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Methyl CpG binding protein 2

MECP2, Methyl-CpG-Binding Protein 2, RTS
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. [provided by RefSeq, Jul 2009] (from NCBI)
Top mentioned proteins: CAN, HAD, Histone, AGE, ACID
Papers on MECP2
Poly(ADP-ribosyl)ation of Methyl CpG Binding Domain Protein 2 Regulates Chromatin Structure.
New
Cardoso et al., Darmstadt, Germany. In J Biol Chem, Feb 2016
UNASSIGNED: The epigenetic information encoded in the genomic DNA methylation pattern is translated by methyl-cytosine binding proteins like MeCP2 into chromatin topology and structure and gene activity states.
Homozygous c.1160C>T (P38L) in the MECP2 gene in a female Rett syndrome patient.
New
Das et al., Mumbai, India. In J Clin Neurosci, Feb 2016
Mutations in the MECP2 gene on chromosome Xq28 have been shown to be the cause of Rett syndrome.
CREBBP and EP300 mutational spectrum and clinical presentations in a cohort of Swedish patients with Rubinstein-Taybi syndrome.
New
Anderlid et al., Stockholm, Sweden. In Mol Genet Genomic Med, Jan 2016
Rubinstein-Taybi syndrome (RTS) is a rare autosomal dominant congenital disorder characterized by distinctive facial features, broad thumbs and halluces, growth retardation, and a variable degree of cognitive impairment.
Reversal of phenotypes in MECP2 duplication mice using genetic rescue or antisense oligonucleotides.
New
Impact
Zoghbi et al., Houston, United States. In Nature, Jan 2016
The broad range of deficits caused by methyl-CpG-binding protein 2 (MeCP2) overexpression poses a daunting challenge to traditional biochemical-pathway-based therapeutic approaches.
The March Toward Malaria Vaccines.
Review
New
Duffy et al., Rockville, United States. In Am J Prev Med, Dec 2015
In this limited review, we focus on four approaches to malaria vaccines, (1) a recombinant protein with adjuvant vaccine aimed at Plasmodium falciparum (Pf) pre-erythrocytic stages of the parasite cycle (RTS,S/AS01), (2) whole sporozoite vaccines aimed at Pf pre-erythrocytic stages (PfSPZ Vaccine and PfSPZ-CVac), (3) prime boost vaccines that include recombinant DNA, viruses and bacteria, and protein with adjuvant aimed primarily at Pf pre-erythrocytic, but also asexual erythrocytic stages, and (4) recombinant protein with adjuvant vaccines aimed at Pf and Plasmodium vivax sexual erythrocytic and mosquito stages.
The march toward malaria vaccines.
Review
New
Duffy et al., Rockville, United States. In Vaccine, Dec 2015
In this limited review, we focus on four approaches to malaria vaccines, (1) a recombinant protein with adjuvant vaccine aimed at Plasmodium falciparum (Pf) pre-erythrocytic stages of the parasite cycle (RTS,S/AS01), (2) whole sporozoite vaccines aimed at Pf pre-erythrocytic stages (PfSPZ Vaccine and PfSPZ-CVac), (3) prime boost vaccines that include recombinant DNA, viruses and bacteria, and protein with adjuvant aimed primarily at Pf pre-erythrocytic, but also asexual erythrocytic stages, and (4) recombinant protein with adjuvant vaccines aimed at Pf and Plasmodium vivax sexual erythrocytic and mosquito stages.
Genetic Diversity and Protective Efficacy of the RTS,S/AS01 Malaria Vaccine.
New
Impact
Wirth et al., Boston, United States. In N Engl J Med, Dec 2015
BACKGROUND: The RTS,S/AS01 vaccine targets the circumsporozoite protein of Plasmodium falciparum and has partial protective efficacy against clinical and severe malaria disease in infants and children.
Forniceal deep brain stimulation rescues hippocampal memory in Rett syndrome mice.
New
Impact
Tang et al., Houston, United States. In Nature, Nov 2015
We therefore studied the effects of forniceal DBS in a well-characterized mouse model of Rett syndrome (RTT), which is a leading cause of intellectual disability in females.
Brief report: systematic review of Rett syndrome in males.
Review
New
Volkmar et al., Farmington, United States. In J Autism Dev Disord, Oct 2015
Rett syndrome (RTT) is a neurogenetic disorder in which a period of typical development is followed by loss of previously acquired skills.
Profiling the host response to malaria vaccination and malaria challenge.
Review
New
Fletcher et al., Oxford, United Kingdom. In Vaccine, Oct 2015
The RTS,S vaccine represents major progress, but is only partially effective.
A high-resolution imaging approach to investigate chromatin architecture in complex tissues.
New
Impact
Mandel et al., Portland, United States. In Cell, Oct 2015
We then apply this approach to examine how the genome is organized in the mammalian brain using female Rett syndrome mice, which are a mosaic of normal and Mecp2-null cells.
MECP2 disorders: from the clinic to mice and back.
Review
New
Zoghbi et al., In J Clin Invest, Sep 2015
Two severe, progressive neurological disorders characterized by intellectual disability, autism, and developmental regression, Rett syndrome and MECP2 duplication syndrome, result from loss and gain of function, respectively, of the same critical gene, methyl-CpG-binding protein 2 (MECP2).
Methyl-CpG Binding Protein 2 Regulates Microglia and Macrophage Gene Expression in Response to Inflammatory Stimuli.
New
Impact
Kipnis et al., Charlottesville, United States. In Immunity, May 2015
Mutations in MECP2, encoding the epigenetic regulator methyl-CpG-binding protein 2, are the predominant cause of Rett syndrome, a disease characterized by both neurological symptoms and systemic abnormalities.
Association between PDCD1, CTLA4, and MECP2 gene polymorphisms and systemic lupus erythematosus in the Chinese Northern Han.
Chang et al., Hohhot, China. In Genet Mol Res, 2014
The programmed cell death 1 gene (PDCD1), the cytotoxic T-lymphocyte-associated protein 4 (CTLA4) gene, and the methyl-CpG-binding protein 2 gene (MECP2) are considered to be the candidate genes associated with SLE.
RAPADILINO RECQL4 mutant protein lacks helicase and ATPase activity.
GeneRIF
Bohr et al., Baltimore, United States. In Biochim Biophys Acta, 2012
These observations help explain the underlying molecular etiology of the disease and our findings provide insight into the genotype and phenotype association among RECQL4 syndromes
Nuclear calcium signaling controls methyl-CpG-binding protein 2 (MeCP2) phosphorylation on serine 421 following synaptic activity.
GeneRIF
Bading et al., Heidelberg, Germany. In J Biol Chem, 2012
Nuclear calcium signaling controls methyl-CpG-binding protein 2 (MeCP2) phosphorylation on serine 421 following synaptic activity
Up-regulated methyl CpG binding protein-2 in intractable temporal lobe epilepsy patients and a rat model.
GeneRIF
Wang et al., Chongqing, China. In Neurochem Res, 2012
Up-regulated expression of MeCP2 in intractable temporal lobe epilepsy patients and experimental animals suggested that MeCP2 may be involved in the pathogenesis of temporal lobe epilepsy
MeCP2 is critical for maintaining mature neuronal networks and global brain anatomy during late stages of postnatal brain development and in the mature adult brain.
GeneRIF
Ballas et al., Stony Brook, United States. In J Neurosci, 2012
Our data suggest a crucial role for MeCP2 in post-transcriptional regulation of critical synaptic proteins involved in maintaining mature neuronal networks during late stages of postnatal brain development.
Hippocampal CA1 pyramidal neurons of Mecp2 mutant mice show a dendritic spine phenotype only in the presymptomatic stage.
GeneRIF
Pozzo-Miller et al., Birmingham, United States. In Neural Plast, 2011
These results raise caution regarding the use of dendritic spine density in hippocampal neurons as a phenotypic endpoint for the evaluation of therapeutic interventions in symptomatic Mecp2-deficient mice
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