about
Pathogenesis of lethal cardiac arrhythmias in Mecp2 mutant mice: implication for therapy in Rett syndromeLoss of MeCP2 in aminergic neurons causes cell-autonomous defects in neurotransmitter synthesis and specific behavioral abnormalitiesInsulinotropic treatments exacerbate metabolic syndrome in mice lacking MeCP2 function.Female Mecp2(+/-) mice display robust behavioral deficits on two different genetic backgrounds providing a framework for pre-clinical studies.Regional rescue of spinocerebellar ataxia type 1 phenotypes by 14-3-3epsilon haploinsufficiency in mice underscores complex pathogenicity in neurodegenerationMeCP2 is critical within HoxB1-derived tissues of mice for normal lifespanTreatment of cardiac arrhythmias in a mouse model of Rett syndrome with Na+-channel-blocking antiepileptic drugs.Atoh1 governs the migration of postmitotic neurons that shape respiratory effectiveness at birth and chemoresponsiveness in adulthood.Progressive Changes in a Distributed Neural Circuit Underlie Breathing Abnormalities in Mice Lacking MeCP2.Breathing challenges in Rett syndrome: lessons learned from humans and animal models.Overexpression of methyl-CpG binding protein 2 impairs T(H)1 responses.Reduced hydroperoxidase (HPI and HPII) activity in the Deltafur mutant contributes to increased sensitivity to UVA radiation in Escherichia coli.Effects of sublethal UVA irradiation on activity levels of oxidative defense enzymes and protein oxidation in Escherichia coli.rRNA promoter regulation by nonoptimal binding of sigma region 1.2: an additional recognition element for RNA polymerase.
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description
hulumtues
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researcher
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wetenschapper
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հետազոտող
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name
Christopher S. Ward
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Christopher S. Ward
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Christopher S. Ward
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Christopher S. Ward
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Christopher S. Ward
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type
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Christopher S. Ward
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Christopher S. Ward
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Christopher S. Ward
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Christopher S. Ward
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Christopher S. Ward
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Christopher S. Ward
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Christopher S. Ward
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Christopher S. Ward
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Christopher S. Ward
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Christopher S. Ward
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0000-0002-3445-6327