src kinase inhibitor pp1  (Biomol GmbH)

Journal: Endocrine-Related Cancer

Article Title: Targeting Src tyrosine kinase to enhance radioiodide uptake in breast cancer

doi: 10.1530/ERC-24-0312

Figure Lengend Snippet: Src inhibition inhibits PBF phosphorylation and restores RAIU. (A) MCF-7 (i) and MDA-MB-231 (ii) cells were treated with varying doses of PP1 (0–2 μM) for 24 h before PBF-pY174 and total PBF expression levels were determined by Western blot. (B) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. (C) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 cells treated with ATRA and dexamethasone. (D) PBF-pY174 and total PBF expression levels following dasatinib dose response (0–2 μM) treatment for 24 h in MCF-7 (i) and MDA-MB-231 (ii) cells. (E) Effect of 1 nM dasatinib or 10 nM saracatinib treatment on PBF-repressed RAIU in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. n = 3 for all experiments. Error bars = SEM. * = P < 0.05, ** = P < 0.01, *** = P < 0.001.

Article Snippet: Src family kinase inhibitors PP1 (Tocris, UK), dasatinib and saracatinib (Selleck Chemicals, USA) and NMT inhibitor (DDD85646; Drug Discovery Unit, University of Dundee) were dissolved in DMSO to a 10 mM stock concentration.

Techniques: Inhibition, Phospho-proteomics, Expressing, Western Blot, Transfection

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Oxysophocarpine reduces oxidative stress and inflammation in tuberculosis-infected neutrophils and mouse lungs

doi:

Figure Lengend Snippet: OSC hindered the adhesion and F-actin polymerization in the H37Rv-infected neutrophils by the inhibition of the TLR2/MyD88/Src/ERK1/2 signaling pathway. A-C. The neutrophils were uninfected or infected with H37Rv (5 MOI) in the presence or absence of 5 μM OSC. A. The firmly adherent neutrophils were counted after the H37Rv infection for 6, 12, 18, and 24 h. B. F-actin polymerization was monitored using immunofluorescent microscopy at 24 h after the H37Rv infection. C. A Western blot analysis was performed to assess the expressions of TLR2, MyD88, Src, p-ERK1/2, ERK1/2, p-p38 MAPK, p38 MAPK, p-JNK, and JNK at 24 h after the H37Rv infection. β-actin was used as an endogenous control. D and E. The neutrophils were preincubated with the Src kinase inhibitor PP1 (5 μM), ERK1/2 inhibitor U0126 (10 μM), p38MAPK inhibitor SB202190 (10 μM), or the JNK inhibitor AG490 (25 μM) for 30 min or pretransfected with siTLR2 (100 nM) for 24 h, and then uninfected or infected with H37Rv (5 MOI) in the presence or absence of OSC (5 μM) for 24 h. D. The firmly adherent neutrophils were counted. E. F-actin polymerization was monitored. Data are expressed as the mean ± SD of the three independent experiments. *P < 0.05, **P < 0.01 compared with Ctrl group. #P < 0.05 compared with the Mtb group. Ctrl: control; OSC: Oxysophocarpine; NS: no significance.

Article Snippet: Adhesion assay After pretreatment with the Src kinase inhibitor PP1 (5 μM), ERK1/2 inhibitor U0126 (10 μM), p38MAPK inhibitor SB202190 (10 μM), or JNK inhibitor AG490 (25 μM; Biomol, Plymouth Meeting, PA, USA) for 30 min or with siRNA targeting TLR2 (siTLR2; 100 nM; Santa Cruz Biotechnology, Inc., Dallas, Texas, USA) for 24 h, neutrophils (3 × 10 5 cells/well) were then uninfected or infected with H37Rv (5 MOI) in the presence or absence of 5 μM OSC and allowed to adhere to 48-well plates for 6, 12, 18, and 24 h. The non-adherent cells were washed away, and the adherent neutrophils were quantified using a myeloperoxidase (MPO) assay.

Techniques: Infection, Inhibition, Microscopy, Western Blot, Control