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PMID |
Sentence |
1 |
17468742
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The histone H3K4 demethylase SMCX links REST target genes to X-linked mental retardation.
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2 |
17468742
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An SMCX complex isolated from HeLa cells contains additional chromatin modifiers (the histone deacetylases HDAC1 and HDAC2, and the histone H3K9 methyltransferase G9a) and the transcriptional repressor REST, suggesting a direct role for SMCX in chromatin dynamics and REST-mediated repression.
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3 |
17468742
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Chromatin immunoprecipitation reveals that SMCX and REST co-occupy the neuron-restrictive silencing elements in the promoters of a subset of REST target genes.
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4 |
17468742
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RNA-interference-mediated depletion of SMCX derepresses several of these targets and simultaneously increases H3K4 trimethylation at the sodium channel type 2A (SCN2A) and synapsin I (SYN1) promoters.
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5 |
17468742
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We propose that loss of SMCX activity impairs REST-mediated neuronal gene regulation, thereby contributing to SMCX-associated X-linked mental retardation.
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6 |
19139378
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Endothelin-stimulated human B-type natriuretic peptide gene expression is mediated by Yin Yang 1 in association with histone deacetylase 2.
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7 |
19139378
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Here we demonstrate that both basal- and endothelin-1-dependent stimulation of human (h) BNP gene transcription requires the presence of an intact Yin Yang 1 (YY1) binding site positioned at -62 bp relative to the transcription start site.
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8 |
19139378
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Exposure to endothelin-1 also resulted in increased nuclear localization of YY1 and a reduction in acetylation of the YY1 protein.
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9 |
19139378
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Overexpression of wild-type YY1 increased both basal and endothelin-stimulated hBNP promoter activity, whereas a carboxy-terminal deletion mutant of YY1 was devoid of activity.
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10 |
19139378
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YY1 was shown to associate with histone deacetylase 2, and histone deacetylase 2 was shown to associate directly with the hBNP promoter in the intact cell.
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11 |
19139378
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Collectively these findings demonstrate that YY1 plays an important role in regulating the transcriptional activity of the hBNP gene promoter.
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12 |
19139378
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These data suggest a model in which YY1 activates hBNP transcription through interaction with histone deacetylase 2.
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13 |
19139378
|
Endothelin-stimulated human B-type natriuretic peptide gene expression is mediated by Yin Yang 1 in association with histone deacetylase 2.
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14 |
19139378
|
Here we demonstrate that both basal- and endothelin-1-dependent stimulation of human (h) BNP gene transcription requires the presence of an intact Yin Yang 1 (YY1) binding site positioned at -62 bp relative to the transcription start site.
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15 |
19139378
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Exposure to endothelin-1 also resulted in increased nuclear localization of YY1 and a reduction in acetylation of the YY1 protein.
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16 |
19139378
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Overexpression of wild-type YY1 increased both basal and endothelin-stimulated hBNP promoter activity, whereas a carboxy-terminal deletion mutant of YY1 was devoid of activity.
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17 |
19139378
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YY1 was shown to associate with histone deacetylase 2, and histone deacetylase 2 was shown to associate directly with the hBNP promoter in the intact cell.
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18 |
19139378
|
Collectively these findings demonstrate that YY1 plays an important role in regulating the transcriptional activity of the hBNP gene promoter.
|
19 |
19139378
|
These data suggest a model in which YY1 activates hBNP transcription through interaction with histone deacetylase 2.
|
20 |
19139378
|
Endothelin-stimulated human B-type natriuretic peptide gene expression is mediated by Yin Yang 1 in association with histone deacetylase 2.
|
21 |
19139378
|
Here we demonstrate that both basal- and endothelin-1-dependent stimulation of human (h) BNP gene transcription requires the presence of an intact Yin Yang 1 (YY1) binding site positioned at -62 bp relative to the transcription start site.
|
22 |
19139378
|
Exposure to endothelin-1 also resulted in increased nuclear localization of YY1 and a reduction in acetylation of the YY1 protein.
|
23 |
19139378
|
Overexpression of wild-type YY1 increased both basal and endothelin-stimulated hBNP promoter activity, whereas a carboxy-terminal deletion mutant of YY1 was devoid of activity.
|
24 |
19139378
|
YY1 was shown to associate with histone deacetylase 2, and histone deacetylase 2 was shown to associate directly with the hBNP promoter in the intact cell.
|
25 |
19139378
|
Collectively these findings demonstrate that YY1 plays an important role in regulating the transcriptional activity of the hBNP gene promoter.
|
26 |
19139378
|
These data suggest a model in which YY1 activates hBNP transcription through interaction with histone deacetylase 2.
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27 |
19553350
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Histone deacetylase-2 is a key regulator of diabetes- and transforming growth factor-beta1-induced renal injury.
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28 |
19553350
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This study examined the effect of HDAC inhibition on renal fibrosis induced by diabetes or transforming growth factor (TGF)-beta1 and determined the role of reactive oxygen species (ROS) as mediators of HDAC activation.
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29 |
19553350
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Among the six HDACs tested (HDAC-1 through -5 and HDAC-8), HDAC-2 activity significantly increased in the kidneys of STZ-induced diabetic rats and db/db mice and TGF-beta1-treated NRK52-E cells.
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30 |
19553350
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Levels of mRNA expression of fibronectin and alpha-smooth muscle actin were decreased, whereas E-cadherin mRNA was increased when HDAC-2 was knocked down using RNA interference in NRK52-E cells.
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31 |
19553350
|
Histone deacetylase-2 is a key regulator of diabetes- and transforming growth factor-beta1-induced renal injury.
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32 |
19553350
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This study examined the effect of HDAC inhibition on renal fibrosis induced by diabetes or transforming growth factor (TGF)-beta1 and determined the role of reactive oxygen species (ROS) as mediators of HDAC activation.
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33 |
19553350
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Among the six HDACs tested (HDAC-1 through -5 and HDAC-8), HDAC-2 activity significantly increased in the kidneys of STZ-induced diabetic rats and db/db mice and TGF-beta1-treated NRK52-E cells.
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34 |
19553350
|
Levels of mRNA expression of fibronectin and alpha-smooth muscle actin were decreased, whereas E-cadherin mRNA was increased when HDAC-2 was knocked down using RNA interference in NRK52-E cells.
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35 |
19553350
|
Histone deacetylase-2 is a key regulator of diabetes- and transforming growth factor-beta1-induced renal injury.
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36 |
19553350
|
This study examined the effect of HDAC inhibition on renal fibrosis induced by diabetes or transforming growth factor (TGF)-beta1 and determined the role of reactive oxygen species (ROS) as mediators of HDAC activation.
|
37 |
19553350
|
Among the six HDACs tested (HDAC-1 through -5 and HDAC-8), HDAC-2 activity significantly increased in the kidneys of STZ-induced diabetic rats and db/db mice and TGF-beta1-treated NRK52-E cells.
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38 |
19553350
|
Levels of mRNA expression of fibronectin and alpha-smooth muscle actin were decreased, whereas E-cadherin mRNA was increased when HDAC-2 was knocked down using RNA interference in NRK52-E cells.
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39 |
20175943
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Also, EGCG decreased NF-kappaB activity and increased HDAC activity and HDAC-2 expression in Tregs (P < 0.05) in both groups.
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40 |
20175943
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IL-10 production and number by suppressing the NF-kappaB signalling pathway via inducing epigenetic changes.
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41 |
20655188
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HG significantly induced histone acetylation, NF-κB activity and proinflammatory cytokine (interleukin 6, tumor necrosis factor α and MCP-1) release from THP-1 cells.
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42 |
20655188
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Also, since p300 histone acetyltransferase is a coactivator of NF-κB, we examined its acetylation.
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43 |
20655188
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Curcumin treatment also significantly reduced HAT activity, level of p300 and acetylated CBP/p300 gene expression, and induced HDAC2 expression by curcumin.
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44 |
22638581
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This oxidative stress causes the accumulation of reactive oxygen species (ROS) and depletion of reduced glutathione (GSH) that together inhibited histone deacetylases (HDACs) activity, reduced protein levels of HDAC2 and increased acetylation in miR-466h-5p promoter region, which led to the activation of this miRNA.
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45 |
22733364
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Co-location of HDAC2 and insulin signaling components in the adult mouse hippocampus.
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46 |
22733364
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However, the recent studies indicated that HDAC2, a member of HDACs family, played a role in insulin signaling pathway and synaptic plasticity.
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47 |
22733364
|
Here, we are concerned about whether HDAC2 was co-located with insulin signaling components in postsynaptic glutamatergic neurons (PSGNs) of the adult mouse hippocampus using double immunofluorescence staining.
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48 |
22733364
|
The results displayed that HDAC2 was present in PSGNs marked by N-methyl-D-aspartate receptor subunit 2B, in which major components of insulin signaling pathway such as insulin receptor alpha and beta and insulin receptor substrate-1 were also involved.
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49 |
22733364
|
Accordingly, we speculate that the interaction of HDAC2 and insulin signaling system in PSGNs observed in the present study may serve as a potential mechanism in memory formation.
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50 |
22733364
|
We hope this could provide a valuable basis for understanding the roles of HDAC2 and insulin on cognitive impairment of diabetes mellitus, involved Alzheimer's disease, which is also called type 3 diabetes recently.
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51 |
22733364
|
Co-location of HDAC2 and insulin signaling components in the adult mouse hippocampus.
|
52 |
22733364
|
However, the recent studies indicated that HDAC2, a member of HDACs family, played a role in insulin signaling pathway and synaptic plasticity.
|
53 |
22733364
|
Here, we are concerned about whether HDAC2 was co-located with insulin signaling components in postsynaptic glutamatergic neurons (PSGNs) of the adult mouse hippocampus using double immunofluorescence staining.
|
54 |
22733364
|
The results displayed that HDAC2 was present in PSGNs marked by N-methyl-D-aspartate receptor subunit 2B, in which major components of insulin signaling pathway such as insulin receptor alpha and beta and insulin receptor substrate-1 were also involved.
|
55 |
22733364
|
Accordingly, we speculate that the interaction of HDAC2 and insulin signaling system in PSGNs observed in the present study may serve as a potential mechanism in memory formation.
|
56 |
22733364
|
We hope this could provide a valuable basis for understanding the roles of HDAC2 and insulin on cognitive impairment of diabetes mellitus, involved Alzheimer's disease, which is also called type 3 diabetes recently.
|
57 |
22733364
|
Co-location of HDAC2 and insulin signaling components in the adult mouse hippocampus.
|
58 |
22733364
|
However, the recent studies indicated that HDAC2, a member of HDACs family, played a role in insulin signaling pathway and synaptic plasticity.
|
59 |
22733364
|
Here, we are concerned about whether HDAC2 was co-located with insulin signaling components in postsynaptic glutamatergic neurons (PSGNs) of the adult mouse hippocampus using double immunofluorescence staining.
|
60 |
22733364
|
The results displayed that HDAC2 was present in PSGNs marked by N-methyl-D-aspartate receptor subunit 2B, in which major components of insulin signaling pathway such as insulin receptor alpha and beta and insulin receptor substrate-1 were also involved.
|
61 |
22733364
|
Accordingly, we speculate that the interaction of HDAC2 and insulin signaling system in PSGNs observed in the present study may serve as a potential mechanism in memory formation.
|
62 |
22733364
|
We hope this could provide a valuable basis for understanding the roles of HDAC2 and insulin on cognitive impairment of diabetes mellitus, involved Alzheimer's disease, which is also called type 3 diabetes recently.
|
63 |
22733364
|
Co-location of HDAC2 and insulin signaling components in the adult mouse hippocampus.
|
64 |
22733364
|
However, the recent studies indicated that HDAC2, a member of HDACs family, played a role in insulin signaling pathway and synaptic plasticity.
|
65 |
22733364
|
Here, we are concerned about whether HDAC2 was co-located with insulin signaling components in postsynaptic glutamatergic neurons (PSGNs) of the adult mouse hippocampus using double immunofluorescence staining.
|
66 |
22733364
|
The results displayed that HDAC2 was present in PSGNs marked by N-methyl-D-aspartate receptor subunit 2B, in which major components of insulin signaling pathway such as insulin receptor alpha and beta and insulin receptor substrate-1 were also involved.
|
67 |
22733364
|
Accordingly, we speculate that the interaction of HDAC2 and insulin signaling system in PSGNs observed in the present study may serve as a potential mechanism in memory formation.
|
68 |
22733364
|
We hope this could provide a valuable basis for understanding the roles of HDAC2 and insulin on cognitive impairment of diabetes mellitus, involved Alzheimer's disease, which is also called type 3 diabetes recently.
|
69 |
22733364
|
Co-location of HDAC2 and insulin signaling components in the adult mouse hippocampus.
|
70 |
22733364
|
However, the recent studies indicated that HDAC2, a member of HDACs family, played a role in insulin signaling pathway and synaptic plasticity.
|
71 |
22733364
|
Here, we are concerned about whether HDAC2 was co-located with insulin signaling components in postsynaptic glutamatergic neurons (PSGNs) of the adult mouse hippocampus using double immunofluorescence staining.
|
72 |
22733364
|
The results displayed that HDAC2 was present in PSGNs marked by N-methyl-D-aspartate receptor subunit 2B, in which major components of insulin signaling pathway such as insulin receptor alpha and beta and insulin receptor substrate-1 were also involved.
|
73 |
22733364
|
Accordingly, we speculate that the interaction of HDAC2 and insulin signaling system in PSGNs observed in the present study may serve as a potential mechanism in memory formation.
|
74 |
22733364
|
We hope this could provide a valuable basis for understanding the roles of HDAC2 and insulin on cognitive impairment of diabetes mellitus, involved Alzheimer's disease, which is also called type 3 diabetes recently.
|
75 |
22733364
|
Co-location of HDAC2 and insulin signaling components in the adult mouse hippocampus.
|
76 |
22733364
|
However, the recent studies indicated that HDAC2, a member of HDACs family, played a role in insulin signaling pathway and synaptic plasticity.
|
77 |
22733364
|
Here, we are concerned about whether HDAC2 was co-located with insulin signaling components in postsynaptic glutamatergic neurons (PSGNs) of the adult mouse hippocampus using double immunofluorescence staining.
|
78 |
22733364
|
The results displayed that HDAC2 was present in PSGNs marked by N-methyl-D-aspartate receptor subunit 2B, in which major components of insulin signaling pathway such as insulin receptor alpha and beta and insulin receptor substrate-1 were also involved.
|
79 |
22733364
|
Accordingly, we speculate that the interaction of HDAC2 and insulin signaling system in PSGNs observed in the present study may serve as a potential mechanism in memory formation.
|
80 |
22733364
|
We hope this could provide a valuable basis for understanding the roles of HDAC2 and insulin on cognitive impairment of diabetes mellitus, involved Alzheimer's disease, which is also called type 3 diabetes recently.
|