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PMID |
Sentence |
1 |
18644868
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Prep1 deficiency induces protection from diabetes and increased insulin sensitivity through a p160-mediated mechanism.
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2 |
18644868
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Prep1-hypomorphic (Prep1(i/i)) mice exhibit an absolute reduction in circulating insulin levels but normal glucose tolerance.
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3 |
18644868
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Instead, in Prep1(i/i) muscle, we find normal Pbx1 but reduced levels of the recently identified novel Prep1 interactor p160.
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4 |
18644868
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Consistent with this reduction, we find a muscle-selective increase in mRNA and protein levels of PGC-1alpha, accompanied by enhanced expression of the GLUT4 transporter, responsible for insulin-stimulated glucose uptake in muscle.
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5 |
18644868
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Indeed, using L6 skeletal muscle cells, we induced the opposite effects by overexpressing Prep1 or p160, but not Pbx1.
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6 |
18644868
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In vivo skeletal muscle delivery of p160 cDNA in Prep1(i/i) mice also reverses the molecular phenotype.
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7 |
18644868
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Finally, we show that Prep1 controls the stability of the p160 protein.
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8 |
18644868
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We conclude that Prep1 controls insulin sensitivity through the p160-GLUT4 pathway.
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9 |
18644868
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Prep1 deficiency induces protection from diabetes and increased insulin sensitivity through a p160-mediated mechanism.
|
10 |
18644868
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Prep1-hypomorphic (Prep1(i/i)) mice exhibit an absolute reduction in circulating insulin levels but normal glucose tolerance.
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11 |
18644868
|
Instead, in Prep1(i/i) muscle, we find normal Pbx1 but reduced levels of the recently identified novel Prep1 interactor p160.
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12 |
18644868
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Consistent with this reduction, we find a muscle-selective increase in mRNA and protein levels of PGC-1alpha, accompanied by enhanced expression of the GLUT4 transporter, responsible for insulin-stimulated glucose uptake in muscle.
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13 |
18644868
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Indeed, using L6 skeletal muscle cells, we induced the opposite effects by overexpressing Prep1 or p160, but not Pbx1.
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14 |
18644868
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In vivo skeletal muscle delivery of p160 cDNA in Prep1(i/i) mice also reverses the molecular phenotype.
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15 |
18644868
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Finally, we show that Prep1 controls the stability of the p160 protein.
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16 |
18644868
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We conclude that Prep1 controls insulin sensitivity through the p160-GLUT4 pathway.
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17 |
18644868
|
Prep1 deficiency induces protection from diabetes and increased insulin sensitivity through a p160-mediated mechanism.
|
18 |
18644868
|
Prep1-hypomorphic (Prep1(i/i)) mice exhibit an absolute reduction in circulating insulin levels but normal glucose tolerance.
|
19 |
18644868
|
Instead, in Prep1(i/i) muscle, we find normal Pbx1 but reduced levels of the recently identified novel Prep1 interactor p160.
|
20 |
18644868
|
Consistent with this reduction, we find a muscle-selective increase in mRNA and protein levels of PGC-1alpha, accompanied by enhanced expression of the GLUT4 transporter, responsible for insulin-stimulated glucose uptake in muscle.
|
21 |
18644868
|
Indeed, using L6 skeletal muscle cells, we induced the opposite effects by overexpressing Prep1 or p160, but not Pbx1.
|
22 |
18644868
|
In vivo skeletal muscle delivery of p160 cDNA in Prep1(i/i) mice also reverses the molecular phenotype.
|
23 |
18644868
|
Finally, we show that Prep1 controls the stability of the p160 protein.
|
24 |
18644868
|
We conclude that Prep1 controls insulin sensitivity through the p160-GLUT4 pathway.
|
25 |
18644868
|
Prep1 deficiency induces protection from diabetes and increased insulin sensitivity through a p160-mediated mechanism.
|
26 |
18644868
|
Prep1-hypomorphic (Prep1(i/i)) mice exhibit an absolute reduction in circulating insulin levels but normal glucose tolerance.
|
27 |
18644868
|
Instead, in Prep1(i/i) muscle, we find normal Pbx1 but reduced levels of the recently identified novel Prep1 interactor p160.
|
28 |
18644868
|
Consistent with this reduction, we find a muscle-selective increase in mRNA and protein levels of PGC-1alpha, accompanied by enhanced expression of the GLUT4 transporter, responsible for insulin-stimulated glucose uptake in muscle.
|
29 |
18644868
|
Indeed, using L6 skeletal muscle cells, we induced the opposite effects by overexpressing Prep1 or p160, but not Pbx1.
|
30 |
18644868
|
In vivo skeletal muscle delivery of p160 cDNA in Prep1(i/i) mice also reverses the molecular phenotype.
|
31 |
18644868
|
Finally, we show that Prep1 controls the stability of the p160 protein.
|
32 |
18644868
|
We conclude that Prep1 controls insulin sensitivity through the p160-GLUT4 pathway.
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33 |
18644868
|
Prep1 deficiency induces protection from diabetes and increased insulin sensitivity through a p160-mediated mechanism.
|
34 |
18644868
|
Prep1-hypomorphic (Prep1(i/i)) mice exhibit an absolute reduction in circulating insulin levels but normal glucose tolerance.
|
35 |
18644868
|
Instead, in Prep1(i/i) muscle, we find normal Pbx1 but reduced levels of the recently identified novel Prep1 interactor p160.
|
36 |
18644868
|
Consistent with this reduction, we find a muscle-selective increase in mRNA and protein levels of PGC-1alpha, accompanied by enhanced expression of the GLUT4 transporter, responsible for insulin-stimulated glucose uptake in muscle.
|
37 |
18644868
|
Indeed, using L6 skeletal muscle cells, we induced the opposite effects by overexpressing Prep1 or p160, but not Pbx1.
|
38 |
18644868
|
In vivo skeletal muscle delivery of p160 cDNA in Prep1(i/i) mice also reverses the molecular phenotype.
|
39 |
18644868
|
Finally, we show that Prep1 controls the stability of the p160 protein.
|
40 |
18644868
|
We conclude that Prep1 controls insulin sensitivity through the p160-GLUT4 pathway.
|
41 |
18644868
|
Prep1 deficiency induces protection from diabetes and increased insulin sensitivity through a p160-mediated mechanism.
|
42 |
18644868
|
Prep1-hypomorphic (Prep1(i/i)) mice exhibit an absolute reduction in circulating insulin levels but normal glucose tolerance.
|
43 |
18644868
|
Instead, in Prep1(i/i) muscle, we find normal Pbx1 but reduced levels of the recently identified novel Prep1 interactor p160.
|
44 |
18644868
|
Consistent with this reduction, we find a muscle-selective increase in mRNA and protein levels of PGC-1alpha, accompanied by enhanced expression of the GLUT4 transporter, responsible for insulin-stimulated glucose uptake in muscle.
|
45 |
18644868
|
Indeed, using L6 skeletal muscle cells, we induced the opposite effects by overexpressing Prep1 or p160, but not Pbx1.
|
46 |
18644868
|
In vivo skeletal muscle delivery of p160 cDNA in Prep1(i/i) mice also reverses the molecular phenotype.
|
47 |
18644868
|
Finally, we show that Prep1 controls the stability of the p160 protein.
|
48 |
18644868
|
We conclude that Prep1 controls insulin sensitivity through the p160-GLUT4 pathway.
|
49 |
18644868
|
Prep1 deficiency induces protection from diabetes and increased insulin sensitivity through a p160-mediated mechanism.
|
50 |
18644868
|
Prep1-hypomorphic (Prep1(i/i)) mice exhibit an absolute reduction in circulating insulin levels but normal glucose tolerance.
|
51 |
18644868
|
Instead, in Prep1(i/i) muscle, we find normal Pbx1 but reduced levels of the recently identified novel Prep1 interactor p160.
|
52 |
18644868
|
Consistent with this reduction, we find a muscle-selective increase in mRNA and protein levels of PGC-1alpha, accompanied by enhanced expression of the GLUT4 transporter, responsible for insulin-stimulated glucose uptake in muscle.
|
53 |
18644868
|
Indeed, using L6 skeletal muscle cells, we induced the opposite effects by overexpressing Prep1 or p160, but not Pbx1.
|
54 |
18644868
|
In vivo skeletal muscle delivery of p160 cDNA in Prep1(i/i) mice also reverses the molecular phenotype.
|
55 |
18644868
|
Finally, we show that Prep1 controls the stability of the p160 protein.
|
56 |
18644868
|
We conclude that Prep1 controls insulin sensitivity through the p160-GLUT4 pathway.
|