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MECP2 is regulated post-transcriptionally during in vitro differentiation of human embryonic stem cells (hESCs) into cortical neurons.
Large nuclear foci of high-copy satellite II RNA form and sequester copious MeCP2 into Cancer-Associated Satellite Transcript (CAST) bodies.
We describe here the first case of MECP2-related severe neonatal encephalopathy caused by a mutation in exon one of MECP2, a mutation rarely identified in females with Rett syndrome
DNA methylation of decoys alone did not affect target search kinetics. In the presence of the MeCP2 methyl-CpG-binding domain (MBD), however, DNA methylation of decoys substantially ( approximately 10-30-fold) accelerated the target search process of the Egr-1 zinc-finger protein. This acceleration did not occur when the target was also methylated.
When it binds methylated/hydroxymethylated DNA, MeCP2 recruits various interacting protein and RNA partners, resulting in a highly specialized chromatin organization wherein linker histones and MeCP2 share an organizational role that dynamically changes during neuronal development. MeCP2 mutations alter its chromatin-binding dynamics and interactions with some of its partners, causing Rett syndrome. Review.
MeCP2 regulates IGF1 (show IGF1 ELISA Kits) and BDNF (show BDNF ELISA Kits) levels, and when this gene is mutated both proteins have their expression decreased. In our study, we show that IGF1 (show IGF1 ELISA Kits) gene expression was not different between control and RTT neurons. Interestingly, IGF1R (show IGF1R ELISA Kits) has its gene expression increased in RTT neural cells compared to control
The expression of Rb and MeCP2 in patients with B-cell non-Hodgkin's lymphoma (B-NHL (show RTEL1 ELISA Kits)) showed that positive staining for MeCP2 or Rb was significantly lower in B-NHL (show RTEL1 ELISA Kits) tumor tissues, and these changes were significantly and negatively correlated with the grade of B-NHL (show RTEL1 ELISA Kits).
MECP2 was increased at both mRNA and protein levels in gastric cancer (GC) compared with paracancerous tissues; MECP2 positive expression was correlated with the TNM stages, histological types, and lymph node metastasis status, but not with sex or age; dysregulated expression of MECP2 in GC and its correlation to clinicopathological parameters indicate that MECP2 may regulate the development of GC
that histone deacetylase 3 (show HDAC3 ELISA Kits) interaction with MeCP2 positively regulates a subset of neuronal genes through FOXO (show FOXO3 ELISA Kits) deacetylation, and disruption of HDAC3 (show HDAC3 ELISA Kits) contributes to cognitive and social impairment
C- and N-terminal interactions are required for healthy function of MeCP2.
Here the authors show that genetically restoring Mecp2 expression only in GABAergic neurons of male Mecp2 null mice enhanced inhibitory signaling, extended lifespan, and rescued ataxia, apraxia, and social abnormalities but did not rescue tremor or anxiety.
MeCP2 deficiency in glutamatergic neurons leads to early lethality, obesity, tremor, altered anxiety-like behaviors, and impaired acoustic startle response, which is distinct from the phenotype of mice lacking MeCP2 only in inhibitory neurons.
these findings demonstrate that increasing MeCP2 T158M protein expression is sufficient to mitigate Rett syndrome-like phenotypes and support the targeting of MeCP2 T158M expression or stability as an alternative therapeutic approach.
Loss of Mecp2 is associated with Rett syndrome.
Mice that lacked Mecp2 in macrophages displayed spontaneous obesity, which was linked to impaired function of brown adipose tissue (BAT (show BAAT ELISA Kits)). Specifically, mutagenesis of a BAT (show BAAT ELISA Kits)-resident Cx3Cr1 (show CX3CR1 ELISA Kits)+ macrophage subpopulation compromised homeostatic thermogenesis but not acute, cold-induced thermogenesis. This was associated with diminished sympathetic innervation and local titers of norepinephrine.
provide new insight into the upstream regulation of Sap90/Psd95 (show DLG4 ELISA Kits)-associated protein 3 (show HSPB3 ELISA Kits) and establish the essential role of striatal Hdac1 (show HDAC1 ELISA Kits), Hdac2 (show HDAC2 ELISA Kits) and MeCP2 for suppression of repetitive behaviors
These findings position MeCP2 as a novel component in metabolic homeostasis. We previously showed that treatment of Mecp2 mice with statin drugs alleviated motor symptoms and improved health and longevity. Lipid metabolism is a highly treatable target; therefore, our results shed light on new metabolic pathways for treatment of Rett syndrome
MeCP2 dysfunction in excitatory neurons mediated elevated synchrony at baseline, while MeCP2 dysfunction in inhibitory neurons increased susceptibility to hypersynchronization in response to perturbations.
Loss of MeCP2 causes urological dysfunction and contributes to death by kidney failure in a mouse model of Rett syndrome.
A mecp2-null allele mutation zebrafish model is developed and the animals are viable and fertile.
DNA methylation is the major modification of eukaryotic genomes and plays an essential role in mammalian development. Human proteins MECP2, MBD1, MBD2, MBD3, and MBD4 comprise a family of nuclear proteins related by the presence in each of a methyl-CpG binding domain (MBD). Each of these proteins, with the exception of MBD3, is capable of binding specifically to methylated DNA. MECP2, MBD1 and MBD2 can also repress transcription from methylated gene promoters. In contrast to other MBD family members, MECP2 is X-linked and subject to X inactivation. MECP2 is dispensible in stem cells, but is essential for embryonic development. MECP2 gene mutations are the cause of most cases of Rett syndrome, a progressive neurologic developmental disorder and one of the most common causes of mental retardation in females.
, methyl-CpG-binding protein 2
, meCP-2 protein
, methyl-CpG-binding protein MeCP2