about
Rett syndrome: revised diagnostic criteria and nomenclaturePathogenesis 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 abnormalitiesRett syndrome: a prototypical neurodevelopmental disorderA partial loss of function allele of methyl-CpG-binding protein 2 predicts a human neurodevelopmental syndromeDysfunction in GABA signalling mediates autism-like stereotypies and Rett syndrome phenotypesFemale Mecp2(+/-) mice display robust behavioral deficits on two different genetic backgrounds providing a framework for pre-clinical studies.Preclinical research in Rett syndrome: setting the foundation for translational success.Developmental delay in Rett syndrome: data from the natural history study.Epilepsy and the natural history of Rett syndrome.Low bone mineral mass is associated with decreased bone formation and diet in girls with Rett syndrome.Rett syndrome diagnostic criteria: lessons from the Natural History StudyPubertal development in Rett syndrome deviates from typical femalesMutual antagonism between Sox10 and NFIA regulates diversification of glial lineages and glioma subtypesComplexities of Rett syndrome and MeCP2MeCP2 is critical within HoxB1-derived tissues of mice for normal lifespanAge of diagnosis in Rett syndrome: patterns of recognition among diagnosticians and risk factors for late diagnosis.Clinical severity and quality of life in children and adolescents with Rett syndromeThe Changing Face of Survival in Rett Syndrome and MECP2-Related Disorders.Origin of a Non-Clarke's Column Division of the Dorsal Spinocerebellar Tract and the Role of Caudal Proprioceptive Neurons in Motor Function.Atoh1 governs the migration of postmitotic neurons that shape respiratory effectiveness at birth and chemoresponsiveness in adulthood.Wild-type microglia do not reverse pathology in mouse models of Rett syndromeProgressive Changes in a Distributed Neural Circuit Underlie Breathing Abnormalities in Mice Lacking MeCP2.Deletion of Mecp2 in Sim1-expressing neurons reveals a critical role for MeCP2 in feeding behavior, aggression, and the response to stress.Specific mutations in methyl-CpG-binding protein 2 confer different severity in Rett syndrome.Breathing challenges in Rett syndrome: lessons learned from humans and animal models.Enrichment of mutations in chromatin regulators in people with Rett syndrome lacking mutations in MECP2.Brief report: MECP2 mutations in people without Rett syndrome.Overexpression of methyl-CpG binding protein 2 impairs T(H)1 responses.Unfolding neurodevelopmental disorders: the mystery of developing connectionsTherapeutic Advances in Autism and Other Neurodevelopmental Disorders.Spinal fluid 5-methyltetrahydrofolate levels are normal in Rett syndrome.Neurologic complications associated with influenza A in children during the 2003-2004 influenza season in Houston, Texas.Increased MECP2 gene copy number as the result of genomic duplication in neurodevelopmentally delayed males.Spatially restricted activation of the SAX receptor by SCW modulates DPP/TKV signaling in Drosophila dorsal-ventral patterning.The Xenopus dorsalizing factor noggin ventralizes Drosophila embryos by preventing DPP from activating its receptor.Erratum: Corrigendum: Wild-type microglia do not reverse pathology in mouse models of Rett syndromeInterested in a career as a clinician-scientist?The array of clinical phenotypes of males with mutations in Methyl-CpG binding protein 2Comparison of core features in four Developmental Encephalopathies in the Rett Natural History Study
P50
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P50
description
onderzoeker
@nl
pediatric researcher
@en
հետազոտող
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name
Jeffrey L. Neul
@ast
Jeffrey L. Neul
@en
Jeffrey L. Neul
@es
Jeffrey L. Neul
@nl
Jeffrey L. Neul
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type
label
Jeffrey L. Neul
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Jeffrey L. Neul
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Jeffrey L. Neul
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Jeffrey L. Neul
@nl
Jeffrey L. Neul
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prefLabel
Jeffrey L. Neul
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Jeffrey L. Neul
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Jeffrey L. Neul
@es
Jeffrey L. Neul
@nl
Jeffrey L. Neul
@sl
P106
P1153
9269111500
P21
P31
P496
0000-0002-5628-5872