Results: 5

1.
Figure 5

Figure 5. From: Deranged transcriptional regulation of cell-volume-sensitive kinase hSGK in diabetic nephropathy.

Stimulation of the thick ascending limb Na+,K+,2Cl cotransporter BSC-1 by hSGK 22Na+ uptake in Xenopus oocytes injected with and without the thick ascending limb Na+,K+,2Cl cotransporter BSC-1 and/or the active kinase hSGK or inactive kinase hSGKK127R. In some of the experiments furosemide (100 μM) was added to inhibit BSC-1. Arithmetic means ± SEM.

F. Lang, et al. Proc Natl Acad Sci U S A. 2000 July 5;97(14):8157-8162.
2.
Figure 2

Figure 2. From: Deranged transcriptional regulation of cell-volume-sensitive kinase hSGK in diabetic nephropathy.

Transcriptional regulation of hSGK in endothelial cells. (A) Effect of 20 mM, 50 mM, or 100 mM glucose within 2 h. (B) Effect of the Ca2+ ionophore ionomycin (1 μM), of phorbol 12,13-didecanoate (PDD; 1 μM) and of both ionomycin and PDD (incubation time 2 h). (C) Effect of glucose (100 mM), nifedipine (10 μM or 100 μM), and glucose (100 mM) in the presence of nifedipine (10 μM or 100 μM) (incubation time 2 h).

F. Lang, et al. Proc Natl Acad Sci U S A. 2000 July 5;97(14):8157-8162.
3.
Figure 4

Figure 4. From: Deranged transcriptional regulation of cell-volume-sensitive kinase hSGK in diabetic nephropathy.

Stimulation of ENaC by hSGK. Amiloride-sensitive currents (30 μM amiloride) in Xenopus oocytes injected with the rat epithelial Na+ channel α,β,γ ENaC or the αS622A,β,γ ENaC mutant with or without hSGK, or with ENaC + hSGK in the presence of staurosporine (1 μM) or chelerythrine (1 μM). (A) Original traces. (B) Effect of hSGK on wild-type ENaC with and without protein kinase inhibitors (arithmetic means ± SEM). (C) Effect of hSGK and of inactive hSGKK127R on ENaC αS622A-mediated currents (arithmetic means ± SEM).

F. Lang, et al. Proc Natl Acad Sci U S A. 2000 July 5;97(14):8157-8162.
4.
Figure 1

Figure 1. From: Deranged transcriptional regulation of cell-volume-sensitive kinase hSGK in diabetic nephropathy.

Transcriptional regulation of the serine/threonine kinase hSGK in 3T3 fibroblasts. (A) Influence on hSGK mRNA of an 8-h increase of extracellular glucose concentration from 5.5 to 30 mM and of an 8-h exposure to 2 ng/ml TGF-β-1. (B) Decay of mRNA levels after addition of 5 μg/ml actinomycin D at 30 mM glucose and at 5.5 mM glucose in hypotonic extracellular fluid. Before the experimental period, the cells were exposed to 30 mM glucose. (C) Effect of an 8-h increase of extracellular glucose concentration from 5.5 to 30 mM in presence and absence of 30 μg/ml anti-TGF-β-1 antibody.

F. Lang, et al. Proc Natl Acad Sci U S A. 2000 July 5;97(14):8157-8162.
5.
Figure 3

Figure 3. From: Deranged transcriptional regulation of cell-volume-sensitive kinase hSGK in diabetic nephropathy.

In situ detection of hSGK mRNA in intact kidneys and diabetic nephropathy. In normal kidney significant transcription of hSGK is found in a few mesangial cells and single epithelial cells of the distal tubule (A) and thick ascending limbs of Henle's loop (B, arrowheads). In diabetic kidneys (C–F), however, high levels of hSGK transcripts are found in numerous glomerular cells (C) and epithelial cells from the thick ascending limb of Henle's loop (D) as well as in clusters of interstitial cells of fibrotic areas (E). No labeling of cells was observed after hybridization with the α-35S-labeled sense hSGK RNA probe (F). (×300.)

F. Lang, et al. Proc Natl Acad Sci U S A. 2000 July 5;97(14):8157-8162.

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