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PMID |
Sentence |
1 |
1725860
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Identification and molecular characterization of insulin-like growth factor binding proteins (IGFBP-1, -2, -3, -4, -5 and -6).
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2 |
1725860
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Six different insulin-like growth factor binding proteins (IGFBPs) have been identified by molecular cloning of their cDNAs from rat and human tissues and designated as IGFBP-1, -2, -3, -4, -5 and -6.
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3 |
1725860
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The total number of amino acid residues for the mature rat BPs ranges from 201 for IGFBP-6 to 270 for IGFBP-2, while the human homologs range from 216 for IGFBP-6 to 289 for IGFBP-2.
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4 |
1725860
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One potential N-linked glycosylation site is located at the mid-region of rat and human IGFBP-4, whereas only human but not rat IGFBP-6 possesses one N-linked glycosylation site at the extreme C-terminal of the molecule.
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5 |
1725860
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An RGD sequence is found in the C-terminal of IGFBP-1 and -2.
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6 |
8159583
|
[Distribution of new cases of insulin-dependent diabetes mellitus (IDDM) by age, sex, seasonality, and clinical characteristics at onset in youngsters from the Friuli Venezia Giulia region from 1987 to 1990].
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7 |
8159583
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A retrospective study was undertaken to estimate the incidence of insulin-dependent diabetes mellitus (IDDM) in youngs (< 18 years) in a North-East Province of Italy: Friuli Venezia Giulia (total population: 1,211,320; under age 18: 185,860).
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8 |
8159583
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All IDDM cases diagnosed between 1987 and 1990, with age onset < 18 years, and using insulin at discharge from hospital, were included. 73 new IDDM cases under 18 years (47 M, 26 F) were observed during the considered period.
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9 |
8159583
|
First admission rates showed seasonal variations, with peaks in Oct/Nov and Jan/Feb.
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10 |
12904165
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The CCN family comprises cysteine-rich 61 (CYR61/CCN1), connective tIssue growth factor (CTGF/CCN2), nephroblastoma overexpressed (NOV/CCN3), and Wnt-induced secreted proteins-1 (WISP-1/CCN4), -2 (WISP-2/CCN5) and -3 (WISP-3/CCN6).
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11 |
18676994
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Proteins related to cell growth (CYR61, protein NOV, and clusterin) were increased, whereas growth arrest-specific 6 (GAS6) and growth/differentiation factor 6 were decreased by Ang II stimulation.
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12 |
18676994
|
Ang II-stimulated changes of plasminogen activator inhibitor-1, GAS6, cathepsin B, and periostin were validated by Western blot.
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13 |
20195391
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CCN3/CCN2 regulation and the fibrosis of diabetic renal disease.
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14 |
23705021
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Nov/Ccn3, a novel transcriptional target of FoxO1, impairs pancreatic β-cell function.
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15 |
23705021
|
The forkhead transcription factor FoxO1 is a prominent mediator of insulin signaling in β-cells.
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16 |
23705021
|
We reasoned that identification of FoxO1 target genes in β-cells could reveal mechanisms linking β-cell dysfunction to insulin resistance.
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17 |
23705021
|
In this study, we report the characterization of Nov/Ccn3 as a novel transcriptional target of FoxO1 in pancreatic β-cells.
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18 |
23705021
|
FoxO1 binds to an evolutionarily conserved response element in the Ccn3 promoter to regulate its expression.
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19 |
23705021
|
Accordingly, CCN3 levels are elevated in pancreatic islets of mice with overexpression of a constitutively active form of FoxO1 or insulin resistance.
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20 |
23705021
|
Moreover, CCN3 decreases glucose oxidation, which translates into inhibition of glucose-stimulated Ca(2+) entry and insulin secretion.
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21 |
23705021
|
Our results identify CCN3, a novel transcriptional target of FoxO1 in pancreatic β-cells, as a potential target for therapeutic intervention in the treatment of diabetes.
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22 |
23705021
|
Nov/Ccn3, a novel transcriptional target of FoxO1, impairs pancreatic β-cell function.
|
23 |
23705021
|
The forkhead transcription factor FoxO1 is a prominent mediator of insulin signaling in β-cells.
|
24 |
23705021
|
We reasoned that identification of FoxO1 target genes in β-cells could reveal mechanisms linking β-cell dysfunction to insulin resistance.
|
25 |
23705021
|
In this study, we report the characterization of Nov/Ccn3 as a novel transcriptional target of FoxO1 in pancreatic β-cells.
|
26 |
23705021
|
FoxO1 binds to an evolutionarily conserved response element in the Ccn3 promoter to regulate its expression.
|
27 |
23705021
|
Accordingly, CCN3 levels are elevated in pancreatic islets of mice with overexpression of a constitutively active form of FoxO1 or insulin resistance.
|
28 |
23705021
|
Moreover, CCN3 decreases glucose oxidation, which translates into inhibition of glucose-stimulated Ca(2+) entry and insulin secretion.
|
29 |
23705021
|
Our results identify CCN3, a novel transcriptional target of FoxO1 in pancreatic β-cells, as a potential target for therapeutic intervention in the treatment of diabetes.
|
30 |
23705021
|
Nov/Ccn3, a novel transcriptional target of FoxO1, impairs pancreatic β-cell function.
|
31 |
23705021
|
The forkhead transcription factor FoxO1 is a prominent mediator of insulin signaling in β-cells.
|
32 |
23705021
|
We reasoned that identification of FoxO1 target genes in β-cells could reveal mechanisms linking β-cell dysfunction to insulin resistance.
|
33 |
23705021
|
In this study, we report the characterization of Nov/Ccn3 as a novel transcriptional target of FoxO1 in pancreatic β-cells.
|
34 |
23705021
|
FoxO1 binds to an evolutionarily conserved response element in the Ccn3 promoter to regulate its expression.
|
35 |
23705021
|
Accordingly, CCN3 levels are elevated in pancreatic islets of mice with overexpression of a constitutively active form of FoxO1 or insulin resistance.
|
36 |
23705021
|
Moreover, CCN3 decreases glucose oxidation, which translates into inhibition of glucose-stimulated Ca(2+) entry and insulin secretion.
|
37 |
23705021
|
Our results identify CCN3, a novel transcriptional target of FoxO1 in pancreatic β-cells, as a potential target for therapeutic intervention in the treatment of diabetes.
|
38 |
23705021
|
Nov/Ccn3, a novel transcriptional target of FoxO1, impairs pancreatic β-cell function.
|
39 |
23705021
|
The forkhead transcription factor FoxO1 is a prominent mediator of insulin signaling in β-cells.
|
40 |
23705021
|
We reasoned that identification of FoxO1 target genes in β-cells could reveal mechanisms linking β-cell dysfunction to insulin resistance.
|
41 |
23705021
|
In this study, we report the characterization of Nov/Ccn3 as a novel transcriptional target of FoxO1 in pancreatic β-cells.
|
42 |
23705021
|
FoxO1 binds to an evolutionarily conserved response element in the Ccn3 promoter to regulate its expression.
|
43 |
23705021
|
Accordingly, CCN3 levels are elevated in pancreatic islets of mice with overexpression of a constitutively active form of FoxO1 or insulin resistance.
|
44 |
23705021
|
Moreover, CCN3 decreases glucose oxidation, which translates into inhibition of glucose-stimulated Ca(2+) entry and insulin secretion.
|
45 |
23705021
|
Our results identify CCN3, a novel transcriptional target of FoxO1 in pancreatic β-cells, as a potential target for therapeutic intervention in the treatment of diabetes.
|
46 |
23705021
|
Nov/Ccn3, a novel transcriptional target of FoxO1, impairs pancreatic β-cell function.
|
47 |
23705021
|
The forkhead transcription factor FoxO1 is a prominent mediator of insulin signaling in β-cells.
|
48 |
23705021
|
We reasoned that identification of FoxO1 target genes in β-cells could reveal mechanisms linking β-cell dysfunction to insulin resistance.
|
49 |
23705021
|
In this study, we report the characterization of Nov/Ccn3 as a novel transcriptional target of FoxO1 in pancreatic β-cells.
|
50 |
23705021
|
FoxO1 binds to an evolutionarily conserved response element in the Ccn3 promoter to regulate its expression.
|
51 |
23705021
|
Accordingly, CCN3 levels are elevated in pancreatic islets of mice with overexpression of a constitutively active form of FoxO1 or insulin resistance.
|
52 |
23705021
|
Moreover, CCN3 decreases glucose oxidation, which translates into inhibition of glucose-stimulated Ca(2+) entry and insulin secretion.
|
53 |
23705021
|
Our results identify CCN3, a novel transcriptional target of FoxO1 in pancreatic β-cells, as a potential target for therapeutic intervention in the treatment of diabetes.
|
54 |
23705021
|
Nov/Ccn3, a novel transcriptional target of FoxO1, impairs pancreatic β-cell function.
|
55 |
23705021
|
The forkhead transcription factor FoxO1 is a prominent mediator of insulin signaling in β-cells.
|
56 |
23705021
|
We reasoned that identification of FoxO1 target genes in β-cells could reveal mechanisms linking β-cell dysfunction to insulin resistance.
|
57 |
23705021
|
In this study, we report the characterization of Nov/Ccn3 as a novel transcriptional target of FoxO1 in pancreatic β-cells.
|
58 |
23705021
|
FoxO1 binds to an evolutionarily conserved response element in the Ccn3 promoter to regulate its expression.
|
59 |
23705021
|
Accordingly, CCN3 levels are elevated in pancreatic islets of mice with overexpression of a constitutively active form of FoxO1 or insulin resistance.
|
60 |
23705021
|
Moreover, CCN3 decreases glucose oxidation, which translates into inhibition of glucose-stimulated Ca(2+) entry and insulin secretion.
|
61 |
23705021
|
Our results identify CCN3, a novel transcriptional target of FoxO1 in pancreatic β-cells, as a potential target for therapeutic intervention in the treatment of diabetes.
|