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Proteome analysis of schizophrenia patients Wernicke's area reveals an energy metabolism dysregulationSTOP-like protein 21 is a novel member of the STOP family, revealing a Golgi localization of STOP proteinsMicrotubule-associated protein 6 mediates neuronal connectivity through Semaphorin 3E-dependent signalling for axonal growth.Reduced expression of STOP/MAP6 in mice leads to cognitive deficitsBehavioral genetic contributions to the study of addiction-related amphetamine effects.When clocks go bad: neurobehavioural consequences of disrupted circadian timing.Epothilone D prevents binge methamphetamine-mediated loss of striatal dopaminergic markers.Loss of STOP protein impairs peripheral olfactory neurogenesis.Abnormal nociception and opiate sensitivity of STOP null mice exhibiting elevated levels of the endogenous alkaloid morphineNitric oxide synthase mediates the ability of darbepoetin alpha to improve the cognitive performance of STOP null miceUnderstanding schizophrenia as a disorder of consciousness: biological correlates and translational implications from quantum theory perspectives.New horizons in schizophrenia treatment: autophagy protection is coupled with behavioral improvements in a mouse model of schizophreniaSchizophrenia: an integrative approach to modelling a complex disorder.Deletion of the STOP gene, a microtubule stabilizing factor, leads only to discrete cerebral metabolic changes in miceProteome analysis of schizophrenia brain tissue.Phosphorylation of the tubulin-binding protein, stathmin, by Cdk5 and MAP kinases in the brain.Increased Stability of Microtubules in Cultured Olfactory Neuroepithelial Cells from Individuals with Schizophrenia.Chronic administration of atypical antipsychotics improves behavioral and synaptic defects of STOP null mice.3D imaging of the brain morphology and connectivity defects in a model of psychiatric disorders: MAP6-KO mice.Disruptions of Sleep/Wake Patterns in the Stable Tubule Only Polypeptide (STOP) Null Mouse Model of SchizophreniaMicrotubule-associated STOP protein deletion triggers restricted changes in dopaminergic neurotransmission.The deletion of STOP/MAP6 protein in mice triggers highly altered mood and impaired cognitive performances.SHATI/NAT8L regulates neurite outgrowth via microtubule stabilization.MAP6 interacts with Tctex1 and Cav 2.2/N-type calcium channels to regulate calcium signalling in neurons.Both chronic treatments by epothilone D and fluoxetine increase the short-term memory and differentially alter the mood status of STOP/MAP6 KO mice.Altered expression of synaptic protein mRNAs in STOP (MAP6) mutant mice.STOP--in the name of mood: microtubule-associated proteins in mood and cognition.Deficits in social behavior and sensorimotor gating in mice lacking phospholipase Cbeta1.Cytoskeletal changes in diseases of the nervous system
P2860
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P2860
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年学术文章
@wuu
2005年学术文章
@zh
2005年学术文章
@zh-cn
2005年学术文章
@zh-hans
2005年学术文章
@zh-my
2005年学术文章
@zh-sg
2005年學術文章
@yue
2005年學術文章
@zh-hant
name
Dopaminergic transmission in STOP null mice.
@en
Dopaminergic transmission in STOP null mice.
@nl
type
label
Dopaminergic transmission in STOP null mice.
@en
Dopaminergic transmission in STOP null mice.
@nl
prefLabel
Dopaminergic transmission in STOP null mice.
@en
Dopaminergic transmission in STOP null mice.
@nl
P2093
P2860
P1476
Dopaminergic transmission in STOP null mice.
@en
P2093
Annie Schweitzer
Bernard Renaud
Didier Job
Hélène Scarna
Laurence Mouly-Badina
Magali Clerget
Mélina Bégou
Philippe Brun
P2860
P356
10.1111/J.1471-4159.2005.03166.X
P407
P577
2005-07-01T00:00:00Z