A common mechanism of action for three mood-stabilizing drugs. - Wikidata - wikimedia - TriplyDB

A common mechanism of action for three mood-stabilizing drugs.

A common mechanism of action for three mood-stabilizing drugs.

http://www.wikidata.org/entity/Q34128871

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Evaluation of expression and function of the H+/myo-inositol transporter HMIT Deletion of PREPL, a gene encoding a putative serine oligopeptidase, in patients with hypotonia-cystinuria syndrome.An epigenetic mouse model for molecular and behavioral neuropathologies related to schizophrenia vulnerability.Calbindin D28k targets myo-inositol monophosphatase in spines and dendrites of cerebellar Purkinje neurons A safe lithium mimetic for bipolar disorder GSK-3: tricks of the trade for a multi-tasking kinase The role of lithium in the treatment of bipolar disorder: convergent evidence for neurotrophic effects as a unifying hypothesis The mood stabiliser lithium suppresses PIP3 signalling in Dictyostelium and human cells.Crawling into a new era-the Dictyostelium genome project Mitochondrial dysfunction in psychiatric morbidity: current evidence and therapeutic prospects Review of pharmacological treatment in mood disorders and future directions for drug development.Lithium and autophagy A review of MR spectroscopy studies of pediatric bipolar disorder The delicate balance between secreted protein folding and endoplasmic reticulum-associated degradation in human physiology Investigating the effect of emetic compounds on chemotaxis in Dictyostelium identifies a non-sentient model for bitter and hot tastant research Electrostatic effects and binding determinants in the catalysis of prolyl oligopeptidase. Site specific mutagenesis at the oxyanion binding site The structure of the 1L-myo-inositol-1-phosphate synthase-NAD+-2-deoxy-D-glucitol 6-(E)-vinylhomophosphonate complex demands a revision of the enzyme mechanism Cellular plasticity cascades in the pathophysiology and treatment of bipolar disorder The MARCKS family of phospholipid binding proteins: regulation of phospholipase D and other cellular components Lithium and bipolar mood disorder: the inositol-depletion hypothesis revisited Molecular actions and clinical pharmacogenetics of lithium therapy Structural analysis of prolyl oligopeptidases using molecular docking and dynamics: insights into conformational changes and ligand binding Prophylactic valproic acid treatment prevents schizophrenia-related behaviour in Disc1-L100P mutant mice Valproic acid induces astrocyte-dependent neurite outgrowth from cultured rat primary cortical neuron via modulation of tPA/PAI-1 activity Identification of pathways for bipolar disorder: a meta-analysis The effectiveness of anticonvulsants in psychiatric disorders Seizure control by ketogenic diet-associated medium chain fatty acids Glucose transporters in the 21st Century Glycogen synthase kinase-3beta haploinsufficiency mimics the behavioral and molecular effects of lithium Defective craniofacial development and brain function in a mouse model for depletion of intracellular inositol synthesis.Lithium administration to preadolescent rats causes long-lasting increases in anxiety-like behavior and has molecular consequences.Deletion of GSK3β in D2R-expressing neurons reveals distinct roles for β-arrestin signaling in antipsychotic and lithium action.Attenuation of phospholipid signaling provides a novel mechanism for the action of valproic acid.Valproate attenuates accelerated atherosclerosis in hyperglycemic apoE-deficient mice: evidence in support of a role for endoplasmic reticulum stress and glycogen synthase kinase-3 in lesion development and hepatic steatosis.Label-free, live optical imaging of reprogrammed bipolar disorder patient-derived cells reveals a functional correlate of lithium responsiveness.Myo-inositol monophosphatase is an activated target of calbindin D28k.Subtraction libraries for the molecular characterization of gene-environmental interactions in bipolar disorder.Peptidomics of prolyl endopeptidase in the central nervous system.Bipolar disorder and myo-inositol: a review of the magnetic resonance spectroscopy findings.Comparative analysis of the effects of four mood stabilizers in SH-SY5Y cells and in primary neurons.

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P2860

A common mechanism of action for three mood-stabilizing drugs.

http://www.wikidata.org/entity/Q34128871

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2002 nî lūn-bûn

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2002 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年论文

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name

A common mechanism of action for three mood-stabilizing drugs.

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A common mechanism of action for three mood-stabilizing drugs.

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A common mechanism of action for three mood-stabilizing drugs.

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type

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A common mechanism of action for three mood-stabilizing drugs.

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A common mechanism of action for three mood-stabilizing drugs.

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A common mechanism of action for three mood-stabilizing drugs.

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A common mechanism of action for three mood-stabilizing drugs.

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A common mechanism of action for three mood-stabilizing drugs.

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A common mechanism of action for three mood-stabilizing drugs.

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Adrian J Harwood

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Anne W Mudge

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Lili Cheng

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Robin S B Williams

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P2860

A molecular mechanism for the effect of lithium on development

Chronic lithium and sodium valproate both decrease the concentration of myo-inositol and increase the concentration of inositol monophosphates in rat brain

Neural and developmental actions of lithium: a unifying hypothesis

Alterations in plasma prolyl endopeptidase activity in depression, mania, and schizophrenia: effects of antidepressants, mood stabilizers, and antipsychotic drugs

Axonal remodeling and synaptic differentiation in the cerebellum is regulated by WNT-7a signaling

Cultured Schwann cells constitutively express the myelin protein P0

WNT-7a induces axonal remodeling and increases synapsin I levels in cerebellar neurons

Identification of Novel Graded Polarity Actin Filament Bundles in Locomoting Heart Fibroblasts: Implications for the Generation of Motile Force

The axis-inducing activity, stability, and subcellular distribution of beta-catenin is regulated in Xenopus embryos by glycogen synthase kinase 3

Histone deacetylase is a direct target of valproic acid, a potent anticonvulsant, mood stabilizer, and teratogen

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