N-cadherin and p21 transcript and protein expression levels in HSC5 cells treated with arsenic.

<p>A and C) transcript expression levels of N-cadherin and p21 were measured by real-time PCR. ***, significantly different (p<0.001) from the control by Student's t-test. B and D) Protein expression levels of N-cadherin and p21 were measured by immunoblot. TUBULIN was used as a positive control. Three independent experiments were performed and the same results were obtained.</p

Effects of arsenic on apoptosis of HSC5 cells.

<p>Viability of HSC5 cells treated with 0, 1.0, 3.0 and 5.0 µM of arsenic was evaluated by crystal violet (CV). Cells were presented in photographs (A) and ratios of arsenic treated live cells and control live cells were presented in a graph (B). **, Significantly different (p<0.01) from the control by the Student's t-test.</p

MT1-MMP and P14 transcript and protein expression levels in HSC5 cells treated with arsenic.

<p>A and C) transcript expression levels of MT1-MMP and p14 were measured by real-time PCR. **, significantly different (p<0.01) from the control by Student's t-test. B and D) Protein expression levels of MT1-MMP and p14 were measured by immunoblot. TUBULIN was used as a positive control. Three independent experiments were performed and the same results were obtained.</p

Effects of arsenic on invasion of HSC5 cells.

<p>Invasive ability of of HSC5 cells treated 0, 1.0, 3.0 and 5.0 µM of arsenic were evaluated by invasion assay. Number of invading HSC5 cells treated with arsenic in the invasion assay were presented in photographs (A) and a graph (B). **, Significantly different (p<0.01) from the control by the Student's t-test.</p

Effects of arsenic on invasive activity and phosphorylation and/or expression levels of MT1-MMP and ERK 4 in HSC5 cells.

<p>A), Invasive activity of HSC5 treated with 3 µM of arsenic was evaluated invasion assay. Level of invasive ability is presented as number of invading cells in a graph (left) and photographs (right). **, Significantly different (p<0.01) from the control by the Student's t-test. Phosphorylated levels of ERK (P-ERK) and protein expression levels of MT1-MMP and ERK in HSC5 cells treated with 3 µM arsenic for 24 hours are presented. TUBULIN protein expression levels are presented as an internal control.</p

Thiamine synthesis regulates the fermentation mechanisms in the fungus <i>Aspergillus nidulans</i>

<p>Thiamine pyrophosphate (TPP) is a critical cofactor and its biosynthesis is under the control of TPP availability. Here we disrupted a predicted <i>thiA</i> gene of the fungus <i>Aspergillus nidulans</i> and demonstrated that it is essential for synthesizing cellular thiamine. The thiamine riboswitch is a post-transcriptional mechanism for TPP to repress gene expression and it is located on <i>A. nidulans thiA</i> pre-messenger RNA. The <i>thiA</i> riboswitch was not fully derepressed under thiamine-limited conditions, and fully derepressed under environmental stressors. Upon exposure to hypoxic stress, the fungus accumulated more ThiA and NmtA proteins, and more thiamine than under aerobic conditions. The <i>thiA</i> gene was required for the fungus to upregulate hypoxic branched-chain amino acids and ethanol fermentation that involve enzymes containing TPP. These findings indicate that hypoxia modulates <i>thiA</i> expression through the thiamine riboswitch, and alters cellular fermentation mechanisms by regulating the activity of the TPP enzymes.</p> <p>Upon exposure to hypoxic stress (B; –O₂), the fungus accumulated more ThiA and NmtA proteins that involve in thiamine biosynthesis (A), and more thiamine than under aerobic conditions (B;+O₂).</p

Effects of dietary intervention on lipid metabolism.

<p>Hepatic DGAT-1, DGAT-2, CPT-1, and ACC protein levels were analyzed by Western blotting (A), means and SD (n = 6) were shown by columns and bars, respectively (B). GAPDH was used as a loading control. <i>P</i> < 0.05 was used as a criterion of statistical significance. ^a Significantly different from the control rats of the same age. ^b Significant differences were observed between control diet intervention for 6 or 12 weeks and HFC diet feeding after 2 or 8 weeks.</p

Proliferation of HM3KO cells.

<p>Proliferation of HM3KO cells treated with a solvent (0.1% of DMSO) (open circle in A, lane 1 in B), GDNF (100 ng/ml) (closed circle in A, lane 2 in B), SU5416 (5µM) (open square in A, lane 3 in B) and GDNF plus SU5416 (closed square in A, lane 4 in B) for 24 (A) and 48 hours (A, B) was examined by cell counting with trypan blue staining (A) and MTT assay (B). Difference between proliferation levels of DMSO-treated control cells and other cells was statistically analyzed by the Kruskal-Wallis test. *, Significantly different (P<0.05) from the control.</p

Hepatic fibrosis in HFC rats and intervention groups.

<p>Original magnifications of AZAN stain and α-SMA immunostaining were ×100 and ×200, respectively. Representative images of Azan staining, (A) liver tissue of rats fed HFC diet for 8 weeks, (B) the dietary intervention group at 6 weeks after HFC diet feeding for 8 weeks, (C) the group fed HFC diet for 14 weeks, and representative images of α-SMA immunostaining, (D) liver tissue of rats fed HFC diet for 8 weeks, (E) the dietary intervention group at 6 weeks after HFC diet feeding for 8 weeks, (F) the group fed HFC diet for 14 weeks. Small window of (E) shows the image of central region of liver. (G) and (H) show means and SD (n = 6) of hydroxyproline content and quantitative analysis of fibrotic areas using EVG staining, respectively. <i>P</i> < 0.05 was used as a criterion of statistical significance. ^a Significantly different from control rats of the same age. ^b Significantly different from HFC diet feeding for 14 weeks. * The data were analyzed using Mann-Whitney U test due to the significant variance.</p

Levels of c-RET protein expression in human malignant melanoma cell lines.

<p>The levels of c-RET protein expression were examined in c-RET-transfected NIH3T3 cells as a positive control (c-RET transfectant; lane 1), primary-cultured normal human epithelial melanocytes (NHEM; lane 2), G361 (lane 3), HM3KO (lane 4) and MNT-1 (lane 5) by immunoblotting analysis with anti-RET antibody after immunoprecipitation with anti-RET antibody.</p