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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 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 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
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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Severe MECP2 mutations (R106W, R168X, R255X, R270X, and large deletions) showed a higher proportion of scoliosis.
Authors have identified mutations in PAK3, CASK, and MECP2 that likely contribute to intellectual disability, and the findings extend the spectrum of mutations and phenotypes associated with X-linked intellectual disability.
a mechanism how L1 elements get activated in the absence of Mecp2
MeCP2 in cholinergic neurons is necessary and sufficient for autonomic cardiac control, thermoregulation, and survival.
MECP2 mutation is associated with Rett syndrome.
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 (显示 CTCF 抗体), a constitutive transcriptional insulator.
A mouse model in which Mecp2 is silenced in peripheral tissues, but reactivated prenatally at near normal levels within the nervous system. Major features that characterise RTT result from lack of MeCP2 in the nervous system. Lack of MeCP2 in the periphery, however, resulted in phenotypes that match specific clinical features associated with RTT, including reduced stamina and bone abnormalities.
mice expressing truncated MeCP2 lacking both the N- and C-terminal regions are phenotypically near-normal; and those expressing a minimal MeCP2 additionally lacking a central domain survive for over one year with only mild symptoms; this minimal protein is able to prevent or reverse neurological symptoms when introduced into MeCP2-deficient mice by genetic activation or virus-mediated delivery to the brain
MeCP2 is required for proper gastrointestinal motility and normal nNOS (显示 NOS1 抗体) levels.
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.
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