differentiation...
  36. ncbi request reprint Primed phosphorylation of tau at Thr231 by glycogen synthase kinase 3beta (GSK3beta) plays a critical role in regulating tau's ability to bind and stabilize microtubules
    Jae Hyeon Cho
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Neurochem 88:349-58. 2004
    ..These results strongly indicate that phosphorylation of Thr231 in tau by GSK3beta plays a critical role in regulating tau's ability to bind and stabilize microtubules...
  37. ncbi request reprint The protective effects of cystamine in the R6/2 Huntington's disease mouse involve mechanisms other than the inhibition of tissue transglutaminase
    Craig D C Bailey
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 1720 7th Avenue South, Sparks Center Room 1061, Birmingham, AL 35294 0017, USA
    Neurobiol Aging 27:871-9. 2006
    ..Since the magnitude of cystamine's therapeutic effects was not affected by the genetic deletion of tTG, these results suggest that the mechanism of action for cystamine in this HD mouse model involves targets other than tTG inhibition...
  38. ncbi request reprint Glycogen synthase kinase 3beta phosphorylates tau at both primed and unprimed sites. Differential impact on microtubule binding
    Jae Hyeon Cho
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Biol Chem 278:187-93. 2003
    ..These results demonstrate that GSK3beta-mediated phosphorylation of tau at primed sites plays a more significant role in regulating the interaction of tau with microtubules than phosphorylation at unprimed epitopes...
  39. ncbi request reprint Axin negatively affects tau phosphorylation by glycogen synthase kinase 3beta
    William H Stoothoff
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA
    J Neurochem 83:904-13. 2002
    ..This is the first demonstration that axin negatively affects the phosphorylation of a GSK3beta substrate, and provides a novel mechanism by which tau phosphorylation and function can be regulated within the cell...
  40. ncbi request reprint Cystamine inhibits caspase activity. Implications for the treatment of polyglutamine disorders
    Mathieu Lesort
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 35294 0017, USA
    J Biol Chem 278:3825-30. 2003
    ..These findings demonstrate that cystamine may prolong neuronal survival and delay the onset of HD by inhibiting caspases and increasing the level of antioxidants such as glutathione...
  41. 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
    ....
  42. ncbi request reprint Mutant huntingtin expression induces mitochondrial calcium handling defects in clonal striatal cells: functional consequences
    Tamara Milakovic
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Biol Chem 281:34785-95. 2006
    ....
  43. ncbi request reprint Regulated proteolytic processing of LRP6 results in release of its intracellular domain
    Kaihong Mi
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    J Neurochem 101:517-29. 2007
    ....
  44. ncbi request reprint 14-3-3Zeta does not increase GSK3beta-mediated tau phosphorylation in cell culture models
    Tori A Matthews
    Department of Psychiatry, School of Medicine, 1720 7th Avenue South, SC1061, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Neurosci Lett 384:211-6. 2005
    ..These data indicate that 14-3-3zeta may not be directly interacting with GSK3beta and tau in the brain, but may indirectly facilitate the interactions by binding to other proteins...
  45. ncbi request reprint Verification of somatic CAG repeat expansion by pre-PCR fractionation
    Jesse M Hunter
    Department of Cell Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
    J Neurosci Methods 144:11-7. 2005
    ..The application of this method confirms the presence of somatic expansions in the brains of a knock-in mouse model of HD...
  46. ncbi request reprint Transglutaminases in neurodegenerative disorders
    Craig D C Bailey
    Department of Psychiatry, University of Alabama at Birmingham School of Medicine, 1720 7th Avenue South, Birmingham, AL 35294 0017, USA
    Prog Exp Tumor Res 38:139-57. 2005
  47. ncbi request reprint Tau phosphorylation: physiological and pathological consequences
    William H Stoothoff
    Department of Psychiatry, School of Medicine, University of Alabama at Birmingham, 1061 Sparks Center, 1720 7th Avenue South, Birmingham, AL 35294 0017, USA
    Biochim Biophys Acta 1739:280-97. 2005
    ....
  48. ncbi request reprint 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...
  49. pmc The role of tau kinases in Alzheimer's disease
    Philip J Dolan
    University of Alabama at Birmingham, Department of Cell Biology, 1530 3rd Avenue South, Birmingham, AL 35294, USA
    Curr Opin Drug Discov Devel 13:595-603. 2010
    ..The evolving concepts of the roles tau plays in cellular biology, and the mechanisms by which phosphorylation regulates tau function, is reshaping the framework for the development of therapeutics targeting tau to treat AD...
  50. ncbi request reprint Transglutaminase 2 in neurodegenerative disorders
    Qingmin Ruan
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, 1720 Seventh Avenue South, SC1061, Birmingham, AL 35294 0017, USA
    Front Biosci 12:891-904. 2007
    ....
  51. ncbi request reprint Identification of the N-terminal functional domains of Cdk5 by molecular truncation and computer modeling
    Jianwen Zhang
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama 35294 0017, USA
    Proteins 48:447-53. 2002
    ....
  52. ncbi request reprint Role of the intracellular domains of LRP5 and LRP6 in activating the Wnt canonical pathway
    Kaihong Mi
    Department of Psychiatry, University of Alabama at Birmingham, Alabama 35294 0017, USA
    J Cell Biochem 95:328-38. 2005
    ..These findings provide significant new insights into the roles of LRP5/6 in modulating canonical Wnt signaling...
  53. ncbi request reprint Developmental regulation of tissue transglutaminase in the mouse forebrain
    Craig D C Bailey
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama, USA
    J Neurochem 91:1369-79. 2004
    ..These results demonstrate for the first time that tTG enzymatic activity in the mammalian forebrain is developmentally regulated by post-translational mechanisms...
  54. ncbi request reprint The role of tau phosphorylation in the pathogenesis of Alzheimer's disease
    Kaihong Mi
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Curr Alzheimer Res 3:449-63. 2006
    ..This review focuses on recent literature pertaining to the regulation of tau phosphorylation and function, and the role that a dysregulation of tau phosphorylation may play in the neuronal dysfunction in Alzheimer's disease...
  55. ncbi request reprint Intracellular localization and activity state of tissue transglutaminase differentially impacts cell death
    Tamara Milakovic
    Department of Psychiatry, University of Alabama at Birmingham, Alabama 35294 0017, USA
    J Biol Chem 279:8715-22. 2004
    ....
  56. pmc New application of beta-galactosidase complementation to monitor tau self-association
    Huiping Ding
    Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama, USA
    J Neurochem 106:1545-51. 2008
    ..Overall, this study suggests that beta-gal complementation assay can be a useful tool to monitor tau self-association...
  57. ncbi request reprint Cyclin-dependent kinase-5 in neurodegeneration
    Shirley B Shelton
    Department of Psychiatry, University of Alabama at Birmingham, Birmingham, Alabama, USA
    J Neurochem 88:1313-26. 2004
    ..This review will highlight recent data on the possible roles of CDK5 in neurodegeneration...
  58. pmc The last tangle of tau
    Huiping Ding
    Department of Cell Biology, University of Alabama at Birmingham, Birmingham, AL, USA
    J Alzheimers Dis 14:441-7. 2008
    ..Further studies on the mechanisms of tau aggregation, the structure of intermediate tau forms and their toxicity are needed to settle this debate...
  59. 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...
  60. ncbi request reprint Validity of mouse models for the study of tissue transglutaminase in neurodegenerative diseases
    Craig D C Bailey
    Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294 0017, USA
    Mol Cell Neurosci 25:493-503. 2004
    ..However, tTG contributes to the majority of transglutaminase activity within mouse forebrain. Thus, although tTG is expressed at lower levels in mouse compared with human forebrain, it likely plays important roles in neuronal function...
  61. ncbi request reprint Does tissue transglutaminase play a role in Huntington's disease?
    Mathieu Lesort
    Department of Psychiatry and Behavioral Neurobiology, 1720 7th Avenue, South, SC1061, School of Medicine, University of Alabama at Birmingham, 35294 0017, USA
    Neurochem Int 40:37-52. 2002
    ..Further research is required to define the specific role of tTG in Huntington's disease...
  62. ncbi request reprint Tissue transglutaminase is not involved in the aggregate formation of stably expressed alpha-synuclein in SH-SY5Y human neuroblastoma cells
    Myung Duk Suh
    Department of Pharmacology, College of Medicine, Kangwon National University, Chunchon 200 701, Korea
    Arch Pharm Res 27:850-6. 2004
    ..In addition, alpha-synuclein was not modified by activated tTG in situ. These data suggest that tTG is unlikely to be a contributing factor to the formation of aggregates of alpha-synuclein in a stable cell model...
  63. ncbi request reprint Cystamine treatment is neuroprotective in the YAC128 mouse model of Huntington disease
    Jeremy M Van Raamsdonk
    Centre for Molecular Medicine and Therapeutics, Department of Medical Genetics and British Columbia Research Institute for Women and Children s Health, University of British Columbia, Vancouver, British Columbia, Canada
    J Neurochem 95:210-20. 2005
    ..While the exact mechanism responsible for the beneficial effects of cystamine in YAC128 mice is uncertain, our findings suggest that cystamine is neuroprotective and may be beneficial in the treatment of HD...
  64. pmc Rosiglitazone treatment prevents mitochondrial dysfunction in mutant huntingtin-expressing cells: possible role of peroxisome proliferator-activated receptor-gamma (PPARgamma) in the pathogenesis of Huntington disease
    Rodrigo A Quintanilla
    Department of Anesthesiology, University of Rochester, University Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
    J Biol Chem 283:25628-37. 2008
    ....