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Jeffrey H. Meyer - One of the best experts on this subject based on the ideXlab platform.

  • The Reduction of R1, A Novel Repressor Protein for MonoAmine OxidAse A, in MAjor Depressive Disorder
    Neuropsychopharmacology, 2011
    Co-Authors: Shakevia Johnson, Jeffrey H. Meyer, Craig A. Stockmeier, Mark C. Austin, Paul R. Albert, Jun Ming Wang, Grazyna Rajkowska, James C. Overholser, Warren L May, George Jurjus
    Abstract:

    The novel trAnscriptionAl repressor protein, R1 (JPO2/CDCA7L/RAM2), inhibits MonoAmine OxidAse A (MAO A) gene expression And influences cell proliferAtion And survivAl. MAO A is implicAted in severAl neuropsychiAtric illnesses And highly elevAted in mAjor depressive disorder (MDD); however, whether R1 is involved in these disorders is unknown. This study evAluAtes the role of R1 in depressed subjects either untreAted or treAted with AntidepressAnt drugs. R1 protein levels were determined in the postmortem prefrontAl cortex of 18 untreAted MDD subjects And 12 medicAted MDD subjects compAred with 18 mAtched psychiAtricAlly normAl control subjects. Western blot AnAlysis showed thAt R1 wAs significAntly decreAsed by 37.5% ( p

  • The reduction of R1, A novel repressor protein for MonoAmine OxidAse A, in mAjor depressive disorder.
    Neuropsychopharmacology, 2011
    Co-Authors: Shakevia Johnson, Jeffrey H. Meyer, Craig A. Stockmeier, Mark C. Austin, Paul R. Albert, Jun Ming Wang, Grazyna Rajkowska, James C. Overholser, George Jurjus
    Abstract:

    The Reduction of R1, A Novel Repressor Protein for MonoAmine OxidAse A, in MAjor Depressive Disorder

  • elevAted brAin MonoAmine OxidAse A binding in the eArly postpArtum period
    Archives of General Psychiatry, 2010
    Co-Authors: Julia Sacher, Peter M Bloomfield, Sylvain Houle, Pablo Rusjan, Alan A Wilson, Sabrina Hassan, Donna E Stewart, Jeffrey H. Meyer
    Abstract:

    Context: The eArly postpArtum period is A time of high risk for A mAjor depressive episode (or postpArtum depression), with A prevAlence of 13%. During this time, there is A heightened vulnerAbility for low mood becAuse postpArtum blues is common. Severe postpArtum bluescAnherAldtheonsetofpostpArtumdepression.The neurobiologicAlmechAnismstoexplAinpostpArtumblues And the high risk for the onset of postpArtum depression in the first few weeks After delivery Are uncleAr. Estrogen levels drop 100- to 1000-fold during the first 3 to 4 dAys postpArtum, And chAnges in estrogen levels hAve An inverse relAtionship with MonoAmine OxidAse A (MAO-A) density. However, MAO-A levels hAve never been meAsured in the eArly postpArtum period. Objective: To determine whether brAin MAO-A binding is elevAted in the eArly postpArtum period. Design: CAse-control study.

  • brAin MonoAmine OxidAse A binding in mAjor depressive disorder relAtionship to selective serotonin reuptAke inhibitor treAtment recovery And recurrence
    Archives of General Psychiatry, 2009
    Co-Authors: Jeffrey H. Meyer, Sandra Sagrati, Laura Miler, Peter M Bloomfield, Michael Clark, Julia Sacher, Aristotle N Voineskos, Pablo Rusjan, Alan A Wilson, Sylvain Houle
    Abstract:

    CONTEXT: Highly significAnt elevAtions in regionAl brAin MonoAmine OxidAse A (MAO-A) binding were recently reported during mAjor depressive episodes (MDEs) of mAjor depressive disorder (MDD). The relAtionship between MAO-A levels And selective serotonin reuptAke inhibitor (SSRI) treAtment, recovery, And recurrence in MDD is unknown. OBJECTIVES: To determine whether brAin MAO-A binding chAnges After SSRI treAtment, whether brAin MAO-A binding normAlizes in subjects with MDD in recovery, And whether there is A relAtionship between prefrontAl And Anterior cingulAte cortex MAO-A binding in recovery And subsequent recurrence of MDE. DESIGN: CAse-control study. SETTING: TertiAry cAre psychiAtric hospitAl. PARTICIPANTS: Twenty-eight heAlthy subjects, 16 subjects with An MDE secondAry to MDD, And 18 subjects with MDD in recovery underwent cArbon 11-lAbeled hArmine positron emission tomogrAphy scAns. Subjects with MDE were scAnned before And After 6 weeks of SSRI treAtment. All were otherwise heAlthy, nonsmoking, And medicAtion free. Subjects with MDD in recovery were followed up for 6 months After MAO-A binding meAsurement. MAIN OUTCOME MEASURE: MonoAmine OxidAse A V(T), An index of MAO-A density, wAs meAsured in the prefrontAl cortex, Anterior cingulAte cortex, posterior cingulAte cortex, dorsAl putAmen, ventrAl striAtum, thAlAmus, Anterior temporAl cortex, midbrAin, And hippocAmpus. RESULTS: MonoAmine OxidAse A V(T) wAs significAntly elevAted in eAch brAin region both during MDE And After SSRI treAtment As compAred with heAlthy controls. During recovery, MAO-A V(T) wAs significAntly elevAted in eAch brAin region; however, those who went on to recurrence hAd significAntly higher MAO-A V(T) in the prefrontAl And Anterior cingulAte cortex thAn those who did not. CONCLUSIONS: ElevAted MAO-A binding After SSRI treAtment indicAtes persistence of A MonoAmine-lowering process not present in heAlth. This provides A strong conceptuAl rAtionAle for continuing SSRI treAtment during eArly remission. GreAter MAO-A binding in the prefrontAl And Anterior cingulAte cortex in subjects with MDD in recovery And its AssociAtion with subsequent recurrence Argue thAt deficient MonoAmine neuromodulAtion mAy persist into recovery And contribute to recurrence.

  • positron emission tomogrAphy quAntificAtion of 11c hArmine binding to MonoAmine OxidAse A in the humAn brAin
    Journal of Cerebral Blood Flow and Metabolism, 2006
    Co-Authors: Sylvain Houle, Jeffrey H. Meyer, Nathalie Ginovart, Anahita Boovariwala, Doug Hussey, Eugenii A Rabiner, Alan A Wilson
    Abstract:

    This Article describes the kinetic modeling of [11C]-hArmine binding to MonoAmine OxidAse A (MAO-A) binding sites in the humAn brAin using positron emission tomogrAphy (PET). Positron emission tomogrAphy studies were performed in heAlthy volunteers At plAcebo conditions And After treAtment with clinicAl doses of moclobemide. In either condition, A two-tissue compArtment model (2CM) provided better fits to the dAtA thAn A one-tissue model. EstimAtes of k3/k4 vAlues from An unconstrAined 2CM were highly vAriAble. In contrAst, estimAtes of the specificAlly bound rAdioligAnd distribution volume (DVB) from An unconstrAined 2CM were exceptionAlly stAble, correlAted well with the known distribution of MAO-A in the brAin (cerebellum Al cortex ≈ putAmen Al cortex ≈ cingulAte AlAmus) And thus provided reliAble indices of MAO-A density. TotAl distribution volume (DV) vAlues were Also highly stAble And not different from those estimAted with the LogAn ApproAch. Fixing the DV of free And nonspecificAll...

George Jurjus - One of the best experts on this subject based on the ideXlab platform.

  • The Reduction of R1, A Novel Repressor Protein for MonoAmine OxidAse A, in MAjor Depressive Disorder
    Neuropsychopharmacology, 2011
    Co-Authors: Shakevia Johnson, Jeffrey H. Meyer, Craig A. Stockmeier, Mark C. Austin, Paul R. Albert, Jun Ming Wang, Grazyna Rajkowska, James C. Overholser, Warren L May, George Jurjus
    Abstract:

    The novel trAnscriptionAl repressor protein, R1 (JPO2/CDCA7L/RAM2), inhibits MonoAmine OxidAse A (MAO A) gene expression And influences cell proliferAtion And survivAl. MAO A is implicAted in severAl neuropsychiAtric illnesses And highly elevAted in mAjor depressive disorder (MDD); however, whether R1 is involved in these disorders is unknown. This study evAluAtes the role of R1 in depressed subjects either untreAted or treAted with AntidepressAnt drugs. R1 protein levels were determined in the postmortem prefrontAl cortex of 18 untreAted MDD subjects And 12 medicAted MDD subjects compAred with 18 mAtched psychiAtricAlly normAl control subjects. Western blot AnAlysis showed thAt R1 wAs significAntly decreAsed by 37.5% ( p

  • The reduction of R1, A novel repressor protein for MonoAmine OxidAse A, in mAjor depressive disorder.
    Neuropsychopharmacology, 2011
    Co-Authors: Shakevia Johnson, Jeffrey H. Meyer, Craig A. Stockmeier, Mark C. Austin, Paul R. Albert, Jun Ming Wang, Grazyna Rajkowska, James C. Overholser, George Jurjus
    Abstract:

    The Reduction of R1, A Novel Repressor Protein for MonoAmine OxidAse A, in MAjor Depressive Disorder

Jean C. Shih - One of the best experts on this subject based on the ideXlab platform.

  • MonoAmine OxidAse A inhibitor neAr infrAred dye conjugAte reduces prostAte tumor growth
    Journal of the American Chemical Society, 2015
    Co-Authors: Tzuping Lin, Haiyen E Zhau, Leland W K Chung, John Gallagher, Swati Kushal, Bogdan Olenyuk, Jean C. Shih
    Abstract:

    Development of Anti-cAncer Agents with high tumor-tArgeting specificity And efficAcy is criticAl for modern multidisciplinAry cAncer reseArch. MonoAmine OxidAse A (MAOA), A mitochondriA-bound enzyme, degrAdes MonoAmine neurotrAnsmitters And dietAry MonoAmines. Recent evidence suggests A correlAtion between increAsed MAOA expression And prostAte cAncer (PCA) progression with poor outcomes for pAtients. MAOA induces epitheliAl-mesenchymAl trAnsition (EMT) And Augments hypoxic effects by producing excess reActive oxygen species. Thus, development of MAOA inhibitors which selectively tArget tumors becomes An importAnt goAl in cAncer phArmAcology. Here we describe the design, synthesis, And in vitro And in vivo evAluAtion of NMI, A conjugAte thAt combines A neAr-infrAred dye for tumor tArgeting with the moiety derived from the MAOA inhibitor clorgyline. NMI inhibits MAOA with low micromolAr IC50, suppresses PCA cell proliferAtion And colony formAtion, And reduces migrAtion And invAsion. In mouse PCA xenogrAfts, NMI tArgets tumors with no detectAble AccumulAtion in normAl tissues, providing effective reduction of the tumor burden. AnAlysis of tumor specimens shows reduction in Ki-67(+) And CD31(+) cells, suggesting A decreAse of cell proliferAtion And Angiogenesis And An increAse in M30(+) cells, indicAting increAsed Apoptosis. Gene expression profiles of tumors treAted with NMI demonstrAte reduced expression of oncogenes FOS, JUN, NFKB, And MYC And cell cycle regulAtors CCND1, CCNE1, And CDK4/6, Along with increAses in the levels of tumor suppressor gene TP53, cell cycle inhibitors CDKN1A And CDKN2A, And MAOA-downstreAm genes thAt promote EMT, tumor hypoxiA, cAncer cell migrAtion, And invAsion. These dAtA suggest thAt NMI exerts its effect through tumor-tArgeted delivery of A MAOA-inActivAting group, mAking NMI A vAluAble Anti-tumor Agent.

  • MonoAmine OxidAse A mediAtes prostAte tumorigenesis And cAncer metAstAsis
    Journal of Clinical Investigation, 2014
    Co-Authors: Chen Shao, Jean C. Shih, Changhong Shi, Yiting Chen, Fei Yin, Chunpeng Liao, Bangyan L Stiles, Haiyen E Zhau, Leland W K Chung
    Abstract:

    Tumors from pAtients with high-grAde Aggressive prostAte cAncer (PCA) exhibit increAsed expression of MonoAmine OxidAse A (MAOA), A mitochondriAl enzyme thAt degrAdes MonoAmine neurotrAnsmitters And dietAry Amines. Despite the AssociAtion between MAOA And Aggressive PCA, it is uncleAr how MAOA promotes PCA progression. Here, we found thAt MAOA functions to induce epitheliAl-to-mesenchymAl trAnsition (EMT) And stAbilize the trAnscription fActor HIF1α, which mediAtes hypoxiA through An elevAtion of ROS, thus enhAncing growth, invAsiveness, And metAstAsis of PCA cells. Knockdown And overexpression of MAOA in humAn PCA cell lines indicAted thAt MAOA induces EMT through ActivAtion of VEGF And its coreceptor neuropilin-1. MAOA-dependent ActivAtion of neuropilin-1 promoted AKT/FOXO1/TWIST1 signAling, Allowing FOXO1 binding At the TWIST1 promoter. ImportAntly, the MAOA-dependent HIF1α/VEGF-A/FOXO1/TWIST1 pAthwAy wAs ActivAted in high-grAde PCA specimens, And knockdown of MAOA reduced or even eliminAted prostAte tumor growth And metAstAsis in PCA xenogrAft mouse models. PhArmAcologicAl inhibition of MAOA Activity Also reduced PCA xenogrAft growth in mice. Moreover, high MAOA expression in PCA tissues correlAted with worse clinicAl outcomes in PCA pAtients. These findings collectively chArActerize the contribution of MAOA in PCA pAthogenesis And suggest thAt MAOA hAs potentiAl As A therApeutic tArget in PCA.

  • RegulAtion of MonoAmine OxidAse A by the SRY gene on the Y chromosome
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009
    Co-Authors: Kevin Chen, Yun-fai Chris Lau, Jean C. Shih
    Abstract:

    MonoAmine OxidAse A (MAO A), encoded by the X chromosome, cAtAlyzes the oxidAtive deAminAtion of MonoAmine neurotrAnsmitters, such As serotonin, And plAys A criticAlly importAnt role in brAin development And functions. AbnormAl MAO A Activity hAs been implicAted in severAl neuropsychiAtric disorders, such As depression, Autism, And Attention deficit hyperActivity disorder, which show sexuAl dimorphism. However, the moleculAr bAsis for these diseAse processes is uncleAr. Recently, we found thAt MAO A wAs A putAtive tArget gene directly regulAted by A trAnscription fActor encoded by the sex-determining region Y (SRY) gene locAted on the Y chromosome. We demonstrAted thAt SRY ActivAtes both MAO A-promoter And cAtAlytic Activities in A humAn mAle neuroblAstomA BE(2)C cell line. A functionAl SRY-binding site in the MAO A core promoter wAs identified And vAlidAted by electrophoretic mobility shift And chromAtin immunoprecipitAtion (ChIP) AnAlyses. CoimmunoprecipitAtion And ChIP AssAys showed thAt SRY And Sp1 form A trAnscriptionAl complex And synergisticAlly ActivAte MAO A trAnscription. This is the first study demonstrAting thAt the Y-encoded trAnscription fActor SRY is cApAble of regulAting An X-locAted gene, suggesting A novel moleculAr mechAnism for sexuAl dimorphism in neurAl development, brAin functions, And initiAtion/progression of neurAl disorders AssociAted with MAO A dysfunction.—Wu, J. B., Chen, K., Li, Y., LAu, Y.-F. C., Shih, J. C. RegulAtion of MonoAmine OxidAse A by the SRY gene on the Y chromosome.

  • novel MonoAmine OxidAse A knock out mice with humAn like spontAneous mutAtion
    Neuroreport, 2008
    Co-Authors: Anna L Scott, Kevin Chen, Marco Bortolato, Jean C. Shih
    Abstract:

    A novel line of mutAnt mice [MonoAmine OxidAse A knockout (MAOAA863T KO)] hArboring A spontAneous point nonsense mutAtion in exon 8 of the MAO A gene wAs serendipitously identified in A 129/SvEvTAc colony. This mutAtion is AnAlogous to the cAuse of A rAre humAn disorder, Brunner syndrome, chArActerized by complete MAO A deficiency And impulsive Aggressiveness. Concurrent with previous studies of MAO A KO mice generAted by insertionAl mutAgenesis (‘Tg8’), MAOAA863T KO lAck MAO A enzyme Activity And displAy enhAnced Aggression towArd intruder mice. MAOAA863T KO, however, exhibited lower locomotor Activity in A novel, inescApAble open field And similAr immobility during tAil suspension compAred with wild type, observAtions which differ from reports of Tg8. These findings consolidAte evidence linking MAO A to Aggression And highlight subtle yet distinctive phenotypicAl chArActeristics.

  • glucocorticoid And Androgen ActivAtion of MonoAmine OxidAse A is regulAted differently by r1 And sp1
    Journal of Biological Chemistry, 2006
    Co-Authors: Kevin Chen, Jean C. Shih
    Abstract:

    MonoAmine OxidAse (MAO) A is A key enzyme for the degrAdAtion of neurotrAnsmitters serotonin, norepinephrine, And dopAmine. There Are three consensus glucocorticoid/Androgen response elements And four Sp1-binding sites in the humAn MonoAmine OxidAse A 2-kb promoter. A novel trAnscription fActor R1 (RAM2/CDCA7L) interActs with Sp1-binding sites And represses MAO A gene expression. LuciferAse AssAys show thAt glucocorticoid (dexAmethAsone) And Androgen (R1881) increAse MAO A promoter And cAtAlytic Activities in humAn neuroblAstomA And glioblAstomA cells. Gel-shift AnAlysis demonstrAtes thAt glucocorticoid/Androgen receptors interAct directly with the third glucocorticoid/Androgen response element. Glucocorticoid/Androgen receptors Also interAct with Sp1-binding sites indirectly viA trAnscription fActor Sp1. In Addition, dexAmethAsone induces R1 trAnslocAtion from the cytosol to the nucleus in A time-dependent mAnner in both the neuroblAstomA And wild-type UW228 cell lines but not in R1 knock-down UW228 cells. In summAry, this study shows thAt glucocorticoid enhAnces MonoAmine OxidAse A gene expression by 1) regulAtion of R1 trAnslocAtion; 2) direct interAction of the glucocorticoid receptor with the third glucocorticoid/Androgen response element; And 3) indirect interAction of glucocorticoid receptor with the Sp1 or R1 trAnscription fActor on Sp1-binding sites of the MAO A promoter. Androgen Also up-regulAtes MAO A gene expression by direct interAction of Androgen receptor with the third glucocorticoid/Androgen response element. Androgen receptor indirectly interActs with the Sp1, but not R1 trAnscription fActor, on Sp1-binding sites. This study provides new insights on the differentiAl regulAtion of MAO A by glucocorticoid And Androgen.

Rona R Ramsay - One of the best experts on this subject based on the ideXlab platform.

  • ciproxifAn A histAmine h 3 receptor AntAgonist reversibly inhibits MonoAmine OxidAse A And b
    Scientific Reports, 2017
    Co-Authors: Stefanie Hagenow, Rona R Ramsay, Anna Stasiak, Holger Stark
    Abstract:

    CiproxifAn is A well-investigAted histAmine H3 receptor (H3R) inverse Agonist/AntAgonist, showing An exclusively high species-specific Affinity At rodent compAred to humAn H3R. It is well studied As reference compound for H3R in rodent models for neurologicAl diseAses connected with neurotrAnsmitter dysregulAtion, e.g. Attention deficit hyperActivity disorder or Alzheimer's diseAse. In A screening for potentiAl MonoAmine OxidAse A And B inhibition ciproxifAn showed efficAcy on both enzyme isoforms. Further chArActerizAtion of ciproxifAn reveAled IC50 vAlues in A micromolAr concentrAtion rAnge for humAn And rAt MonoAmine OxidAses with slight preference for MonoAmine OxidAse B in both species. The inhibition by ciproxifAn wAs reversible for both humAn isoforms. RegArding inhibitory potency of ciproxifAn on rAt brAin MAO, these findings should be considered, when using high doses in rAt models for neurologicAl diseAses. As the H3R And MonoAmine OxidAses Are All cApAble of Affecting neurotrAnsmitter modulAtion in brAin, we consider duAl tArgeting ligAnds As interesting ApproAch for treAtment of neurologicAl disorders. Since ciproxifAn shows only moderAte Activity At humAn tArgets, further investigAtions in AnimAls Are not of primAry interest. On the other hAnd, it mAy serve As stArting point for the development of duAl tArgeting ligAnds.

  • DietAry inhibitors of MonoAmine OxidAse A
    Journal of Neural Transmission, 2011
    Co-Authors: Sarah E. Dixon Clarke, Rona R Ramsay
    Abstract:

    Inhibition of MonoAmine OxidAse is one wAy to treAt depression And Anxiety. The informAtion now AvAilAble on the phArmAcokinetics of flAvonoids And of the components of tobAcco prompted An explorAtion of whether A heAlthy diet (with or without smoking) provides Active compounds in Amounts sufficient to pArtiAlly inhibit MonoAmine OxidAse. A literAture seArch wAs used to identify dietAry MonoAmine OxidAse inhibitors, the levels of these compounds in foods, the phArmAcokinetics of the Absorption And distribution, And tissue levels observed. An estimAted dAily intAke And the expected tissue concentrAtions were compAred with the meAsured efficAcies of the compounds As inhibitors of MonoAmine OxidAses. NorhArmAn, hArmAn And quercetin dietAry presence, phArmAcokinetics, And tissue levels were consistent with significAnt levels reAching neuronAl MonoAmine OxidAse from the diet or smoking; 1,2,3,4-tetrAhydroisoquinoline, eugenol, 1-piperoylpiperidine, And coumArin were not. Quercetin wAs equipotent with norhArmAn As A MonoAmine OxidAse A inhibitor And its metAbolite, isorhAmnetin, Also inhibits. TotAl quercetin wAs the highest of the compounds in the sAmple diet. Although bioAvAilAbility wAs vAriAble depending on the source, A heAlthy diet contAins Amounts of quercetin thAt might give sufficient Amounts in brAin to induce, by MonoAmine OxidAse A inhibition, A smAll decreAse in neurotrAnsmitter breAkdown.

  • identificAtion of 4 substituted 1 2 3 triAzoles As novel oxAzolidinone AntibActeriAl Agents with reduced Activity AgAinst MonoAmine OxidAse A
    Journal of Medicinal Chemistry, 2005
    Co-Authors: Folke Reck, Marc Girardo, Charles J Eyerma, Neil James Hales, Rona R Ramsay, Fei Zhou, Michael Gravestock
    Abstract:

    OxAzolidinones represent A new And promising clAss of AntibActeriAl Agents. Current reseArch in this AreA is mAinly concentrAted on improving the sAfety profile And the AntibActeriAl spectrum. MAny oxAzolidinones, including linezolid (mArketed As Zyvox), Are inhibitors of MonoAmine OxidAse A (MAO-A), which presents An undesired side effect. Recently, it wAs found thAt the 1,2,3-triAzole is A good replAcement for the conventionAl AcetAmide functionAlity found in oxAzolidinones. We now disclose the finding thAt 1,2,3-triAzoles beAring A substituent like methyl, smAll substituted methyl, bromo, or A lineAr (sp-hybridized) group At the 4 position (compounds such As 5, 16, 19, And 21) Are good AntibActeriAls with reduced or no Activity, within the detection limit of the AssAy, AgAinst MAO-A. The results Are especiAlly promising for the development of oxAzolidinones with An improved sAfety profile. The MAO-A SAR cAn be rAtionAlized on the bAsis of docking studies to A MAO-A/MAO-B homology model.

  • Kinetic mechAnism of MonoAmine OxidAse A.
    Biochemistry, 1991
    Co-Authors: Rona R Ramsay
    Abstract:

    SteAdy-stAte kinetic dAtA for MonoAmine OxidAse A in crude extrActs suggest An exclusively ping-pong mechAnism, in contrAst to those for MonoAmine OxidAse B, which indicAte AlternAte mechAnisms involving either A binAry or ternAry complex. In this study, with use of purified MonoAmine OxidAse A, steAdy-stAte dAtA for the inhibition by D-AmphetAmine of the oxidAtion of primAry Amines indicAte the possibility of A ternAry complex mechAnism for MonoAmine OxidAse A Also. Stopped-flow studies demonstrAte thAt the rAte of reoxidAtion of reduced enzyme is enhAnced by substrAtes but not by the product, 1-methyl-4-phenylpyridinium. Thus, for the A enzyme, the ternAry complex with substrAte, but not product, is reoxidized At A fAster rAte thAn the free, reduced enzyme. For both the A And B forms of MonoAmine OxidAse, the mechAnism is determined by competition between AlternAte pAthwAys on the bAsis of the relAtive rAte constAnts And dissociAtion constAnts.

Shakevia Johnson - One of the best experts on this subject based on the ideXlab platform.

  • The Reduction of R1, A Novel Repressor Protein for MonoAmine OxidAse A, in MAjor Depressive Disorder
    Neuropsychopharmacology, 2011
    Co-Authors: Shakevia Johnson, Jeffrey H. Meyer, Craig A. Stockmeier, Mark C. Austin, Paul R. Albert, Jun Ming Wang, Grazyna Rajkowska, James C. Overholser, Warren L May, George Jurjus
    Abstract:

    The novel trAnscriptionAl repressor protein, R1 (JPO2/CDCA7L/RAM2), inhibits MonoAmine OxidAse A (MAO A) gene expression And influences cell proliferAtion And survivAl. MAO A is implicAted in severAl neuropsychiAtric illnesses And highly elevAted in mAjor depressive disorder (MDD); however, whether R1 is involved in these disorders is unknown. This study evAluAtes the role of R1 in depressed subjects either untreAted or treAted with AntidepressAnt drugs. R1 protein levels were determined in the postmortem prefrontAl cortex of 18 untreAted MDD subjects And 12 medicAted MDD subjects compAred with 18 mAtched psychiAtricAlly normAl control subjects. Western blot AnAlysis showed thAt R1 wAs significAntly decreAsed by 37.5% ( p

  • The reduction of R1, A novel repressor protein for MonoAmine OxidAse A, in mAjor depressive disorder.
    Neuropsychopharmacology, 2011
    Co-Authors: Shakevia Johnson, Jeffrey H. Meyer, Craig A. Stockmeier, Mark C. Austin, Paul R. Albert, Jun Ming Wang, Grazyna Rajkowska, James C. Overholser, George Jurjus
    Abstract:

    The Reduction of R1, A Novel Repressor Protein for MonoAmine OxidAse A, in MAjor Depressive Disorder