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PMID |
Sentence |
1 |
11754100
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Two novel types of contiguous gene deletion of the AVPR2 and ARHGAP4 genes in unrelated Japanese kindreds with nephrogenic diabetes insipidus.
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2 |
11754100
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Study of two families containing individuals with nephrogenic diabetes insipidus (NDI) indicated different types of 21.3 kb and 26.3 kb deletions involving the AVPR2 and ARHGAP4 (RhoGAP C1) genes.
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3 |
11754100
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We defined three deletion junctions in this rearrangement (DJ1, DJ2, and DJ3) from the 5'-side.
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4 |
21426932
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High glucose upregulation of early-onset Parkinson's disease protein DJ-1 integrates the PRAS40/TORC1 axis to mesangial cell hypertrophy.
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5 |
21426932
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We identified DJ-1 to increase in response to high glucose in renal glomerular mesangial cells concomitant with an increase in phosphorylation of Akt in a time-dependent manner.
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6 |
21426932
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Plasmid-derived overexpression as well as downregulation of DJ-1 by siRNA showed the requirement of this protein in high glucose-stimulated Akt phosphorylation.
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7 |
21426932
|
The tumor suppressor protein PTEN acts as a negative regulator of Akt activation.
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8 |
21426932
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Interestingly, DJ-1 was associated with PTEN and this interaction was significantly increased in response to high glucose.
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9 |
21426932
|
High glucose-induced increase in DJ-1 promoted phosphorylation of the PRAS40, a negative regulator of TORC1 kinase activity, resulting in activating and inactivating phosphorylation of S6 kinase and 4EBP-1, respectively.
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10 |
21426932
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Our results provide evidence for a unique mechanism whereby DJ-1 induces Akt/PRAS40/TORC1-mediated hypertrophy in response to high glucose.
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11 |
21426932
|
High glucose upregulation of early-onset Parkinson's disease protein DJ-1 integrates the PRAS40/TORC1 axis to mesangial cell hypertrophy.
|
12 |
21426932
|
We identified DJ-1 to increase in response to high glucose in renal glomerular mesangial cells concomitant with an increase in phosphorylation of Akt in a time-dependent manner.
|
13 |
21426932
|
Plasmid-derived overexpression as well as downregulation of DJ-1 by siRNA showed the requirement of this protein in high glucose-stimulated Akt phosphorylation.
|
14 |
21426932
|
The tumor suppressor protein PTEN acts as a negative regulator of Akt activation.
|
15 |
21426932
|
Interestingly, DJ-1 was associated with PTEN and this interaction was significantly increased in response to high glucose.
|
16 |
21426932
|
High glucose-induced increase in DJ-1 promoted phosphorylation of the PRAS40, a negative regulator of TORC1 kinase activity, resulting in activating and inactivating phosphorylation of S6 kinase and 4EBP-1, respectively.
|
17 |
21426932
|
Our results provide evidence for a unique mechanism whereby DJ-1 induces Akt/PRAS40/TORC1-mediated hypertrophy in response to high glucose.
|
18 |
21426932
|
High glucose upregulation of early-onset Parkinson's disease protein DJ-1 integrates the PRAS40/TORC1 axis to mesangial cell hypertrophy.
|
19 |
21426932
|
We identified DJ-1 to increase in response to high glucose in renal glomerular mesangial cells concomitant with an increase in phosphorylation of Akt in a time-dependent manner.
|
20 |
21426932
|
Plasmid-derived overexpression as well as downregulation of DJ-1 by siRNA showed the requirement of this protein in high glucose-stimulated Akt phosphorylation.
|
21 |
21426932
|
The tumor suppressor protein PTEN acts as a negative regulator of Akt activation.
|
22 |
21426932
|
Interestingly, DJ-1 was associated with PTEN and this interaction was significantly increased in response to high glucose.
|
23 |
21426932
|
High glucose-induced increase in DJ-1 promoted phosphorylation of the PRAS40, a negative regulator of TORC1 kinase activity, resulting in activating and inactivating phosphorylation of S6 kinase and 4EBP-1, respectively.
|
24 |
21426932
|
Our results provide evidence for a unique mechanism whereby DJ-1 induces Akt/PRAS40/TORC1-mediated hypertrophy in response to high glucose.
|
25 |
21426932
|
High glucose upregulation of early-onset Parkinson's disease protein DJ-1 integrates the PRAS40/TORC1 axis to mesangial cell hypertrophy.
|
26 |
21426932
|
We identified DJ-1 to increase in response to high glucose in renal glomerular mesangial cells concomitant with an increase in phosphorylation of Akt in a time-dependent manner.
|
27 |
21426932
|
Plasmid-derived overexpression as well as downregulation of DJ-1 by siRNA showed the requirement of this protein in high glucose-stimulated Akt phosphorylation.
|
28 |
21426932
|
The tumor suppressor protein PTEN acts as a negative regulator of Akt activation.
|
29 |
21426932
|
Interestingly, DJ-1 was associated with PTEN and this interaction was significantly increased in response to high glucose.
|
30 |
21426932
|
High glucose-induced increase in DJ-1 promoted phosphorylation of the PRAS40, a negative regulator of TORC1 kinase activity, resulting in activating and inactivating phosphorylation of S6 kinase and 4EBP-1, respectively.
|
31 |
21426932
|
Our results provide evidence for a unique mechanism whereby DJ-1 induces Akt/PRAS40/TORC1-mediated hypertrophy in response to high glucose.
|
32 |
21426932
|
High glucose upregulation of early-onset Parkinson's disease protein DJ-1 integrates the PRAS40/TORC1 axis to mesangial cell hypertrophy.
|
33 |
21426932
|
We identified DJ-1 to increase in response to high glucose in renal glomerular mesangial cells concomitant with an increase in phosphorylation of Akt in a time-dependent manner.
|
34 |
21426932
|
Plasmid-derived overexpression as well as downregulation of DJ-1 by siRNA showed the requirement of this protein in high glucose-stimulated Akt phosphorylation.
|
35 |
21426932
|
The tumor suppressor protein PTEN acts as a negative regulator of Akt activation.
|
36 |
21426932
|
Interestingly, DJ-1 was associated with PTEN and this interaction was significantly increased in response to high glucose.
|
37 |
21426932
|
High glucose-induced increase in DJ-1 promoted phosphorylation of the PRAS40, a negative regulator of TORC1 kinase activity, resulting in activating and inactivating phosphorylation of S6 kinase and 4EBP-1, respectively.
|
38 |
21426932
|
Our results provide evidence for a unique mechanism whereby DJ-1 induces Akt/PRAS40/TORC1-mediated hypertrophy in response to high glucose.
|
39 |
21426932
|
High glucose upregulation of early-onset Parkinson's disease protein DJ-1 integrates the PRAS40/TORC1 axis to mesangial cell hypertrophy.
|
40 |
21426932
|
We identified DJ-1 to increase in response to high glucose in renal glomerular mesangial cells concomitant with an increase in phosphorylation of Akt in a time-dependent manner.
|
41 |
21426932
|
Plasmid-derived overexpression as well as downregulation of DJ-1 by siRNA showed the requirement of this protein in high glucose-stimulated Akt phosphorylation.
|
42 |
21426932
|
The tumor suppressor protein PTEN acts as a negative regulator of Akt activation.
|
43 |
21426932
|
Interestingly, DJ-1 was associated with PTEN and this interaction was significantly increased in response to high glucose.
|
44 |
21426932
|
High glucose-induced increase in DJ-1 promoted phosphorylation of the PRAS40, a negative regulator of TORC1 kinase activity, resulting in activating and inactivating phosphorylation of S6 kinase and 4EBP-1, respectively.
|
45 |
21426932
|
Our results provide evidence for a unique mechanism whereby DJ-1 induces Akt/PRAS40/TORC1-mediated hypertrophy in response to high glucose.
|
46 |
23974919
|
We examined the effects of GDM on the proteome, redox status, and nuclear factor erythroid 2-related factor 2 (Nrf2)-mediated antioxidant gene expression in human fetal endothelial cells.
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47 |
23974919
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In GDM cells, the lipid peroxidation product 4-hydroxynonenal (HNE) failed to induce nuclear Nrf2 accumulation and mRNA and/or protein expression of Nrf2 and its target genes NAD(P)H:quinone oxidoreductase 1 (NQO1), Bach1, cystine/glutamate transporter, and glutamate cysteine ligase.
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48 |
23974919
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Although methylation of CpG islands in Nrf2 or NQO1 promoters was unaltered by GDM, decreased DJ-1 and increased phosphorylated glycogen synthase kinase 3β levels may account for impaired Nrf2 signaling.
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49 |
23974919
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HNE-induced increases in GSH and NQO1 levels were abrogated by Nrf2 small interfering RNA in normal cells, and overexpression of Nrf2 in GDM cells partially restored NQO1 induction.
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