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DNA methylation is the major modification of eukaryotic genomes and plays an essential role in mammalian development.
A mecp2-null allele mutation zebrafish model is developed and the animals are viable and fertile.
absence leads to decreased cortical levels of the GAT-1 GABA transporter, facilitating cortical network hyper-excitability by increasing the activity of cortical GABAB receptors
Knockdown of methyl-CpG-binding protein leads to upregulation of microRNA-137, which in turn represses expression of PTEN protein.
Study demonstrates that the time course of N-methyl-D-aspartate receptor (show GRIN1 Proteins) maturation is cell-type specific, and a new cell-type specific role for Mecp2 in the development of -methyl-D-aspartate receptor subunit composition.
Data highlight functional hypoconnectivity in the medial prefrontal cortex as a potential substrate for behavioral disruption in Rett syndrome and other disorders associated with reduced expression of Mecp2 in frontal cortical regions.
These findings indicate that tongue heat sensitivity and hypersensitivity are dependent on the expression of transient receptor potential vanilloid 1 which is regulated via MeCP2 signaling in trigeminal ganglion neurons innervating the tongue.
We treated MeCP2-null mice from postnatal-day 28 for two weeks with desipramine, already tested in Rett syndrome , or mirtazapine, an antidepressant with limited side-effects, known to promote GABA release
these results suggested that MeCP2 facilitated Tet3 activity, enhanced expression of pluripotency-related genes, and eventually improved the development of NT embryos.
The molecular basis of variable phenotypic severity among common MECP2 missense mutations causing Rett syndrome has been described.
Study showed that Mecp2 de fi ciency causes a reduced amplitude in the PER2 (show PER2 Proteins) expression rhythms of the suprachiasmatic nucleus providing a new insight into behavioral dysfunction caused by Mecp2 de fi ciency in Rett syndrome.
Cigarette smoke induces proteosomal-mediated degradation of MeCP-2 in embryonic orofacial cells.
The monkeys transmitted both multiple MECP2 genes and social deficits on to a second generation of monkeys, who did not interact as frequently as did normal monkeys
The MECP2 gene is mutated in 80% of patients with classic Rett syndrome, as well as in 40% of those affected by any of its atypical forms
Xq28 duplication involving MECP2 is associated with brain diseases.
A statistically significant difference was observed in the rs2239464 and rs2075596 polymorphisms of MECP2 between Systemic lupus erythematosus subjects and controls.
We generated induced pluripotent stem cells (iPSCs) from patients with the MECP2 duplication syndrome (MECP2dup), carrying different duplication sizes, to study the impact of increased MeCP2 dosage in human neurons
Study shows that MECP2 is commonly amplified oncogene (show RAB1A Proteins) in human malignancies with a unique epigenetic mechanism of action where its binding to 5-hydroxymethylcytosine is important for its anchorage-independent growth.
The aim of the present study was to evaluate the potential of MeCP2 for use as a therapeutic target for human colorectal cancer.
Functional performance in Rett syndrome patients may relate to the type of Mecp2 mutation
The MECP-2 is the direct targets of miR (show MLXIP Proteins)-370 and miR (show MLXIP Proteins)-373, respectively, in human articular chondrocytes.
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
, meCP-2 protein
, methyl-CpG-binding protein MeCP2