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Multiplexion GmbH
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ATCC
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BioChain Institute
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Korean Cell Line Bank
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The A172 Luciferase cell line is transformed from A172 cell, expressing the firefly luciferase gene. The cell constitutively express Luciferase.
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A172 Cell Lines Complete Growth Medium is a cell lines complete growth medium from Innovative Research, supplied as a ready-to-use liquid. More Details: Formulation: DMEM + 10% FBS + 1% P/S Bacterial detection: Negative Fungal
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Image Search Results
Journal: Oncotarget
Article Title: Type 5 phosphodiesterase regulates glioblastoma multiforme aggressiveness and clinical outcome
doi: 10.18632/oncotarget.14656
Figure Lengend Snippet: A . Wound healing assay and B . Histogram showing the mean percentage ±SD of closure of sh-scrT98G or sh1 or sh2-PDE5 cells monolayers in the presence or absence of 1 μM sildenafil or 100 μM 8br-cGMP. C . Migration assay on matrigel cushions through transwell filters of sh-scr or sh1-PDE5 T98G cells in the presence or absence of 1 μM sildenafil or 100 μM 8br-cGMP. Scale bars= 50 μm. D . Histogram showing the relative migration capacity (fold increase ± SD) of cells that passed through the filter in the different treatments compared to control cells. E . Migration assay on matrigel cushions through transwell filters of mock- or PDE5-overexpressing U87MG (upper panels) or GBM line 83 cells (lower panels). Scale bar= 20 μm. F . Histogram showing the mean percentage ± SD of cells that passed through the filter. G . Histogram of the mean percentage ±SD of secreted MMP-2 in gelatin zymography (bottom image) in sh-scr or sh1-PDE5 T98G and H . in mock- or PDE5-overexpressing U87MG cells and I . in sh-scr T98G stimulated with CNP, GSNO or sildenafil at the indicated concentrations. Data have been obtained from three independent experiments. (*p < 0.05; **p < 0.001).
Article Snippet: The
Techniques: Wound Healing Assay, Migration, Control, Zymography
Journal: Oncotarget
Article Title: Type 5 phosphodiesterase regulates glioblastoma multiforme aggressiveness and clinical outcome
doi: 10.18632/oncotarget.14656
Figure Lengend Snippet: A . PKG1 low and B . PKG1 high GBM samples, as revealed by immuno-histochemistry. Black arrows point to PKG1 expression within the vessel walls. White arrow points to tumor cells. Scale bar=20μm. C . Expression levels of PKGII, PKG1α and PKG1β and total PKG1 in sh-scr and sh1-PDE5 T98G cells and in wtT98G, U87MG, A172, LN18, 83 GBM lines. D . pVASP levels in sh-scr or sh1-PDE5 T98G cells before and after Y-27632, 8br-cGMP (50 μM) treatments. Representative image out of 4 independent experiments. E . Phosphorylation levels of MYPT1 (pSer695) in sh-PDE5 or sh1-scr T98G upon the indicated treatments [8br-cGMP, 50 μM; Y-27632 (RI), 10 μM); KT5823 (PKGi), 2 μM]. F . Densitometric analysis of western blots from three independent experiments is shown. Bars represent the mean ±SD. G . sh-scr and sh1-PDE5 T98G invasion assays on matrigel cushions in the presence of Y-27632 or 8br-cGMP or both. H . Histogram showing the relative migration capacity (fold increase ± SD) of cells that reached the bottom of the matrigel cushion in the different treatments compared to control cells. (**p < 0.001).
Article Snippet: The
Techniques: Immunohistochemistry, Expressing, Phospho-proteomics, Western Blot, Migration, Control
Journal: Oncotarget
Article Title: Type 5 phosphodiesterase regulates glioblastoma multiforme aggressiveness and clinical outcome
doi: 10.18632/oncotarget.14656
Figure Lengend Snippet: A . sh-scr (PDE5+) or sh1-PDE5 (PDE5-) T98G cells were treated with increasing X-ray doses from 2 to 4 Gy and probed with anti-PAR and anti-PARP-1 antibodies. B . sh-scr or sh1-PDE5 T98G cells were exposed to X-rays at 4 Gy in the presence or absence (+/-) of the PARP1 inhibitor olaparib (1 μM). Total protein PARylation levels were assayed after 24 h. C . Schematic representation of cGMP signaling pathway promoting migration and DNA repair in GBM cells.
Article Snippet: The
Techniques: Migration
Journal: Cancer Science
Article Title: Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
doi: 10.1111/cas.16243
Figure Lengend Snippet: Suppression of cancer cell proliferation by AMF at 227 kHz for more than 30 min. (A) The effect of different frequencies (kHz) of AMF (250 Amrs) on the proliferation of GB cell lines (U87 and LN229). XTT cell proliferation assays were conducted at various AMF frequencies (kHz) for 30 min, with evaluation occurring 24 h post‐AMF exposure ( n = 4, * p < 0.05, ** p < 0.01, *** p < 0.001 vs. 0 kHz). (B) The impact of varying electric current intensities (Arms) in AMF (227 kHz) on the proliferation of GBM cell lines (U87 and LN229) ( n = 4, ns, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001 vs. 0 Arms). (C) The effect of different exposure durations (min) to AMF (227 kHz, 250 Amrs) on the proliferation of GBM cell lines (LN229, U251) ( n = 4, ns, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001 vs. 0 min). (D) The influence of AMF (227 kHz, 250 Amrs) on other GB cell lines (U251, T98, and A172), a pancreatic cell line (PANC1), human breast cancer cell lines (MCF7, MDA‐MB‐231, MDA‐MB‐453), normal human astrocyte (NHA), human cardiac fibroblast (HCF), and human umbilical vein endothelial cells (HUVEC) ( n = 4, ns, not significant, * p < 0.05, ** p < 0.01, *** p < 0.001 vs. CTRL). (E, F) Continuous monitoring of cell growth with and without a 30‐min AMF exposure (227 kHz, 250 Arms) in U251 and LN229 cell lines. In vitro cell proliferation was measured using the xCELLigence Real‐Time Cellular Analysis system. (G) Cell cycle analysis 3 and 24 h post‐AMF exposure (227 kHz, 250 Arms, 30 min), revealing the inhibitory effect of AMF, notably the induction of S and G2 phase arrest ( n = 4, ns, not significant, ** p < 0.01, *** p < 0.001 vs. CTRL). (H) Immunoblot analysis of phosphorylated and unphosphorylated forms of p53, p21, CDK2, Cyclin A, Cyclin B1, Cyclin D1, Cyclin E, and GAPDH 24 h after a 30‐min AMF exposure (227 kHz, 250 Arms) ( n = 4, ns, not significant, ** p < 0.01, *** p < 0.001 vs. CTRL).
Article Snippet: Human GBM cell lines,
Techniques: In Vitro, Cell Cycle Assay, Western Blot