Journal: Oncogene

Article Title: Oncogenic mutations and dysregulated pathways in obesity-associated hepatocellular carcinoma.

doi: 10.1038/onc.2016.162

Figure Lengend Snippet: Figure 3. Mutations in Cel and growth-promoting effect of loss of CEL. (a) Schematic illustration of the somatic non-synonymous mutations in Cel identified in liver tumors from obese mice (16 genetic, 13 dietary) and control lean mice (n = 16). (b) The mRNA expression of CEL in nutrition-associated HCC (n = 78) was significantly lower than in virus infection-associated HCC (n = 56) that was available in TCGA database (independent t-test). (c) Stable knock-down of CEL in normal hepatocyte cell line MIHA by two shCEL vectors (SH1 and SH2) was confirmed by real-time PCR and western blot. (d) CEL downregulation in MIHA cells increased cell growth as shown by MTT assay. (e) CEL downregulation in MIHA cells promoted colony formation ability of MIHA cells. Data are mean ± s.e.m. in (b) and mean ± s.d. elsewhere. *Po0.05, **Po0.01. NC, negative control shRNA; SH1&SH2, shRNAs targeting CEL.

Article Snippet: Gene expression knock-down Commercially available vectors expressing shRNAs against CEL (TR313998) and control vector (TR30012) were purchased (Origene).

Techniques: Control, Expressing, Virus, Infection, Knockdown, Real-time Polymerase Chain Reaction, Western Blot, MTT Assay, Negative Control, shRNA

Journal: Oncogene

Article Title: Oncogenic mutations and dysregulated pathways in obesity-associated hepatocellular carcinoma.

doi: 10.1038/onc.2016.162

Figure Lengend Snippet: Figure 4. Loss of CEL caused intracellular accumulation of cholesteryl ester to induce ER stress and activation of IRE1α/JNK/c-Jun/AP-1 pathway. (a1) CEL knock-down increased the level of cholesteryl ester in MIHA cells. (a2) Treatment with 25 nM cholesteryl palmitate, a form of cholesteryl ester having liquid-crystalline states, promoted cell growth as shown by MTT assay. (b1) CEL knock-down in MIHA cells activated the signaling cascade in ER stress as shown by western blot analysis of key proteins. (b2) CEL knock-down increased the transcriptional activity of AP-1 in MIHA as determined by luciferase reporter assay. (c1) MIHA cells expressing CEL mutants (Mut-1, Mut-2) caused significantly higher levels of cholesteryl ester as compared with cells overexpressing wild-type CEL. (c2) CEL mutants promoted MIHA cell growth as shown by MTT assay. (d1) CEL mutants activated the signaling cascade of ER stress in MIHA. (d2) CEL mutants increased the transcriptional activity of AP-1 in MIHA. (e) Cholesteryl ester levels (e1) and protein levels of p-IRE1a and p-c-Jun (e2) in NAFLD-HCC and lean HCC from mouse models. Proteins from two lean HCC were not adequate for both tests. (f) Mechanistic scheme of CEL knock-down or inactivating mutation in promoting liver cancer growth. Data are means ± s.d. *Po0.05; **Po0.01; ***Po0.001. NC, negative control shRNA; SH1&SH2, shRNAs targeting CEL.

Article Snippet: Gene expression knock-down Commercially available vectors expressing shRNAs against CEL (TR313998) and control vector (TR30012) were purchased (Origene).

Techniques: Activation Assay, Knockdown, MTT Assay, Western Blot, Activity Assay, Luciferase, Reporter Assay, Expressing, Mutagenesis, Negative Control, shRNA

Journal: Food Chemistry: X

Article Title: Improvement of cake baking properties by lipases compared to a traditional emulsifier

doi: 10.1016/j.fochx.2022.100442

Figure Lengend Snippet: Lipases, dosage and lipase activity measured using the three different lipase activity assay kits MAK046, MAK047 and MAK048. Values are given as mean (n = 3) ± standard deviation.

Article Snippet: The three commercially available lipase activity assay kits MAK046, MAK047 and MAK048 (Merck KGaA, Darmstadt, Germany) were used for lipase activity measurements.

Techniques: Activity Assay