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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.
Study shows that embryonic primary cortical neurons of Mecp2 null mice display reduced neurite complexity possibly reflecting transcriptional changes that occur long before onset of Rett symptoms.
MeCP2 binding downstream of promoters correlates with increased expression in Mecp2-deficient neurons. Genome-wide association with methylation is in part due to MeCP2's affinity to GC-rich (show RELB Proteins) chromatin.
MeCP2 induced aggregation of heterochromatin that was enhanced in PARP1 (show PARP1 Proteins)-/- cells.
Findings establish miR (show MLXIP Proteins)-199a as a critical downstream target of MeCP2 in RTT pathogenesis by linking MeCP2 with mTOR (show FRAP1 Proteins) signaling.
Results together reveal an important role of MeCP2 SUMOylation in social interaction, memory and synaptic plasticity, and that abnormal MeCP2 SUMOylation is implicated in Rett syndrome.
These results provide new insight into both the fundamental neurobiology of RTT, and potential therapeutic strategies via NF-kappaB (show NFKB1 Proteins) pathway modulation.
Loss of MeCP2 in astrocytes alone is sufficient to result in a dramatic attenuation of the HCVR.
Disturbance of cardiac gene expression and cardiomyocyte structure predisposes Mecp2-null mice to arrhythmias.
a general deficiency of MeCP2 causes an important muscle hypotrophy that is probably the main cause of hypotonia characterizing most Rett syndrome patients.
The data of this study demonstrated a role for MeCP2 in growth and maturation of newborn granule cells in developing fetal and adult hippocampus
The MECP-2 is the direct targets of miR (show MLXIP Proteins)-370 and miR (show MLXIP Proteins)-373, respectively, in human articular chondrocytes.
revealed a genotype-specific effect of methyl-CpG-binding protein-2 (MeCP2) dysfunction on iPSC-derived neuronal migration and maturation (reduced neurite outgrowth and fewer synapses) in 3D layered hydrogels
Rett Syndrome Mutant Neural Cells Lacks MeCP2 Immunoreactive Bands.
Study suggests that polymorphism in the MECP2 locus is associated with the susceptibility of Iranian patients to systemic lupus erythematosus.
The authors identify NUDT21 (show NUDT21 Proteins) as a novel candidate for intellectual disability and neuropsychiatric disease, and elucidate a mechanism of pathogenesis by MeCP2 dysregulation via altered alternative polyadenylation.
MeCP2 is expressed throughout the gastrointestinal tract (GI). MeCP2 is expressed specifically in the enteric nervous system of the GI.
Study describes the various mutations of MECP2 associated with specific phenotypes and symptoms of Rett syndrome in a large cohort.
MECP2 targets short interspersed nuclear elements, but does not exclude RNA Polymerase III.
MECP2, a gene associated with Rett syndrome in humans, shows conserved coding regions, independent Alu insertions, and a novel transcript across primate evolution
Results show that these antibodies are highly specific for dense fine speckles 70 (show PSIP1 Proteins) protein DFS70 (show PSIP1 Proteins)/LEDGFp75 and do not target methyl CpG binding protein 2 (MeCP2).
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