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PMID |
Sentence |
1 |
10826522
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In order to assess radiation-induced alterations in cultured thyroid cells, the occurrence of apoptosis and necrosis as well as the expression of thyroid peroxidase (TPO) and of two members of the 70 kD heat shock family, HSP-73 and HSP-72, were analysed following gamma irradiation.
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2 |
10826522
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TPO and HSP expression by SDS-PAGE and Western blotting.
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3 |
10826522
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Interestingly, the expression of TPO, a key enzyme of thyroid hormone synthesis, decreased significantly in irradiated TEC, while HSP-73 expression remained unchanged.
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4 |
10826522
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In order to assess radiation-induced alterations in cultured thyroid cells, the occurrence of apoptosis and necrosis as well as the expression of thyroid peroxidase (TPO) and of two members of the 70 kD heat shock family, HSP-73 and HSP-72, were analysed following gamma irradiation.
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5 |
10826522
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TPO and HSP expression by SDS-PAGE and Western blotting.
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6 |
10826522
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Interestingly, the expression of TPO, a key enzyme of thyroid hormone synthesis, decreased significantly in irradiated TEC, while HSP-73 expression remained unchanged.
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7 |
10976917
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Previously recognized intracellular proteins with an affinity for vitamin D metabolites include the vitamin D receptor and the cytochrome P-450-based vitamin D metabolizing mixed-function oxidases.
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8 |
10976917
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The full-length cDNAs for IDBP-1 and IDBP-2 demonstrated 95% and 94% nucleotide homology, respectively, with the cDNAs for human constitutively expressed heat shock protein 70 (hsc-70) and hsp-70.
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9 |
10976917
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Stable overexpression of IDBP-1 in wild-type cells enhanced vitamin D-directed responsiveness of endogenous vitamin D-24-hydroxylase, osteopontin, and osteocalcin genes by several-fold over that observed in cells transfected with an empty vector.
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10 |
11712664
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Here, we examined the cellular levels of stress proteins such as HSP105, HSP90 and HSC70/HSP70 in various tissues of streptozotocin-induced diabetic rats.
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11 |
11712664
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Furthermore, the induction of HSP70 as well as HSC70 by hyperthermia was significantly reduced in the liver and adrenal gland of diabetic rats.
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12 |
11712664
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These results suggested that the expression and induction of HSC70/HSP70 may be altered during the course of diabetic disease and may result in impairment of the cytoprotective ability of diabetic rats.
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13 |
11712664
|
Here, we examined the cellular levels of stress proteins such as HSP105, HSP90 and HSC70/HSP70 in various tissues of streptozotocin-induced diabetic rats.
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14 |
11712664
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Furthermore, the induction of HSP70 as well as HSC70 by hyperthermia was significantly reduced in the liver and adrenal gland of diabetic rats.
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15 |
11712664
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These results suggested that the expression and induction of HSC70/HSP70 may be altered during the course of diabetic disease and may result in impairment of the cytoprotective ability of diabetic rats.
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16 |
11712664
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Here, we examined the cellular levels of stress proteins such as HSP105, HSP90 and HSC70/HSP70 in various tissues of streptozotocin-induced diabetic rats.
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17 |
11712664
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Furthermore, the induction of HSP70 as well as HSC70 by hyperthermia was significantly reduced in the liver and adrenal gland of diabetic rats.
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18 |
11712664
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These results suggested that the expression and induction of HSC70/HSP70 may be altered during the course of diabetic disease and may result in impairment of the cytoprotective ability of diabetic rats.
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19 |
16899576
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Downregulation of the constitutively expressed Hsc70 in diabetic myocardium is mediated by insulin deficiency.
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20 |
16899576
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This study was carried out to define the changes in the 70 kDa heat shock protein family in the myocardium in the of streptozotocin-diabetes rats, and to explore the mechanisms through which diabetes alters the abundance of Hsp70/Hsc70 in cardiac muscle.
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21 |
16899576
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Unlike Hsp60, Hsp70 and Hsc70 did not augment insulin-like growth factor-I receptor signaling in cardiac muscle cells.
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22 |
16899576
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In cultured cardiomyocytes, insulin directly increased the abundance of Hsc70, whereas insulin could not modulate Hsp70.
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23 |
16899576
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Treating diabetic rats with insulin restored myocardial Hsc70 level, but phlorizin treatment failed to restore myocardial Hsc70.
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24 |
16899576
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These in vivo and in vitro studies showed that downregulation of Hsc70 in diabetic myocardium was secondary to insulin deficiency.
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25 |
16899576
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Thus, insulin played a major role in maintaining adequate expression of Hsc70 in cardiac muscle.
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26 |
16899576
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Downregulation of the constitutively expressed Hsc70 in diabetic myocardium is mediated by insulin deficiency.
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27 |
16899576
|
This study was carried out to define the changes in the 70 kDa heat shock protein family in the myocardium in the of streptozotocin-diabetes rats, and to explore the mechanisms through which diabetes alters the abundance of Hsp70/Hsc70 in cardiac muscle.
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28 |
16899576
|
Unlike Hsp60, Hsp70 and Hsc70 did not augment insulin-like growth factor-I receptor signaling in cardiac muscle cells.
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29 |
16899576
|
In cultured cardiomyocytes, insulin directly increased the abundance of Hsc70, whereas insulin could not modulate Hsp70.
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30 |
16899576
|
Treating diabetic rats with insulin restored myocardial Hsc70 level, but phlorizin treatment failed to restore myocardial Hsc70.
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31 |
16899576
|
These in vivo and in vitro studies showed that downregulation of Hsc70 in diabetic myocardium was secondary to insulin deficiency.
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32 |
16899576
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Thus, insulin played a major role in maintaining adequate expression of Hsc70 in cardiac muscle.
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33 |
16899576
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Downregulation of the constitutively expressed Hsc70 in diabetic myocardium is mediated by insulin deficiency.
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34 |
16899576
|
This study was carried out to define the changes in the 70 kDa heat shock protein family in the myocardium in the of streptozotocin-diabetes rats, and to explore the mechanisms through which diabetes alters the abundance of Hsp70/Hsc70 in cardiac muscle.
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35 |
16899576
|
Unlike Hsp60, Hsp70 and Hsc70 did not augment insulin-like growth factor-I receptor signaling in cardiac muscle cells.
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36 |
16899576
|
In cultured cardiomyocytes, insulin directly increased the abundance of Hsc70, whereas insulin could not modulate Hsp70.
|
37 |
16899576
|
Treating diabetic rats with insulin restored myocardial Hsc70 level, but phlorizin treatment failed to restore myocardial Hsc70.
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38 |
16899576
|
These in vivo and in vitro studies showed that downregulation of Hsc70 in diabetic myocardium was secondary to insulin deficiency.
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39 |
16899576
|
Thus, insulin played a major role in maintaining adequate expression of Hsc70 in cardiac muscle.
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40 |
16899576
|
Downregulation of the constitutively expressed Hsc70 in diabetic myocardium is mediated by insulin deficiency.
|
41 |
16899576
|
This study was carried out to define the changes in the 70 kDa heat shock protein family in the myocardium in the of streptozotocin-diabetes rats, and to explore the mechanisms through which diabetes alters the abundance of Hsp70/Hsc70 in cardiac muscle.
|
42 |
16899576
|
Unlike Hsp60, Hsp70 and Hsc70 did not augment insulin-like growth factor-I receptor signaling in cardiac muscle cells.
|
43 |
16899576
|
In cultured cardiomyocytes, insulin directly increased the abundance of Hsc70, whereas insulin could not modulate Hsp70.
|
44 |
16899576
|
Treating diabetic rats with insulin restored myocardial Hsc70 level, but phlorizin treatment failed to restore myocardial Hsc70.
|
45 |
16899576
|
These in vivo and in vitro studies showed that downregulation of Hsc70 in diabetic myocardium was secondary to insulin deficiency.
|
46 |
16899576
|
Thus, insulin played a major role in maintaining adequate expression of Hsc70 in cardiac muscle.
|
47 |
16899576
|
Downregulation of the constitutively expressed Hsc70 in diabetic myocardium is mediated by insulin deficiency.
|
48 |
16899576
|
This study was carried out to define the changes in the 70 kDa heat shock protein family in the myocardium in the of streptozotocin-diabetes rats, and to explore the mechanisms through which diabetes alters the abundance of Hsp70/Hsc70 in cardiac muscle.
|
49 |
16899576
|
Unlike Hsp60, Hsp70 and Hsc70 did not augment insulin-like growth factor-I receptor signaling in cardiac muscle cells.
|
50 |
16899576
|
In cultured cardiomyocytes, insulin directly increased the abundance of Hsc70, whereas insulin could not modulate Hsp70.
|
51 |
16899576
|
Treating diabetic rats with insulin restored myocardial Hsc70 level, but phlorizin treatment failed to restore myocardial Hsc70.
|
52 |
16899576
|
These in vivo and in vitro studies showed that downregulation of Hsc70 in diabetic myocardium was secondary to insulin deficiency.
|
53 |
16899576
|
Thus, insulin played a major role in maintaining adequate expression of Hsc70 in cardiac muscle.
|
54 |
16899576
|
Downregulation of the constitutively expressed Hsc70 in diabetic myocardium is mediated by insulin deficiency.
|
55 |
16899576
|
This study was carried out to define the changes in the 70 kDa heat shock protein family in the myocardium in the of streptozotocin-diabetes rats, and to explore the mechanisms through which diabetes alters the abundance of Hsp70/Hsc70 in cardiac muscle.
|
56 |
16899576
|
Unlike Hsp60, Hsp70 and Hsc70 did not augment insulin-like growth factor-I receptor signaling in cardiac muscle cells.
|
57 |
16899576
|
In cultured cardiomyocytes, insulin directly increased the abundance of Hsc70, whereas insulin could not modulate Hsp70.
|
58 |
16899576
|
Treating diabetic rats with insulin restored myocardial Hsc70 level, but phlorizin treatment failed to restore myocardial Hsc70.
|
59 |
16899576
|
These in vivo and in vitro studies showed that downregulation of Hsc70 in diabetic myocardium was secondary to insulin deficiency.
|
60 |
16899576
|
Thus, insulin played a major role in maintaining adequate expression of Hsc70 in cardiac muscle.
|
61 |
16899576
|
Downregulation of the constitutively expressed Hsc70 in diabetic myocardium is mediated by insulin deficiency.
|
62 |
16899576
|
This study was carried out to define the changes in the 70 kDa heat shock protein family in the myocardium in the of streptozotocin-diabetes rats, and to explore the mechanisms through which diabetes alters the abundance of Hsp70/Hsc70 in cardiac muscle.
|
63 |
16899576
|
Unlike Hsp60, Hsp70 and Hsc70 did not augment insulin-like growth factor-I receptor signaling in cardiac muscle cells.
|
64 |
16899576
|
In cultured cardiomyocytes, insulin directly increased the abundance of Hsc70, whereas insulin could not modulate Hsp70.
|
65 |
16899576
|
Treating diabetic rats with insulin restored myocardial Hsc70 level, but phlorizin treatment failed to restore myocardial Hsc70.
|
66 |
16899576
|
These in vivo and in vitro studies showed that downregulation of Hsc70 in diabetic myocardium was secondary to insulin deficiency.
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67 |
16899576
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Thus, insulin played a major role in maintaining adequate expression of Hsc70 in cardiac muscle.
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68 |
17330940
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They also had increased levels of heat shock protein (HSP) 60 kDa isoform #A4, of HSP71 kDa isoform #A30, and of HSP27 kDa isoform #6, whereas the HSP27 kDa isoforms #A90 and #A71 were decreased.
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69 |
17330940
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Cathepsin beta-2 (#40), the cation-independent mannose 6-phosphate receptor binding protein 1 (CIMPR) (#A27), and annexin 2 (#A9) were also decreased in the [DN+] T1DM patients, whereas the RNA-binding protein regulatory subunity (#38) and the translationally-controlled tumor protein (TCTP) (#A45) were increased.
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70 |
17693608
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Co-chaperone potentiation of vitamin D receptor-mediated transactivation: a role for Bcl2-associated athanogene-1 as an intracellular-binding protein for 1,25-dihydroxyvitamin D3.
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71 |
17693608
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Hsc70 also recruits and interacts with the co-chaperone Bcl2-associated athanogene (BAG)-1 via the ATP-binding domain that resides on hsc70.
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72 |
17693608
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To investigate the functional significance of this, we transiently overexpressed the S, M, and L variants of BAG-1 into human kidney HKC-8 cells stably transfected with a 1,25(OH)2D3-responsive 24-hydroxylase (CYP24) promoter-reporter construct.
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73 |
17693608
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These data highlight a novel role for BAG-1 as an intracellular-binding protein for 1,25(OH)2D3 and further suggest that BAG-1 is able to potentiate vitamin D receptor-mediated transactivation by acting as a nuclear chaperone for 1,25(OH)2D3.
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74 |
21104931
|
Diabetes increased constitutive HSC70 mRNA, and decreased HSP90 and glucose-regulated protein 75 (GRP75) mRNA without affecting protein levels.
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75 |
21104931
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Exercise increased HSP90 protein and mRNA, and also GRP75 and heme oxygenase-1 (HO-1) mRNA only in non-diabetic animals.
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76 |
21104931
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LA had no significant effect on brain HSPs, although LA increased HSC70 and HO-1 mRNA in diabetic animals and decreased HSC70 mRNA in non-diabetic animals.
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77 |
21104931
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Eukaryotic translation elongation factor-2, essential for protein synthesis, was decreased by diabetes and suggesting a mechanism for the impaired HSP response related to translocation of the nascent chain during protein synthesis.
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78 |
21104931
|
Diabetes increased constitutive HSC70 mRNA, and decreased HSP90 and glucose-regulated protein 75 (GRP75) mRNA without affecting protein levels.
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79 |
21104931
|
Exercise increased HSP90 protein and mRNA, and also GRP75 and heme oxygenase-1 (HO-1) mRNA only in non-diabetic animals.
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80 |
21104931
|
LA had no significant effect on brain HSPs, although LA increased HSC70 and HO-1 mRNA in diabetic animals and decreased HSC70 mRNA in non-diabetic animals.
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81 |
21104931
|
Eukaryotic translation elongation factor-2, essential for protein synthesis, was decreased by diabetes and suggesting a mechanism for the impaired HSP response related to translocation of the nascent chain during protein synthesis.
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82 |
21475814
|
Association of polymorphisms of THBS2 and HSPA8 with hypertension in Japanese individuals with chronic kidney disease.
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83 |
21475814
|
Subsequent multivariable logistic regression analysis with adjustment for age, gender and the prevalence of diabetes mellitus revealed that these two polymorphisms, 3949T↷G (3'-UTR) of the thrombospondin 2 gene (THBS2; odds ratio in recessive model, 8.31) and -110A↷C of the heat shock 70-kDa protein 8 gene (HSPA8; odds ratio in recessive model, 0.72) were significantly (P<0.05) associated with the prevalence of hypertension.
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84 |
21475814
|
The variant G allele of THBS2 was a risk factor for hypertension, whereas the variant C allele of HSPA8 was protective against this condition.
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85 |
21475814
|
A stepwise forward selection procedure also demonstrated that the THBS2 and HSPA8 genotypes were significant (P<0.05) and independent determinants of hypertension.
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86 |
21475814
|
Association of polymorphisms of THBS2 and HSPA8 with hypertension in Japanese individuals with chronic kidney disease.
|
87 |
21475814
|
Subsequent multivariable logistic regression analysis with adjustment for age, gender and the prevalence of diabetes mellitus revealed that these two polymorphisms, 3949T↷G (3'-UTR) of the thrombospondin 2 gene (THBS2; odds ratio in recessive model, 8.31) and -110A↷C of the heat shock 70-kDa protein 8 gene (HSPA8; odds ratio in recessive model, 0.72) were significantly (P<0.05) associated with the prevalence of hypertension.
|
88 |
21475814
|
The variant G allele of THBS2 was a risk factor for hypertension, whereas the variant C allele of HSPA8 was protective against this condition.
|
89 |
21475814
|
A stepwise forward selection procedure also demonstrated that the THBS2 and HSPA8 genotypes were significant (P<0.05) and independent determinants of hypertension.
|
90 |
21475814
|
Association of polymorphisms of THBS2 and HSPA8 with hypertension in Japanese individuals with chronic kidney disease.
|
91 |
21475814
|
Subsequent multivariable logistic regression analysis with adjustment for age, gender and the prevalence of diabetes mellitus revealed that these two polymorphisms, 3949T↷G (3'-UTR) of the thrombospondin 2 gene (THBS2; odds ratio in recessive model, 8.31) and -110A↷C of the heat shock 70-kDa protein 8 gene (HSPA8; odds ratio in recessive model, 0.72) were significantly (P<0.05) associated with the prevalence of hypertension.
|
92 |
21475814
|
The variant G allele of THBS2 was a risk factor for hypertension, whereas the variant C allele of HSPA8 was protective against this condition.
|
93 |
21475814
|
A stepwise forward selection procedure also demonstrated that the THBS2 and HSPA8 genotypes were significant (P<0.05) and independent determinants of hypertension.
|
94 |
21475814
|
Association of polymorphisms of THBS2 and HSPA8 with hypertension in Japanese individuals with chronic kidney disease.
|
95 |
21475814
|
Subsequent multivariable logistic regression analysis with adjustment for age, gender and the prevalence of diabetes mellitus revealed that these two polymorphisms, 3949T↷G (3'-UTR) of the thrombospondin 2 gene (THBS2; odds ratio in recessive model, 8.31) and -110A↷C of the heat shock 70-kDa protein 8 gene (HSPA8; odds ratio in recessive model, 0.72) were significantly (P<0.05) associated with the prevalence of hypertension.
|
96 |
21475814
|
The variant G allele of THBS2 was a risk factor for hypertension, whereas the variant C allele of HSPA8 was protective against this condition.
|
97 |
21475814
|
A stepwise forward selection procedure also demonstrated that the THBS2 and HSPA8 genotypes were significant (P<0.05) and independent determinants of hypertension.
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98 |
22311732
|
Tadalafil reversed the coordinated alterations of cytoskeletal/contractile proteins such as myosin light chain (MLY) 2 and 4, myosin heavy chain α and myosin-binding protein C which contributes to contractile dysfunction.
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99 |
22311732
|
The expression of intermediate filament protein vimentin and extra-cellular matrix proteins like cysteine and glycine rich protein-3 and collagen type VI α were upregulated in db/db mice indicating cardiac remodeling in diabetes.
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100 |
22311732
|
Tadalafil also enhanced antioxidant enzyme glutathione S-transferase Kappa-1 (GSKT-1) and downregulated redox regulatory chaperones like heat shock protein 8 (HSPA8), and 75 kD glucose regulatory protein (75GRP).
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101 |
22719926
|
We identified an arsenic exposure related 51-gene signature at PND1 and PND70 with several hubs of interaction (Hspa8, IgM and Hnf4a).
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102 |
22719926
|
Western blot analysis confirmed changes in the liver at PND70 that included increases of heat shock protein 70 (Hspa8) and active SREBP1.
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103 |
22719926
|
We identified an arsenic exposure related 51-gene signature at PND1 and PND70 with several hubs of interaction (Hspa8, IgM and Hnf4a).
|
104 |
22719926
|
Western blot analysis confirmed changes in the liver at PND70 that included increases of heat shock protein 70 (Hspa8) and active SREBP1.
|