Journal: Toxicological Research

Article Title: 1,2-Dichloropropane (1,2-DCP)-Induced Angiogenesis in Dermatitis

doi: 10.5487/TR.2019.35.4.361

Figure Lengend Snippet: Protein expression of VEGF, phosphorylated protein kinase B (p-PKB), and phosphorylated mammalian target of rapamycin (p-mTOR) in the angiogenic sites. (A) Western blot analysis of VEGF, p-PKB, and p-mTOR following 1,2-DCP treatment in mice. Actin was used as a loading control. (B, C) Graph shows densitometric quantification of bands. The results are means ± SD of two independent experiments. * p < 0.05; ** p <0.01.

Article Snippet: The following antibodies were used: anti-VEGF (Santa Cruz Biotechnology Inc., Dallas, TX, USA), anti-phosphorylated PKB (p-PKB; Cell Signaling, Danvers, MA, USA), anti-PKB (Cell Signaling), anti-phosphorylated mTOR (p-mTOR; Cell Signaling), anti-mTOR (Cell Signaling), anti-TNF-α (Abcam, Cambridge, UK), anti-IL-6 (Invitrogen, Carlsbad, CA, USA), anti-actin (Sigma-Aldrich Co.), and anti-mouse or anti-rabbit secondary antibodies (Koma Biotech, Seoul, Korea).

Techniques: Expressing, Western Blot

Journal: Toxicological Research

Article Title: 1,2-Dichloropropane (1,2-DCP)-Induced Angiogenesis in Dermatitis

doi: 10.5487/TR.2019.35.4.361

Figure Lengend Snippet: 1,2-DCP induces inflammation and activates angiogenic signals in NHFD cells. (A) NHFD cells (1 × 10 6 ) were grown in 3.5 mm diameter cell culture dishes and treated with 1,2-DCP at doses of 0, 2.73, 5.75, and 8.75 μL/mL for 24 hr and imaged. (B, E) Western blot analysis of IL-6, TNF-α, VEGF, p-PKB, and p-mTOR following 1,2-DCP treatment in NHFD cells. Actin was used as a loading control. The graph shows densitometric quantification of bands. (C, D, F–H) The results are means ± SD of two independent experiments. * p < 0.05; ** p < 0.01.

Article Snippet: The following antibodies were used: anti-VEGF (Santa Cruz Biotechnology Inc., Dallas, TX, USA), anti-phosphorylated PKB (p-PKB; Cell Signaling, Danvers, MA, USA), anti-PKB (Cell Signaling), anti-phosphorylated mTOR (p-mTOR; Cell Signaling), anti-mTOR (Cell Signaling), anti-TNF-α (Abcam, Cambridge, UK), anti-IL-6 (Invitrogen, Carlsbad, CA, USA), anti-actin (Sigma-Aldrich Co.), and anti-mouse or anti-rabbit secondary antibodies (Koma Biotech, Seoul, Korea).

Techniques: Cell Culture, Western Blot

Journal: Cells

Article Title: Effective Synergy of Sorafenib and Nutrient Shortage in Inducing Melanoma Cell Death through Energy Stress

doi: 10.3390/cells9030640

Figure Lengend Snippet: Combined exposure to sorafenib and starvation stimulates biogenesis in human melanoma cells. ( A ) The activity of the AMPK and mTOR signaling pathways were evaluated by measuring the phosphorylation status of AMPK (p-AMPK on Thr172) or the mTOR target p70S6K1 (p-p70S6K1 on Thr389) in CHL-1 and SK Mel 28 cells treated or untreated (4 or 6 h) as indicated, by western blotting analysis. Total AMPK, p70S6K1, and GAPDH were used as internal/loading controls ( n = 3). ( B ) The expression of PGC1α was evaluated by qRT-PCR in the same experimental condition described in A. (Histograms represent mean ± SD; n = 3) * p < 0.005 compared to control cells.

Article Snippet: Primary antibodies were: anti-PARP (1:1000, Cell Signaling, Danvers, MA, USA); anti-Mcl-1 (1:1000, Cell Signaling, Danvers, MA, USA), anti-LC3B (1:1000, Cell Signaling, Danvers, MA, USA), anti-ATG5 (1:1000, Cell Signaling, Danvers, MA, USA); anti-AMPK (1:1000, Cell Signaling, Danvers, MA, USA); anti-p-AMPK (Thr172) (1:1000, Cell Signaling, Danvers, MA, USA); anti-p70S6K1 (1:1000, Cell Signaling, Danvers, MA, USA), anti-p-p70S6K1 (Thr 389; 1:1000, Cell Signaling, Danvers, MA, USA), anti-GAPDH (1:5000, Sigma-Aldrich, St. Louis, MO, USA), and anti-Tubulin (1:5000, Sigma-Aldrich, St. Louis, MO, USA).

Techniques: Activity Assay, Western Blot, Expressing, Quantitative RT-PCR