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Human MECP2 Protein expressed in Wheat germ - ABIN1310622
Nott, Cheng, Gao, Lin, Gjoneska, Ko, Minhas, Zamudio, Meng, Zhang, Jin, Tsai: Histone deacetylase 3 associates with MeCP2 to regulate FOXO and social behavior. in Nature neuroscience 2016
The reported loss of the MECP2 function induced by the simulated mutations can be ascribed to both stabilizing and destabilizing effect on DNA binding.
Low MECP2 expression is associated with pancreatic cancer.
There are AT-hook motifs in MeCP2 which can bind with AT-rich DNA, suggesting a role in chromatin binding. This study reports the identification and characterization of another AT-rich DNA binding motif (residues 295 to 313) from the C-terminal transcription repression domain of MeCP2 by nuclear magnetic resonance (NMR) and isothermal calorimetry .
glycogenes can be either up- or down-regulated by MeCP2 directly or indirectly to alter the glycopatterning and affect the proliferation and apoptosis of gastric cancer cells.
The MeCP2, a protein whose mutated forms are involved in Rett syndrome; and CTCF (zeige CTCF Proteine), a constitutive transcriptional insulator.
MECP2 promotes the proliferation of gastric cancer cells via miR (zeige MLXIP Proteine)-338 (miR (zeige MLXIP Proteine)-338-3p and miR (zeige MLXIP Proteine)-338-5p)-mediated antitumor and gene regulatory effect.
The genetic etiology of Rett syndrome (RTT) without MECP2, CDKL5 (zeige CDKL5 Proteine), and FOXG1 (zeige FOXG1 Proteine) mutations is heterogeneous, overlaps with other NDDs, and complicated by a high mutation burden. Dysregulation of chromatin structure and abnormal excitatory synaptic signaling may form two common pathological bases of RTT.
We provided the largest known Chinese pedigree with MECP2 duplication syndrome. X-chromosome inactivation (XCI) analysis on AR gene was detected for all female family members, and the microsatellite analysis on MECP2 was used to validate the recombination event on MECP2 region.
Until the mechanisms of sudden death and the basis for the QTc prolongation in a few RTT subjects are better understood, caution is advised when attempting to predict risk of sudden death in individuals with MECP2 mutations based on minimally increased QTc interval
MECP2 is regulated post-transcriptionally during in vitro differentiation of human embryonic stem cells (hESCs) into cortical neurons.
Here the authors show that hyperactivation of the interleukin 1 pathway, through either ablation of the interleukin 1 receptor 8 (IL-1R8, also known as SIGIRR or Tir8) or activation of IL-1R, leads to up-regulation of the mTOR pathway and increased levels of the epigenetic regulator MeCP2, bringing to disruption of dendritic spine morphology, synaptic plasticity and plasticity-related gene expression.
The authors show that BDNF acts cell autonomous and autocrine, as wildtype neurons are not capable of rescuing growth deficits in neighboring MeCP2 deficient neurons in vitro and in vivo.
MeCP2 is critical for normal function of cholinergic neurons and dysfunction of cholinergic neurons can contribute to numerous neuropsychiatric phenotypes.
Study found that cholinergic MeCP2 preservation could reverse some aspects of the Rett syndrome-like phenotypes in mice including hypolocomotion and increased anxiety level, and delay the onset of underweight, instead of improving the hypersocial abnormality and the poor general conditions such as short lifespan, low brain weight, and increasing severity score.
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 (zeige BAAT Proteine)). Specifically, mutagenesis of a BAT (zeige BAAT Proteine)-resident Cx3Cr1 (zeige CX3CR1 Proteine)+ macrophage subpopulation compromised homeostatic thermogenesis but not acute, cold-induced thermogenesis. This was associated with diminished sympathetic innervation and local titers of norepinephrine.
that histone deacetylase 3 (zeige HDAC3 Proteine) interaction with MeCP2 positively regulates a subset of neuronal genes through FOXO (zeige FOXO3 Proteine) deacetylation, and disruption of HDAC3 (zeige HDAC3 Proteine) contributes to cognitive and social impairment
a proteomic analysis to examine protein expression changes in mecp2-null vs. wild-type larvae and adult zebrafish
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