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p38 MAPK Antibody

BHA12913752
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Western blot analysis of extracts from Rat lung, using p38 MAPK Antibody. The lane on the left was treated with blocking peptide.Western blot analysis of extracts from Rat lung, using p38 MAPK Antibody.
Fig. 5. NK diminished LPS-induced TLR4 activation likely due to promoting TRL4 proteolysis in RAW264.7 cells. (A) Effect of NK on LPS-induced TLR4signaling pathways. Cells were pretreated with indicated concentrations of NK for 1 h and then exposed to LPS (0.1 ?g/mL) for 12 h. Equal amounts of total celllysates were loaded and subjected to immunoblot analysis. Data represent the mean ± SD from three independent experiments. (B) NK induced TRL4 degradationvia its serine protease activity in RAW264.7 cells. Cells were treated with NK (0.3 FU/mL) for indicated time points with or without PMSF pretreatment for 30 min.Equal amounts of total cell lysates were loaded and subjected to immunoblot analysis. Data represent mean ± SD from three independent experiments. *P< 0.05,**P< 0.01 compared to control group; #P< 0.05, ##P< 0.05 compared to NK 12h group; $P< 0.05, $$P< 0.05 compared to NK 24h group.Fig.
Western blot analysis of extracts from various samples, using p38 MAPK Antibody. Lane 1: Mouse brain lysates treated with blocking peptide; Lane 2: Mouse brain lysates;Lane 3: Hybridoma cell lysates;Lane 4: Hela cell lysates;Lane 5: Vero cell lysates.Western blot analysis of extracts from various samples, using p38 MAPK Antibody.
Western blot analysis of extracts from Mouse brain, using p38 MAPK Antibody. Lane 1 was treated with the blocking peptide.Western blot analysis of extracts from Mouse brain, using p38 MAPK Antibody.
Western blot analysis of extracts from Rat lung, using p38 MAPK Antibody. The lane on the left was treated with blocking peptide.Western blot analysis of extracts from Rat lung, using p38 MAPK Antibody.
Fig. 5. NK diminished LPS-induced TLR4 activation likely due to promoting TRL4 proteolysis in RAW264.7 cells. (A) Effect of NK on LPS-induced TLR4signaling pathways. Cells were pretreated with indicated concentrations of NK for 1 h and then exposed to LPS (0.1 ?g/mL) for 12 h. Equal amounts of total celllysates were loaded and subjected to immunoblot analysis. Data represent the mean ± SD from three independent experiments. (B) NK induced TRL4 degradationvia its serine protease activity in RAW264.7 cells. Cells were treated with NK (0.3 FU/mL) for indicated time points with or without PMSF pretreatment for 30 min.Equal amounts of total cell lysates were loaded and subjected to immunoblot analysis. Data represent mean ± SD from three independent experiments. *P< 0.05,**P< 0.01 compared to control group; #P< 0.05, ##P< 0.05 compared to NK 12h group; $P< 0.05, $$P< 0.05 compared to NK 24h group.Fig.