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PMID |
Sentence |
1 |
16685406
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Expression of thioredoxin and thioredoxin-binding protein-2 in the liver of patients with chronic hepatitis C as a predictor of response to interferon therapy.
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2 |
16685406
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The aim of this study was to evaluate the clinical significance of the expression of TRX and thioredoxin-binding protein-2 (TBP-2), which is a negative regulator of TRX function, in the liver of patients with chronic hepatitis C and the relationship of this to the efficacy of interferon (IFN) treatment.
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3 |
16685406
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TRX and TBP-2 mRNA levels in the liver biopsy specimens were amplified by real-time RT-PCR.
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4 |
16685406
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TRX and TBP-2 levels in the liver tended to decrease slightly with increased fibrosis stage, although not significantly.
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5 |
16685406
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TBP-2 mRNA levels in the liver were significantly higher in responders than non-responders to the IFN therapy (p<0.05).
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6 |
16685406
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TRX and TBP-2 mRNA levels in the liver before IFN therapy may predict the outcome of IFN therapy in patients with chronic serotype 1 HCV infection.
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7 |
16685406
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Expression of thioredoxin and thioredoxin-binding protein-2 in the liver of patients with chronic hepatitis C as a predictor of response to interferon therapy.
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8 |
16685406
|
The aim of this study was to evaluate the clinical significance of the expression of TRX and thioredoxin-binding protein-2 (TBP-2), which is a negative regulator of TRX function, in the liver of patients with chronic hepatitis C and the relationship of this to the efficacy of interferon (IFN) treatment.
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9 |
16685406
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TRX and TBP-2 mRNA levels in the liver biopsy specimens were amplified by real-time RT-PCR.
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10 |
16685406
|
TRX and TBP-2 levels in the liver tended to decrease slightly with increased fibrosis stage, although not significantly.
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11 |
16685406
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TBP-2 mRNA levels in the liver were significantly higher in responders than non-responders to the IFN therapy (p<0.05).
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12 |
16685406
|
TRX and TBP-2 mRNA levels in the liver before IFN therapy may predict the outcome of IFN therapy in patients with chronic serotype 1 HCV infection.
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13 |
16685406
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Expression of thioredoxin and thioredoxin-binding protein-2 in the liver of patients with chronic hepatitis C as a predictor of response to interferon therapy.
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14 |
16685406
|
The aim of this study was to evaluate the clinical significance of the expression of TRX and thioredoxin-binding protein-2 (TBP-2), which is a negative regulator of TRX function, in the liver of patients with chronic hepatitis C and the relationship of this to the efficacy of interferon (IFN) treatment.
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15 |
16685406
|
TRX and TBP-2 mRNA levels in the liver biopsy specimens were amplified by real-time RT-PCR.
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16 |
16685406
|
TRX and TBP-2 levels in the liver tended to decrease slightly with increased fibrosis stage, although not significantly.
|
17 |
16685406
|
TBP-2 mRNA levels in the liver were significantly higher in responders than non-responders to the IFN therapy (p<0.05).
|
18 |
16685406
|
TRX and TBP-2 mRNA levels in the liver before IFN therapy may predict the outcome of IFN therapy in patients with chronic serotype 1 HCV infection.
|
19 |
16685406
|
Expression of thioredoxin and thioredoxin-binding protein-2 in the liver of patients with chronic hepatitis C as a predictor of response to interferon therapy.
|
20 |
16685406
|
The aim of this study was to evaluate the clinical significance of the expression of TRX and thioredoxin-binding protein-2 (TBP-2), which is a negative regulator of TRX function, in the liver of patients with chronic hepatitis C and the relationship of this to the efficacy of interferon (IFN) treatment.
|
21 |
16685406
|
TRX and TBP-2 mRNA levels in the liver biopsy specimens were amplified by real-time RT-PCR.
|
22 |
16685406
|
TRX and TBP-2 levels in the liver tended to decrease slightly with increased fibrosis stage, although not significantly.
|
23 |
16685406
|
TBP-2 mRNA levels in the liver were significantly higher in responders than non-responders to the IFN therapy (p<0.05).
|
24 |
16685406
|
TRX and TBP-2 mRNA levels in the liver before IFN therapy may predict the outcome of IFN therapy in patients with chronic serotype 1 HCV infection.
|
25 |
16685406
|
Expression of thioredoxin and thioredoxin-binding protein-2 in the liver of patients with chronic hepatitis C as a predictor of response to interferon therapy.
|
26 |
16685406
|
The aim of this study was to evaluate the clinical significance of the expression of TRX and thioredoxin-binding protein-2 (TBP-2), which is a negative regulator of TRX function, in the liver of patients with chronic hepatitis C and the relationship of this to the efficacy of interferon (IFN) treatment.
|
27 |
16685406
|
TRX and TBP-2 mRNA levels in the liver biopsy specimens were amplified by real-time RT-PCR.
|
28 |
16685406
|
TRX and TBP-2 levels in the liver tended to decrease slightly with increased fibrosis stage, although not significantly.
|
29 |
16685406
|
TBP-2 mRNA levels in the liver were significantly higher in responders than non-responders to the IFN therapy (p<0.05).
|
30 |
16685406
|
TRX and TBP-2 mRNA levels in the liver before IFN therapy may predict the outcome of IFN therapy in patients with chronic serotype 1 HCV infection.
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31 |
17115886
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Thioredoxin and glutaredoxin systems in mammalian cells utilize thiol and selenol groups to maintain a reducing intracellular redox state acting as antioxidants and reducing agents in redox signaling with oxidizing reactive oxygen species.
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32 |
17115886
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The role of thioredoxin and glutaredoxin in antioxidant defense and the role of thioredoxin in controlling recruitment of inflammatory cells offer potential use in clinical therapy.
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33 |
17115886
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Thioredoxin and binding proteins (ASK1 and TBP2) appear to control apoptosis or metabolic states such as carbohydrate and lipid metabolism related to diseases such as diabetes and atherosclerosis.
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34 |
21119640
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Disruption of TBP-2 ameliorates insulin sensitivity and secretion without affecting obesity.
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35 |
21119640
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In this study, we show that disruption of thioredoxin binding protein-2 (TBP-2, also called Txnip) in obese mice (ob/ob) dramatically improves hyperglycaemia and glucose intolerance, without affecting obesity or adipocytokine concentrations.
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36 |
21119640
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TBP-2-deficient ob/ob mice exhibited enhanced insulin sensitivity with activated insulin receptor substrate-1/Akt signalling in skeletal muscle and GSIS in islets compared with ob/ob mice.
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37 |
21119640
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The elevation of uncoupling protein-2 (UCP-2) expression in ob/ob islets was downregulated by TBP-2 deficiency.
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38 |
21119640
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In β-cells, TBP-2 enhanced the expression level and transcriptional activity of UCP-2 by recruitment of peroxisome proliferator-activated receptor-γ co-activator-1α to the UCP-2 promoter.
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39 |
21119640
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Thus, TBP-2 is a key regulatory molecule of both insulin sensitivity and GSIS in diabetes, raising the possibility that inhibition of TBP-2 may be a novel therapeutic approach for T2DM.
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40 |
21119640
|
Disruption of TBP-2 ameliorates insulin sensitivity and secretion without affecting obesity.
|
41 |
21119640
|
In this study, we show that disruption of thioredoxin binding protein-2 (TBP-2, also called Txnip) in obese mice (ob/ob) dramatically improves hyperglycaemia and glucose intolerance, without affecting obesity or adipocytokine concentrations.
|
42 |
21119640
|
TBP-2-deficient ob/ob mice exhibited enhanced insulin sensitivity with activated insulin receptor substrate-1/Akt signalling in skeletal muscle and GSIS in islets compared with ob/ob mice.
|
43 |
21119640
|
The elevation of uncoupling protein-2 (UCP-2) expression in ob/ob islets was downregulated by TBP-2 deficiency.
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44 |
21119640
|
In β-cells, TBP-2 enhanced the expression level and transcriptional activity of UCP-2 by recruitment of peroxisome proliferator-activated receptor-γ co-activator-1α to the UCP-2 promoter.
|
45 |
21119640
|
Thus, TBP-2 is a key regulatory molecule of both insulin sensitivity and GSIS in diabetes, raising the possibility that inhibition of TBP-2 may be a novel therapeutic approach for T2DM.
|
46 |
21119640
|
Disruption of TBP-2 ameliorates insulin sensitivity and secretion without affecting obesity.
|
47 |
21119640
|
In this study, we show that disruption of thioredoxin binding protein-2 (TBP-2, also called Txnip) in obese mice (ob/ob) dramatically improves hyperglycaemia and glucose intolerance, without affecting obesity or adipocytokine concentrations.
|
48 |
21119640
|
TBP-2-deficient ob/ob mice exhibited enhanced insulin sensitivity with activated insulin receptor substrate-1/Akt signalling in skeletal muscle and GSIS in islets compared with ob/ob mice.
|
49 |
21119640
|
The elevation of uncoupling protein-2 (UCP-2) expression in ob/ob islets was downregulated by TBP-2 deficiency.
|
50 |
21119640
|
In β-cells, TBP-2 enhanced the expression level and transcriptional activity of UCP-2 by recruitment of peroxisome proliferator-activated receptor-γ co-activator-1α to the UCP-2 promoter.
|
51 |
21119640
|
Thus, TBP-2 is a key regulatory molecule of both insulin sensitivity and GSIS in diabetes, raising the possibility that inhibition of TBP-2 may be a novel therapeutic approach for T2DM.
|
52 |
21119640
|
Disruption of TBP-2 ameliorates insulin sensitivity and secretion without affecting obesity.
|
53 |
21119640
|
In this study, we show that disruption of thioredoxin binding protein-2 (TBP-2, also called Txnip) in obese mice (ob/ob) dramatically improves hyperglycaemia and glucose intolerance, without affecting obesity or adipocytokine concentrations.
|
54 |
21119640
|
TBP-2-deficient ob/ob mice exhibited enhanced insulin sensitivity with activated insulin receptor substrate-1/Akt signalling in skeletal muscle and GSIS in islets compared with ob/ob mice.
|
55 |
21119640
|
The elevation of uncoupling protein-2 (UCP-2) expression in ob/ob islets was downregulated by TBP-2 deficiency.
|
56 |
21119640
|
In β-cells, TBP-2 enhanced the expression level and transcriptional activity of UCP-2 by recruitment of peroxisome proliferator-activated receptor-γ co-activator-1α to the UCP-2 promoter.
|
57 |
21119640
|
Thus, TBP-2 is a key regulatory molecule of both insulin sensitivity and GSIS in diabetes, raising the possibility that inhibition of TBP-2 may be a novel therapeutic approach for T2DM.
|
58 |
21119640
|
Disruption of TBP-2 ameliorates insulin sensitivity and secretion without affecting obesity.
|
59 |
21119640
|
In this study, we show that disruption of thioredoxin binding protein-2 (TBP-2, also called Txnip) in obese mice (ob/ob) dramatically improves hyperglycaemia and glucose intolerance, without affecting obesity or adipocytokine concentrations.
|
60 |
21119640
|
TBP-2-deficient ob/ob mice exhibited enhanced insulin sensitivity with activated insulin receptor substrate-1/Akt signalling in skeletal muscle and GSIS in islets compared with ob/ob mice.
|
61 |
21119640
|
The elevation of uncoupling protein-2 (UCP-2) expression in ob/ob islets was downregulated by TBP-2 deficiency.
|
62 |
21119640
|
In β-cells, TBP-2 enhanced the expression level and transcriptional activity of UCP-2 by recruitment of peroxisome proliferator-activated receptor-γ co-activator-1α to the UCP-2 promoter.
|
63 |
21119640
|
Thus, TBP-2 is a key regulatory molecule of both insulin sensitivity and GSIS in diabetes, raising the possibility that inhibition of TBP-2 may be a novel therapeutic approach for T2DM.
|