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Human Polyclonal MECP2 Primary Antibody for ICC, IF - ABIN269308
LaSalle, Goldstine, Balmer, Greco: Quantitative localization of heterogeneous methyl-CpG-binding protein 2 (MeCP2) expression phenotypes in normal and Rett syndrome brain by laser scanning cytometry. in Human molecular genetics 2001
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Human Monoclonal MECP2 Primary Antibody for ChIP, ICC - ABIN2668836
Ganguly, Chen, Shin, Devaskar: Prenatal caloric restriction enhances DNA methylation and MeCP2 recruitment with reduced murine placental glucose transporter isoform 3 expression. in The Journal of nutritional biochemistry 2014
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Human Polyclonal MECP2 Primary Antibody for DB - ABIN650833
Qiu, Sylwestrak, Lieberman, Zhang, Liu, Ghosh: The Rett syndrome protein MeCP2 regulates synaptic scaling. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2012
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Human Polyclonal MECP2 Primary Antibody for ICC, IF - ABIN252309
Ruddock-DCruz, Xue, Wilson, Heffernan, Prashadkumar, Cooney, Sanchez-Partida, French, Holland: Dynamic changes in the localization of five members of the methyl binding domain (MBD) gene family during murine and bovine preimplantation embryo development. in Molecular reproduction and development 2007
Human Monoclonal MECP2 Primary Antibody for ChIP, ICC - ABIN2668837
Jost, Rottach, Milden, Bertulat, Becker, Wolf, Sandoval, Petazzi, Huertas, Esteller, Kremmer, Leonhardt, Cardoso: Generation and characterization of rat and mouse monoclonal antibodies specific for MeCP2 and their use in X-inactivation studies. in PLoS ONE 2011
Cow (Bovine) Polyclonal MECP2 Primary Antibody for WB - ABIN2781332
Robertson, Hall, Jacoby, Ellaway, de Klerk, Leonard: The association between behavior and genotype in Rett syndrome using the Australian Rett Syndrome Database. in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics 2006
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Human Polyclonal MECP2 Primary Antibody for WB - ABIN6143681
Liu, Lai, Ma, Ke, Zhang, Liu, Zhang, Pei, Li, Yi, Shu, Shang, Liang, Huang: CDYL suppresses epileptogenesis in mice through repression of axonal Nav1.6 sodium channel expression. in Nature communications 2017
Human Polyclonal MECP2 Primary Antibody for DB - ABIN389978
Liu, Ni, Sun: Expression of Phospho-MeCP2s in the Developing Rat Brain and Function of Postnatal MeCP2 in Cerebellar Neural Cell Development. in Neuroscience bulletin 2017
Human Polyclonal MECP2 Primary Antibody for ICC, IF - ABIN4333391
Stadler, Rexhepaj, Singan, Murphy, Pepperkok, Uhlén, Simpson, Lundberg: Immunofluorescence and fluorescent-protein tagging show high correlation for protein localization in mammalian cells. in Nature methods 2013
We studied the molecular consequences of four of these 'non-canonical' mutations in cultured neurons and mice to see if they reveal additional essential domains without affecting known properties of MeCP2..The finding that a stable C-terminal truncation does not compromise MeCP2 function raises the possibility that small molecules which stabilize these mutant proteins may be of therapeutic value.
There is no evidence whether MeCP2_e2 is able to partially compensate the function of the affected MeCP2_e1. More cases of male patients with clinical features of classic RTT are necessary to obtain a better understanding of the genotype-phenotype correlations in cases with MeCP2_e1 mutations.
Mutations in the X-linked gene MECP2 were identified as the main cause of the Rett syndrome - severe progressive Developmental disorder that almost exclusively affects females.
Role of MeCP2 in neurological disorders: current status and future perspectives.
Included in the region distal to Xq28 is the gene MECP2 and this patient presents with features of MECP2 duplication syndrome. We find that this patient has skeletal features not typical with the loss of SHOX that are likely explained by the rearrangement of the X chromosome
MeCP2 reduced angiogenesis of senescent endothelial progenitor cells, promoted apoptosis, and caused senescent EPC dysfunction through SIRT1 promoter hypermethylation and histone modification.
Autism-related protein MeCP2 regulates FGF13 expression and emotional behaviors
the apparent length-dependent trends previously observed in MeCP2 microarray and RNA-sequencing datasets disappear after estimating baseline variability from randomized control samples.
our data suggest that MeCP2 plays an essential role in TGF-beta1-induced myofibroblast differentiation and extracellular matrix production in nasal polyp-derived fibroblasts
These findings highlight the critical role of miR-137-c-Met nexus in colorectal cancer (CRC) development and reveal Mecp2-regulated epigenetic silence causes the downregulation of miR-137 in colorectal adenoma and carcinoma.
Here we report a 10-year--10-months old male patient having overlapping clinical features of MECP2 duplication syndrome, AS and ASDs. He had mental retardation, lack of speech and developmental delay, and also dysmorphic features such as plagiocephaly, retrognathia, hyperextensible joints in fingers and elbows, broad great toe and three different sizes of cafe au laits.
These data showed an intimate interplay among miR-19a/b methylation, MeCP2 activity, and multidrug resistance, revealing a potential therapeutic target for gastric cancer.
In an Indian population, the yield of the mutation detection in MECP2 is higher in classical Rett syndrome. In girls with some Rett like features, but not fulfilling revised Rett syndrome diagnostic criteria, mutation testing for MECP2 gene has a low yield.
C5-cytosine methylation entropically favors complexation by the MBD domain of the human MeCP2 protein with almost no contribution of the binding enthalpy.
The authors find that astrocyte stimulation in wild-type mice increases excitatory synaptic activity that is absent in male mice lacking MeCP2 globally. The defect is dependent upon MeCP2 expression status in the astrocytes and not in the neurons.
These dysregulated genes provide a better understanding of the underlying mechanisms of the effect of MeCP2 on heart failure and might be used as targets and prognostic markers of heart failure.
MECP2 gene rs17435 polymorphism was associated with juvenile idiopathic arthritis predisposition. Considering the involvement of genetic polymorphisms of MECP2 gene in susceptibility to adult-onset RA, this gene might basically play a role in the initiation of arthritis during early stages of life.
MECP2 is not associated with disease susceptibility in JSLE patients, implying the involvement of different susceptibility genes in the pathogenesis of Systemic Lupus Erythematosus and Juvenile-Onset Systemic Lupus Erythematosus
We report on two dizygotic twins with an MECP2-related psychiatric disorder without intellectual disability. We found a c.491G>T [ChrX:153296788C>A (Hg19)] transversion in exon 4 of the MECP2 gene in both patients. It was predicted to change a highly conserved serine to isoleucine, p.(Ser164Ile)
Males with Rett syndrome and missense mutations in MECP2 display a phenotype that correlates with impaired function of MECP2.
Dopaminergic dysfunction in Rett syndrome is also present in Mecp2-deficient mice and reductions in dopamine D2 receptors impairs ambulation.
Study reports that layer 5 pyramidal neuron axonal projections to layer 1 of wild type mouse motor cortex exhibit a selective escalation in bouton elimination during motor training, a plasticity process that is disrupted in the MECP2 duplication syndrome mouse model of autism.
MeCP2-Transgenic mice display elevated GFAP and Tau expression within the hippocampus and cortex followed by neuronal loss in these brain regions.
Study shows that methyl-CpG-binding protein 2 (MeCP2)deficiency leads to loss of glial Kir4.1. These are the first data implicating a direct MeCP2 molecular target in astrocytes and provide novel mechanistic insight explaining a potential mechanism by which astrocytic dysfunction may contribute to Rett syndrome.
MeCP2 interacts with microRNAs in mouse primary cortical neurons.
MeCP2 expression in the excitatory cells of mouse visual thalamus
Pup gathering behaviour and associated auditory cortical plasticity are impaired in female Mecp2 knockout mice.
Decreased MeCP2 binding near splice junctions facilitates intron retention via reduced recruitment of splicing factors, including Tra2b, and increased RNA polymerase II stalling.
we found that MeCP2 plays a critical role in regulating fate determination of adult NSCs. These evidences further suggest that abnormal development of NSCs may play a role in the pathogenesis of the MECP2 duplication syndrome.
MeCP2 regulated mRNA splicing in the brain through interacting with 5-hydroxymethylcytosine and epigenetic changes in histone markers.
Study in female mouse model for Rett syndrome shows that low-level MECP2 expression in the brain can have a disproportionately positive impact on health and survival.
genetic reactivation of Xi-linked Mecp2 in cerebral cortical neurons of living mice bearing a homozygous XCIF deletion. Collectively, our results further establish the feasibility of pharmacological reactivation of Xi-linked MECP2 as a therapeutic approach for RTT.
Authors used a well-characterized motor suppressive effect of nAChR agonists on mouse open field locomotor behavior to probe effects of MeCP2 mutation on cholinergic transmission.
Protein levels of p-MeCP2 were increased in high glucose or TGF-beta-treated mouse glomerular mesangial cells. The SIAH1/HIPK2/MeCP2 axis played a novel role for in suppressing miR-25 processing and thereby upregulating NOX4 in early diabetic nephropathy.
Study shows defective GABAergic neurotransmission in the nucleus tractus solitarius (NTS) methyl-CpG binding protein 2-null mice, a model of Rett syndrome. In addition the study found an increase in the delta subunit of the GABAA-receptors in the NTS in Mecp2-null mice, consistent with increased extrasynaptic receptors.
The results of this study indicated significant structural and functional impairments in the barrel cortex of animal model for the Rett syndrome.
disruption of AT-hook 1 domain in MeCP2 caused behavioral abnormality in mice, which suggests that AT-hook 1 is a critical region for the function of MeCP2 protein
Mecp2 is required for tnfa expression during zebrafish development and inflammation.
The results of this study imply that Mecp2 is an important functional regulator of bdnf gene expression during neural circuit formation in zebrafish embryo
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