The major form of MeCP2 has a novel N-terminus generated by alternative splicing
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The odyssey of MeCP2 and parental imprintingRett syndrome: clinical review and genetic updateModifiers and Readers of DNA Modifications and Their Impact on Genome Structure, Expression, and Stability in DiseaseMeCP2 and the enigmatic organization of brain chromatin. Implications for depression and cocaine addictionDevelopmental Dynamics of Rett SyndromeThe Utility of Next-Generation Sequencing in Gene Discovery for Mutation-Negative Patients with Rett SyndromeRett syndrome - biological pathways leading from MECP2 to disorder phenotypesMeCP2: the chromatin connection and beyondDexamethasone induces a putative repressor complex and chromatin modifications in the CRH promoterA partial loss of function allele of methyl-CpG-binding protein 2 predicts a human neurodevelopmental syndromeAnalysis of protein domains and Rett syndrome mutations indicate that multiple regions influence chromatin-binding dynamics of the chromatin-associated protein MECP2 in vivoGene expression analysis exposes mitochondrial abnormalities in a mouse model of Rett syndromeEx vivo treatment with a novel synthetic aminoglycoside NB54 in primary fibroblasts from Rett syndrome patients suppresses MECP2 nonsense mutationsIUGR differentially alters MeCP2 expression and H3K9Me3 of the PPARĪ³ gene in male and female rat lungs during alveolarizationBdnf overexpression in hippocampal neurons prevents dendritic atrophy caused by Rett-associated MECP2 mutationsThe implications of alternative splicing in the ENCODE protein complementBeyond Widespread Mecp2 Deletions to Model Rett Syndrome: Conditional Spatio-Temporal Knockout, Single-Point Mutations and Transgenic Rescue MiceMice with an isoform-ablating Mecp2 exon 1 mutation recapitulate the neurologic deficits of Rett syndrome.Over-expression of either MECP2_e1 or MECP2_e2 in neuronally differentiated cells results in different patterns of gene expressionExpression profiling of clonal lymphocyte cell cultures from Rett syndrome patientsReduced MeCP2 expression is frequent in autism frontal cortex and correlates with aberrant MECP2 promoter methylationHigh levels of MeCP2 depress MHC class I expression in neuronal cells.Mecp2-null mice provide new neuronal targets for Rett syndrome.Improved MECP2 Gene Therapy Extends the Survival of MeCP2-Null Mice without Apparent Toxicity after Intracisternal Delivery.Experimental Autoimmune Encephalomyelitis (EAE)-Induced Elevated Expression of the E1 Isoform of Methyl CpG Binding Protein 2 (MeCP2E1): Implications in Multiple Sclerosis (MS)-Induced Neurological Disability and Associated Myelin DamageMutations of CDKL5 cause a severe neurodevelopmental disorder with infantile spasms and mental retardation.MeCP2 mutation results in compartment-specific reductions in dendritic branching and spine density in layer 5 motor cortical neurons of YFP-H mice.Cellular commitment in the developing cerebellumNovel MeCP2 isoform-specific antibody reveals the endogenous MeCP2E1 expression in murine brain, primary neurons and astrocytes.Setdb1-mediated histone H3K9 hypermethylation in neurons worsens the neurological phenotype of Mecp2-deficient mice.Experimental models of Rett syndrome based on Mecp2 dysfunction.Brain region-specific expression of MeCP2 isoforms correlates with DNA methylation within Mecp2 regulatory elements.MECP2e1 isoform mutation affects the form and function of neurons derived from Rett syndrome patient iPS cells.CDKL5/STK9 is mutated in Rett syndrome variant with infantile spasmsCAGE-defined promoter regions of the genes implicated in Rett Syndrome.Transgenic complementation of MeCP2 deficiency: phenotypic rescue of Mecp2-null mice by isoform-specific transgenesPartial rescue of MeCP2 deficiency by postnatal activation of MeCP2.Linking epigenetics to human disease and Rett syndrome: the emerging novel and challenging concepts in MeCP2 research.Effects of Mecp2 loss of function in embryonic cortical neurons: a bioinformatics strategy to sort out non-neuronal cells variability from transcriptome profiling.Methyl CpG-binding protein isoform MeCP2_e2 is dispensable for Rett syndrome phenotypes but essential for embryo viability and placenta development.
P2860
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P2860
The major form of MeCP2 has a novel N-terminus generated by alternative splicing
description
2004 Õ©ÕøÖÕ”ÕÆÕ”Õ¶Õ« Õ
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@hyw
2004 Õ©Õ¾Õ”ÕÆÕ”Õ¶Õ« Õ°ÕøÖÕ¶Õ¾Õ”ÖÕ«Õ¶ Õ°ÖÕ”ÕæÕ”ÖÕ”ÕÆÕ¾Õ”Õ® Õ£Õ«ÕæÕ”ÕÆÕ”Õ¶ Õ°ÕøÕ¤Õ¾Õ”Õ®
@hy
artĆculu cientĆficu espublizĆ”u en 2004
@ast
im Januar 2004 verƶffentlichter wissenschaftlicher Artikel
@de
scientific journal article
@en
vedeckĆ½ ÄlĆ”nok (publikovanĆ½ 2004/01/01)
@sk
vÄdeckĆ½ ÄlĆ”nek publikovanĆ½ v roce 2004
@cs
wetenschappelijk artikel (gepubliceerd op 2004/01/01)
@nl
Š½Š°ŃŠŗŠ¾Š²Š° ŃŃŠ°ŃŃŃ, Š¾ŠæŃŠ±Š»ŃŠŗŠ¾Š²Š°Š½Š° Š² ŃŃŃŠ½Ń 2004
@uk
Ł
ŁŲ§ŁŲ© Ų¹ŁŁ
ŁŲ© (ŁŲ“Ų±ŲŖ Ų¹Ų§Ł
2004)
@ar
name
The major form of MeCP2 has a novel N-terminus generated by alternative splicing
@ast
The major form of MeCP2 has a novel N-terminus generated by alternative splicing
@en
The major form of MeCP2 has a novel N-terminus generated by alternative splicing
@nl
type
label
The major form of MeCP2 has a novel N-terminus generated by alternative splicing
@ast
The major form of MeCP2 has a novel N-terminus generated by alternative splicing
@en
The major form of MeCP2 has a novel N-terminus generated by alternative splicing
@nl
prefLabel
The major form of MeCP2 has a novel N-terminus generated by alternative splicing
@ast
The major form of MeCP2 has a novel N-terminus generated by alternative splicing
@en
The major form of MeCP2 has a novel N-terminus generated by alternative splicing
@nl
P2860
P3181
P356
P1476
The major form of MeCP2 has a novel N-terminus generated by alternative splicing
@en
P2860
P304
1818ā1823
P3181
P356
10.1093/NAR/GKH349
P407
P577
2004-01-01T00:00:00Z