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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 ansducin beta-like 1 X-linked receptor 1 and methyl-CpG binding protein 2.
5 of de novo DNA methyltransferase DNMT3a and methyl-CpG-binding protein 2.
6 order caused by mutations in MECP2, encoding methyl-CpG-binding protein 2.
7 from mutation in the mecp2 gene that encodes methyl CpG binding protein 2, a transcriptional represso
8 NA methyltransferases (DNMT1 and DNMT3A) and methyl-CpG binding protein 2, a DNA methylation reader p
9 so notable are two neuron-enriched proteins, methyl CpG-binding protein 2 and polypyrimidine tract-bi
10 in repression of PPARgamma: increased MeCP2 (methyl CpG binding protein 2) and HP-1alpha co-repressor
12 RTT), caused by mutations in MECP2 (encoding methyl CpG binding protein 2), and Angelman syndrome (AS
13 tone methyltransferases and demethylases, or methyl CpG binding protein 2, and a significant decrease
16 in MECP2, encoding the epigenetic regulator methyl-CpG-binding protein 2, are the predominant cause
17 1 and 2, histone methyl-transferase G9a, and methyl CpG binding protein 2 at the promoters of target
20 5-hmC levels were inversely correlated with methyl-CpG-binding protein 2 dosage, a protein encoded b
21 nuclear antigen, heterochromatin protein 1, methyl-CpG binding protein 2, Enhancer of Zeste homolog
23 T) arises from loss-of-function mutations in methyl-CpG binding protein 2 gene (Mecp2), but fundament
26 ace since the identification of mutations in methyl-CpG-binding protein 2 gene (MECP2) was first repo
30 l disorder caused by mutations in the MECP2 (methyl-CpG binding protein 2) gene, because overexpressi
31 n two such factors, CREB-binding protein and methyl-CpG-binding protein 2, have begun to reveal how e
32 se 1, ten-eleven-translocation hydroxylases, methyl CpG binding protein 2, histone deacetylases, and
33 decreased C/EBPbeta and pCREB and increased methyl-CpG binding protein-2, histone-deacetylase-2, and
35 X-linked gene encoding the epigenetic factor methyl-CpG-binding protein-2, is mutated in Rett syndrom
36 nction mutations of the X-linked gene MECP2 (methyl-CpG binding protein 2) lead to severe neurodevelo
37 nteraction between histone deacetylase 2 and methyl-CpG-binding protein 2, leading to suppressed hist
38 n immunoprecipitation analysis revealed that methyl-CpG-binding protein 2 (MBD2) is associated prefer
39 activity by 30%, and reduced the binding of methyl CpG binding protein 2 (MeCP2) and increased the b
41 Mutations in the transcriptional repressor methyl CpG binding protein 2 (MeCP2) are responsible for
43 mal expression of the X-linked gene encoding methyl CpG binding protein 2 (MeCP2) cause a spectrum of
45 tification of mutations in the gene encoding methyl CpG binding protein 2 (MeCP2) in Rett syndrome re
47 mainly caused by mutations of a single gene methyl CpG binding protein 2 (MeCP2) on the X chromosome
48 der caused by mutations in the gene encoding methyl CpG binding protein 2 (MeCP2) that occur sporadic
49 chromatin immunoprecipitation (ChIP) assays, methyl CpG binding protein 2 (MeCP2) was shown to bind t
50 polypeptide backbone dynamics of full-length methyl CpG binding protein 2 (MeCP2) when free in soluti
52 (HP1), polycomb protein complex 1 (PRC1) and methyl CpG binding protein 2 (MeCP2), at the COX-2 promo
54 tone H1, high mobility group D1 (HMGD1), and methyl CpG binding protein 2 (MeCP2), on the biophysical
58 CNV disorder caused by duplications spanning methyl CpG-binding protein 2 (MECP2) and other genes on
59 r the expression of the epigenetic regulator methyl CpG-binding protein 2 (MeCP2) in key brain reward
61 ontal cortex vasopressin receptor (V1aR) and methyl CpG-binding protein 2 (MeCP2) mRNA expression, bu
62 y loss-of-function heterozygous mutations of methyl CpG-binding protein 2 (MECP2) on the X chromosome
63 l activity-induced phosphorylation (NAIP) of methyl CpG-binding protein 2 (MeCP2) precedes its releas
64 munoprecipitation analysis revealed that the methyl CpG-binding protein 2 (MeCP2) was enriched in the
65 eport that HMGN1 modulates the expression of methyl CpG-binding protein 2 (MeCP2), a DNA-binding prot
66 tion in the brain, the Rett syndrome protein methyl CpG-binding protein 2 (MeCP2), and discuss how di
67 structure and domain organization of native methyl CpG-binding protein 2 (MeCP2), the recombinant hu
68 is active epigenetic state was replaced by a methyl CpG-binding protein 2 (MeCP2)-containing repressi
75 inked gene encoding the transcription factor methyl-CpG binding protein 2 (MECP2) are the most freque
77 gene encoding the transcriptional repressor methyl-CpG binding protein 2 (MeCP2) cause the neurodeve
78 ss of function of the X-linked gene encoding methyl-CpG binding protein 2 (MeCP2) causes the progress
79 function and gain-of-function alterations in methyl-CpG binding protein 2 (MeCP2) expression, respect
80 orrelates with the dissociation of DNMT1 and methyl-CpG binding protein 2 (MeCP2) from the promoter,
81 in which most patients have mutations in the methyl-CpG binding protein 2 (MECP2) gene and suffer fro
89 e we report that Htt directly interacts with methyl-CpG binding protein 2 (MeCP2) in mouse and cellul
90 transcription in vitro and are recognized by methyl-CpG binding protein 2 (MeCP2) in neurons in vivo.
96 n intriguing finding about the gene encoding methyl-CpG binding protein 2 (MeCP2) is that the loss-of
100 tation (ChIP) assays assessed the binding of methyl-CpG binding protein 2 (MeCP2) to PPARgamma and ch
101 nding proteins (MBDs) demonstrated that only methyl-CpG binding protein 2 (MeCP2) was associated with
102 with mutations in the X-linked gene encoding methyl-CpG binding protein 2 (MeCp2), a transcriptional
103 is caused by mutations in the gene encoding methyl-CpG binding protein 2 (MeCP2), a transcriptional
104 is caused by mutations in the gene encoding methyl-CpG binding protein 2 (MECP2), an epigenetic regu
105 ssed TFPI-2 promoter was associated with the methyl-CpG binding protein 2 (MeCP2), and that gene reac
107 ene coding for the transcriptional regulator methyl-CpG binding protein 2 (MeCP2), but despite much e
108 and several transcription factors including methyl-CpG binding protein 2 (MeCP2), histone deacetylas
109 is of an X-linked, Rett syndrome (RTT) gene, methyl-CpG binding protein 2 (MECP2), in both rhesus and
110 yndrome (RTT), mainly caused by mutations in methyl-CpG binding protein 2 (MeCP2), is one of the most
111 Mutations in the transcriptional repressor, methyl-CpG binding protein 2 (MeCP2), result in a neurod
123 cts to address CLN3 dosage effects using the methyl-CpG-binding protein 2 (MeCP2) and beta-actin prom
124 cts to address CLN3 dosage effects using the methyl-CpG-binding protein 2 (MeCP2) and beta-actin prom
125 -function mutations in the gene encoding the methyl-CpG-binding protein 2 (MeCP2) and is characterize
126 identify the mechanism of regulation of the methyl-CpG-binding protein 2 (MeCP2) and its functional
127 tions in the gene (MECP2 ) encoding X-linked methyl-CpG-binding protein 2 (MeCP2) as the cause of som
131 s-of-function mutations in the X-linked gene Methyl-CpG-binding protein 2 (MECP2) cause a devastating
135 Mutations in the X-linked gene encoding methyl-CpG-binding protein 2 (MeCP2) cause Rett syndrome
138 and SRFS1-interacting protein 1 (DFS70) and methyl-CpG-binding protein 2 (MeCp2) could be documented
139 dissociation of the transcription repressor methyl-CpG-binding protein 2 (MeCP2) from the promoter,
140 ong with the fact that chimeric mice lacking methyl-CpG-binding protein 2 (MeCP2) function die during
142 of function of the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2) gene, is associated
143 isorder caused primarily by mutations in the methyl-CpG-binding protein 2 (MECP2) gene, which encodes
147 ouse models of the transcriptional modulator Methyl-CpG-Binding Protein 2 (MeCP2) have advanced our u
161 to immunomodulate behavioral impairment in a Methyl-CpG-binding protein 2 (Mecp2) transgenic mouse mo
163 Loss- and gain-of-function mutations in methyl-CpG-binding protein 2 (MECP2) underlie two distin
164 disorder caused by mutations or deletions in Methyl-CpG-binding Protein 2 (MeCP2), a brain-enriched t
166 n in rodents are increased in the absence of methyl-CpG-binding protein 2 (MeCP2), a protein involved
168 evelopmental disorder caused by mutations in methyl-CpG-binding protein 2 (MECP2), a transcriptional
169 which encodes the transcriptional regulator methyl-CpG-binding protein 2 (MeCP2), cause Rett syndrom
172 ipts previously shown to be repressed by the Methyl-CpG-binding protein 2 (MeCP2), including serum- a
173 CA), together with the Rett syndrome protein methyl-CpG-binding protein 2 (MeCP2), to control gene ex
174 Germline mutations in the X-linked gene, methyl-CpG-binding protein 2 (MECP2), underlie most case
176 evelopmental disorder caused by mutations in methyl-CpG-binding protein 2 (MECP2), with known disturb
177 duct Fos in the brains of wild-type (Wt) and methyl-CpG-binding protein 2 (Mecp2)-null (Null) mice, a
207 ological disorder, is caused by mutations in methyl-CpG-binding protein 2 (MECP2; OMIM 300005), a ubi
208 m, we revealed a genotype-specific effect of methyl-CpG-binding protein-2 (MeCP2) dysfunction on iPSC
209 caused by loss-of-function mutations in the Methyl-CpG-binding protein-2 (MECP2) gene and is charact
211 cent identification of mutations in the gene methyl-Cpg-binding protein-2 (MECP2) in girls with Rett
214 d by duplications spanning the gene encoding methyl-CpG-binding protein-2 (MeCP2), a protein involved
215 P-3 promoter influenced the binding of Sp-1, methyl-CpG-binding protein-2 (MeCP2), and histone deacet
220 , peripherin, plasma glutathione peroxidase, methyl CpG-binding protein 2, retinal S-antigen, ErbB2 p
222 e found a significant increase in binding of methyl-CpG binding protein 2 to the "cytosine-phosphate-
223 in remodelling by its interaction with MBD2 (methyl CpG-binding protein 2), underlying FAK regulation