mouse anti p38 mitogen activated protein kinase  (Bioss)

Journal: Cancer Science

Article Title: Loss of GSTO2 contributes to cell growth and mitochondria function via the p38 signaling in lung squamous cell carcinoma

doi: 10.1111/cas.15189

Figure Lengend Snippet: Ectopic expression of GSTO2 downregulated β‐catenin through p38 phosphorylation. (A) Left: Typical images of mock‐transfected and GSTO2 ‐transfected cells. Phosphorylated p38 (red) was visualized by nuclear staining (blue). p38 phosphorylation per nucleus was quantified and presented as the mean ±SD of assays performed in triplicate. *** P < .001. (B) A representative image of normal bronchial samples double‐stained with anti–p38 (green) and anti–CK5/6 (red). (C) A representative image of normal bronchial samples double‐stained with anti–p38 (green) and anti–CC16 (red). The Clara cell is surrounded by a dotted line. (D) Left: Typical images of mock‐transfected and GSTO2 ‐transfected cells after treatment with 50 µmol/L SB203580 or DMSO for 24 h. β‐catenin (red) was visualized by nuclear staining (blue). β‐catenin expression per nucleus was quantified and presented as the mean ±SD of assays performed in triplicate. ** P < .01. (E) CTNNB1 mRNA levels in mock‐transfected and GSTO2 ‐transfected cells. Data are presented as the mean ±SD of assays performed in triplicate. * P < .05. (F) Transcript levels of AXIN2 , VEGF , and MMP2 were determined by quantitative RT‐PCR in mock‐transfected and GSTO2 ‐transfected cells. Data are presented as the mean ±SD of assays performed in triplicate. * P < .05, ** P < .01, *** P < .001

Article Snippet: Cultured LK‐2 and H520 transfectants (5 × 10 4 cells/well) in a poly‐ l ‐lysine–coated slide chamber (Iwaki) were stained with anti–phospho‐p38 mitogen‐activated protein kinase (MAPK) antibody (Cell Signaling Technology) or anti–human β‐catenin antibody (Santa Cruz Biotechnology) as previously described.

Techniques: Expressing, Phospho-proteomics, Transfection, Staining, Quantitative RT-PCR

Journal: Cancer Science

Article Title: Loss of GSTO2 contributes to cell growth and mitochondria function via the p38 signaling in lung squamous cell carcinoma

doi: 10.1111/cas.15189

Figure Lengend Snippet: Ectopic expression of GSTO2 inhibited mitochondrial function through p38 phosphorylation. (A) ECAR (left) and OCR (middle) were measured using an Extracellular Flux Analyzer in four or five separate wells, and the results are presented as the mean ±SD. Injection A = glucose; B = oligomycin; C = 2‐DG; D = FCCP; E = antimycin A + rotenone. The red line denotes mock‐transfected cells, and the blue line denotes GSTO2 ‐transfected cells. The maximum OCRs are presented as the mean ±SD (right). * P < .05, ** P < .01. (B) Mitochondrial membrane potential of mock‐transfected and GSTO2 ‐transfected cells after treatment with 50 µmol/L SB203580 or DMSO for 24 h was assessed using JC‐1 assay. JC‐1 signals per nucleus were quantified and presented as the mean ±SD of assays performed in triplicate. * P < .05, ** P < .01, *** P < .001

Article Snippet: Cultured LK‐2 and H520 transfectants (5 × 10 4 cells/well) in a poly‐ l ‐lysine–coated slide chamber (Iwaki) were stained with anti–phospho‐p38 mitogen‐activated protein kinase (MAPK) antibody (Cell Signaling Technology) or anti–human β‐catenin antibody (Santa Cruz Biotechnology) as previously described.

Techniques: Expressing, Phospho-proteomics, Injection, Transfection, Membrane

Journal: Cancer Science

Article Title: Loss of GSTO2 contributes to cell growth and mitochondria function via the p38 signaling in lung squamous cell carcinoma

doi: 10.1111/cas.15189

Figure Lengend Snippet: Role of GSTO2 in normal lung and LSCC cells. In normal lung cells, GSTO2 activates the p38 mitogen‐activated protein kinase (MAPK), which results in decrease β‐catenin expression probably via ubiquitination. By contrast, silencing of GSTO2 is caused by DNA hypermethylation in LSCC, which allows β‐catenin to escape from degradation, activate mitochondrial OXPHOS, and promote energy production

Article Snippet: Cultured LK‐2 and H520 transfectants (5 × 10 4 cells/well) in a poly‐ l ‐lysine–coated slide chamber (Iwaki) were stained with anti–phospho‐p38 mitogen‐activated protein kinase (MAPK) antibody (Cell Signaling Technology) or anti–human β‐catenin antibody (Santa Cruz Biotechnology) as previously described.

Techniques: Expressing, Ubiquitin Proteomics

Journal: Experimental and Therapeutic Medicine

Article Title: Repairing effects of ICAM-1-expressing mesenchymal stem cells in mice with autoimmune thyroiditis

doi: 10.3892/etm.2017.4131

Figure Lengend Snippet: Phosphorylation of p38 in each group determined via western blot analysis. p, phosphorylated, p38, p38 mitogen-activated protein kinase; model, experimental autoimmune thyroiditis model; MSC, mesenchymal stem cell; ICAM, intercellular adhesion molecule.

Article Snippet: Rabbit anti-mouse antibodies against total-mitogen-activated protein kinase p38 (p38; cat. no. 9212), phosphorylated (p)-P38 (cat. no. 9216), total extracellular signal-regulated kinase (ERK) (cat. no. 9101) and p-ERK (cat. no. 4696), and goat anti-rabbit horseradish peroxidase (HRP)-conjugated antibodies were purchased from Cell Signaling Technology, Inc., (Danvers, MA, USA).

Techniques: Phospho-proteomics, Western Blot