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PMID |
Sentence |
1 |
7791758
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Inhibition of cellular proliferation by the Wilms' tumor suppressor WT1 is associated with suppression of insulin-like growth factor I receptor gene expression.
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2 |
7791758
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We have investigated the regulation of the insulin-like growth factor I receptor (IGF-I-R) gene promoter by the Wilms' tumor suppressor WT1 in intact cells.
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3 |
7791758
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Expression of WT1 mRNA in G401 cells resulted in a significant decrease in the rate of cellular proliferation, which was associated with a reduction in the levels of IGF-I-R mRNA, promoter activity, and ligand binding and with a reduction in IGF-I-stimulated cellular proliferation, thymidine incorporation, and anchorage-independent growth.
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4 |
7791758
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Inhibition of cellular proliferation by the Wilms' tumor suppressor WT1 is associated with suppression of insulin-like growth factor I receptor gene expression.
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5 |
7791758
|
We have investigated the regulation of the insulin-like growth factor I receptor (IGF-I-R) gene promoter by the Wilms' tumor suppressor WT1 in intact cells.
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6 |
7791758
|
Expression of WT1 mRNA in G401 cells resulted in a significant decrease in the rate of cellular proliferation, which was associated with a reduction in the levels of IGF-I-R mRNA, promoter activity, and ligand binding and with a reduction in IGF-I-stimulated cellular proliferation, thymidine incorporation, and anchorage-independent growth.
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7 |
8411713
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On the other hand, only small number of transcribed sequences including G6PD gene, Gdx, P3, factor VIII gene, red and green color pigment genes, GABRA3 gene, L1 adhesion molecule gene, QM gene and so on have been identified at Xq28.
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8 |
8702614
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This rearrangement results in the fusion of the ubiquitously expressed EWS1 gene to the Wilms' tumor suppressor (WT1) gene.
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9 |
8702614
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Because WT1 has been shown previously to bind and repress the insulin-like growth factor I (IGF-I-R) promoter, we investigated whether this promoter is, in addition, a target for the aberrant EWS/WT1 transcription factor.
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10 |
8702614
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EWS/WT1 activated the IGF-I-R promoter approximately 340%, whereas a fusion protein containing a three-amino acid insert (KTS) between zinc fingers 3 and 4 had no effect.
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11 |
8702614
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Results of gel shift assays indicate that the binding affinity of EWS/WT1 to a fragment of the 5'-flanking region of the receptor promoter was higher than the affinity of WT1 itself.
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12 |
8702614
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Consistent with the results of functional assays, the binding of EWS/WT1(+KTS) was significantly reduced.
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13 |
8702614
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Due to the central role of the IGF-I-R in tumorigenesis, activation of the receptor promoter by EWS/WT1 may constitute a potential mechanism for the etiology and/or progression of DSRCT.
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14 |
8873895
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Regulation of insulin-like growth factor I receptor gene expression by the Wilms' tumor suppressor WT1.
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15 |
8873895
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THe insulin-like growth factor I receptor (IGF-I-R) has been implicated in the etiology and/or progression of Wilms' tumor, or nephroblastoma, a pediatric neoplasm of the kidney that is often associated with deletion or mutation of the WT1 tumor suppressor gene.
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16 |
16955103
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Nephrin loss in experimental diabetic nephropathy is prevented by deletion of protein kinase C alpha signaling in-vivo.
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17 |
16955103
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In PKCalpha-/- mice, hyperglycemia-induced downregulation of nephrin was prevented.
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18 |
16955103
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In addition, the nephrin messenger RNA expression was also reduced in hyperglycemic wild-type mice but remained unaltered in PKCalpha-/- mice.
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19 |
16955103
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We postulate that the underlying mechanism of the hyperglycemia-induced regulation of various proteins of the glomerular filtration barrier is a PKCalpha-dependent regulation of the Wilms' Tumor Suppressor (WT1) which previously has been shown to act as a direct transcription factor on the nephrin promoter.
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20 |
16955103
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Our data suggest that PKCalpha activation may be an important intracellular signaling pathway in the regulation of nephrin expression and glomerular albumin permeability in the diabetic state.
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