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1 sed by mutations in the X-linked gene MECP2 (methyl-CpG-binding protein 2).
2 , hypoxia-related transcription factors, and methyl CpG binding protein 2.
3 d with mutations in MECP2, the gene encoding methyl CpG-binding protein 2.
4 of de novo DNA methyltransferase DNMT3a and methyl-CpG-binding protein 2.
5 order caused by mutations in MECP2, encoding methyl-CpG-binding protein 2.
6 from mutation in the mecp2 gene that encodes methyl CpG binding protein 2, a transcriptional represso
7 so notable are two neuron-enriched proteins, methyl CpG-binding protein 2 and polypyrimidine tract-bi
8 in repression of PPARgamma: increased MeCP2 (methyl CpG binding protein 2) and HP-1alpha co-repressor
9 RTT), caused by mutations in MECP2 (encoding methyl CpG binding protein 2), and Angelman syndrome (AS
10 tone methyltransferases and demethylases, or methyl CpG binding protein 2, and a significant decrease
13 in MECP2, encoding the epigenetic regulator methyl-CpG-binding protein 2, are the predominant cause
14 1 and 2, histone methyl-transferase G9a, and methyl CpG binding protein 2 at the promoters of target
17 5-hmC levels were inversely correlated with methyl-CpG-binding protein 2 dosage, a protein encoded b
18 nuclear antigen, heterochromatin protein 1, methyl-CpG binding protein 2, Enhancer of Zeste homolog
20 T) arises from loss-of-function mutations in methyl-CpG binding protein 2 gene (Mecp2), but fundament
23 ace since the identification of mutations in methyl-CpG-binding protein 2 gene (MECP2) was first repo
26 n two such factors, CREB-binding protein and methyl-CpG-binding protein 2, have begun to reveal how e
27 se 1, ten-eleven-translocation hydroxylases, methyl CpG binding protein 2, histone deacetylases, and
28 decreased C/EBPbeta and pCREB and increased methyl-CpG binding protein-2, histone-deacetylase-2, and
30 X-linked gene encoding the epigenetic factor methyl-CpG-binding protein-2, is mutated in Rett syndrom
31 X-linked gene encoding the epigenetic factor methyl-CpG-binding protein-2, is mutated in Rett syndrom
32 nction mutations of the X-linked gene MECP2 (methyl-CpG binding protein 2) lead to severe neurodevelo
33 nteraction between histone deacetylase 2 and methyl-CpG-binding protein 2, leading to suppressed hist
34 n immunoprecipitation analysis revealed that methyl-CpG-binding protein 2 (MBD2) is associated prefer
35 activity by 30%, and reduced the binding of methyl CpG binding protein 2 (MeCP2) and increased the b
37 Mutations in the transcriptional repressor methyl CpG binding protein 2 (MeCP2) are responsible for
39 mal expression of the X-linked gene encoding methyl CpG binding protein 2 (MeCP2) cause a spectrum of
40 tification of mutations in the gene encoding methyl CpG binding protein 2 (MeCP2) in Rett syndrome re
41 mainly caused by mutations of a single gene methyl CpG binding protein 2 (MeCP2) on the X chromosome
42 der caused by mutations in the gene encoding methyl CpG binding protein 2 (MeCP2) that occur sporadic
43 chromatin immunoprecipitation (ChIP) assays, methyl CpG binding protein 2 (MeCP2) was shown to bind t
44 polypeptide backbone dynamics of full-length methyl CpG binding protein 2 (MeCP2) when free in soluti
45 (HP1), polycomb protein complex 1 (PRC1) and methyl CpG binding protein 2 (MeCP2), at the COX-2 promo
47 tone H1, high mobility group D1 (HMGD1), and methyl CpG binding protein 2 (MeCP2), on the biophysical
50 r the expression of the epigenetic regulator methyl CpG-binding protein 2 (MeCP2) in key brain reward
52 l activity-induced phosphorylation (NAIP) of methyl CpG-binding protein 2 (MeCP2) precedes its releas
53 munoprecipitation analysis revealed that the methyl CpG-binding protein 2 (MeCP2) was enriched in the
54 eport that HMGN1 modulates the expression of methyl CpG-binding protein 2 (MeCP2), a DNA-binding prot
55 tion in the brain, the Rett syndrome protein methyl CpG-binding protein 2 (MeCP2), and discuss how di
56 structure and domain organization of native methyl CpG-binding protein 2 (MeCP2), the recombinant hu
57 is active epigenetic state was replaced by a methyl CpG-binding protein 2 (MeCP2)-containing repressi
64 inked gene encoding the transcription factor methyl-CpG binding protein 2 (MECP2) are the most freque
65 gene encoding the transcriptional repressor methyl-CpG binding protein 2 (MeCP2) cause the neurodeve
66 ss of function of the X-linked gene encoding methyl-CpG binding protein 2 (MeCP2) causes the progress
67 function and gain-of-function alterations in methyl-CpG binding protein 2 (MeCP2) expression, respect
68 orrelates with the dissociation of DNMT1 and methyl-CpG binding protein 2 (MeCP2) from the promoter,
69 in which most patients have mutations in the methyl-CpG binding protein 2 (MECP2) gene and suffer fro
74 e we report that Htt directly interacts with methyl-CpG binding protein 2 (MeCP2) in mouse and cellul
75 transcription in vitro and are recognized by methyl-CpG binding protein 2 (MeCP2) in neurons in vivo.
80 n intriguing finding about the gene encoding methyl-CpG binding protein 2 (MeCP2) is that the loss-of
83 tation (ChIP) assays assessed the binding of methyl-CpG binding protein 2 (MeCP2) to PPARgamma and ch
84 nding proteins (MBDs) demonstrated that only methyl-CpG binding protein 2 (MeCP2) was associated with
85 with mutations in the X-linked gene encoding methyl-CpG binding protein 2 (MeCp2), a transcriptional
86 is caused by mutations in the gene encoding methyl-CpG binding protein 2 (MeCP2), a transcriptional
87 is caused by mutations in the gene encoding methyl-CpG binding protein 2 (MECP2), an epigenetic regu
88 ssed TFPI-2 promoter was associated with the methyl-CpG binding protein 2 (MeCP2), and that gene reac
89 ene coding for the transcriptional regulator methyl-CpG binding protein 2 (MeCP2), but despite much e
90 is of an X-linked, Rett syndrome (RTT) gene, methyl-CpG binding protein 2 (MECP2), in both rhesus and
91 Mutations in the transcriptional repressor, methyl-CpG binding protein 2 (MeCP2), result in a neurod
101 cts to address CLN3 dosage effects using the methyl-CpG-binding protein 2 (MeCP2) and beta-actin prom
102 cts to address CLN3 dosage effects using the methyl-CpG-binding protein 2 (MeCP2) and beta-actin prom
103 -function mutations in the gene encoding the methyl-CpG-binding protein 2 (MeCP2) and is characterize
104 identify the mechanism of regulation of the methyl-CpG-binding protein 2 (MeCP2) and its functional
105 tions in the gene (MECP2 ) encoding X-linked methyl-CpG-binding protein 2 (MeCP2) as the cause of som
109 s-of-function mutations in the X-linked gene Methyl-CpG-binding protein 2 (MECP2) cause a devastating
113 Mutations in the X-linked gene encoding methyl-CpG-binding protein 2 (MeCP2) cause Rett syndrome
114 and SRFS1-interacting protein 1 (DFS70) and methyl-CpG-binding protein 2 (MeCp2) could be documented
115 dissociation of the transcription repressor methyl-CpG-binding protein 2 (MeCP2) from the promoter,
116 ong with the fact that chimeric mice lacking methyl-CpG-binding protein 2 (MeCP2) function die during
117 of function of the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2) gene, is associated
118 isorder caused primarily by mutations in the methyl-CpG-binding protein 2 (MECP2) gene, which encodes
122 ouse models of the transcriptional modulator Methyl-CpG-Binding Protein 2 (MeCP2) have advanced our u
134 Loss- and gain-of-function mutations in methyl-CpG-binding protein 2 (MECP2) underlie two distin
136 n in rodents are increased in the absence of methyl-CpG-binding protein 2 (MeCP2), a protein involved
137 evelopmental disorder caused by mutations in methyl-CpG-binding protein 2 (MECP2), a transcriptional
138 which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrom
141 ipts previously shown to be repressed by the Methyl-CpG-binding protein 2 (MeCP2), including serum- a
142 Germline mutations in the X-linked gene, methyl-CpG-binding protein 2 (MECP2), underlie most case
144 evelopmental disorder caused by mutations in methyl-CpG-binding protein 2 (MECP2), with known disturb
145 duct Fos in the brains of wild-type (Wt) and methyl-CpG-binding protein 2 (Mecp2)-null (Null) mice, a
172 ological disorder, is caused by mutations in methyl-CpG-binding protein 2 (MECP2; OMIM 300005), a ubi
173 m, we revealed a genotype-specific effect of methyl-CpG-binding protein-2 (MeCP2) dysfunction on iPSC
174 caused by loss-of-function mutations in the Methyl-CpG-binding protein-2 (MECP2) gene and is charact
176 cent identification of mutations in the gene methyl-Cpg-binding protein-2 (MECP2) in girls with Rett
179 d by duplications spanning the gene encoding methyl-CpG-binding protein-2 (MeCP2), a protein involved
180 P-3 promoter influenced the binding of Sp-1, methyl-CpG-binding protein-2 (MeCP2), and histone deacet
183 , peripherin, plasma glutathione peroxidase, methyl CpG-binding protein 2, retinal S-antigen, ErbB2 p
185 e found a significant increase in binding of methyl-CpG binding protein 2 to the "cytosine-phosphate-
186 in remodelling by its interaction with MBD2 (methyl CpG-binding protein 2), underlying FAK regulation
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