p38i vx702 Search Results


inhibitors p38i  (ApexBio)
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ApexBio inhibitors p38i
Sepsis induces neutrophil differentiation is mediated by p38α-MSK1/-MK2 pathway. a Gene chip showed activation of MAPK and p38α pathways at 0.5 h and 1 h after LPS (1 μg/mL) stimulation. b , c q-PCR results for PD-L1 mRNA expression. Neutrophils were challenged with LPS (1 μg/mL) or pre-treated with <t>p38i</t> (10 μM), MSK1i (25 μM) or MK2i (20 μM) prior to LPS challenge (n = 4). d q-PCR results for PD-L1 mRNA expression. Neutrophils were challenged with LPS (1 μg/mL) or pre-treated with p38i (10 µM), <t>P38(αβ)i</t> (10 µM) prior to LPS challenge (n = 4). e , f Different time points after LPS (1 μg/mL) stimulation of neutrophils, the phosphorylation of p38, p38α, MSK1, MK2 and expression of PD-L1 were observed. g Western blot results of the phosphorylation of MSK1 in neutrophils which stimulated with LPS (1 μg/mL) in 12 and 24 h. P38i (10 µM), P38(αβ)i (10 µM) or MK2i (20 µM) was preloaded. h Western blot results of PD-L1 expression in neutrophils which stimulated with LPS (1 μg/mL) in 12 h. p38i (10 µM), p38(αβ)i (10 µM), MSK1i (25 µM), MK2i (20 µM) were preloaded. i <t>inhibitors.</t> # p < 0.05, ## p < 0.01 and ### p < 0.001, compared with control group; *p < 0.05, **p < 0.01 and ***p < 0.001, compared with LPS group. Data are mean ± SEM
Inhibitors P38i, supplied by ApexBio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/p38i+vx702/p38i+vx702/pmc07865119-102-2-10
Average 90 stars, based on 1 article reviews
inhibitors p38i - by Bioz Stars, 2026-10
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Sepsis induces neutrophil differentiation is mediated by p38α-MSK1/-MK2 pathway. a Gene chip showed activation of MAPK and p38α pathways at 0.5 h and 1 h after LPS (1 μg/mL) stimulation. b , c q-PCR results for PD-L1 mRNA expression. Neutrophils were challenged with LPS (1 μg/mL) or pre-treated with p38i (10 μM), MSK1i (25 μM) or MK2i (20 μM) prior to LPS challenge (n = 4). d q-PCR results for PD-L1 mRNA expression. Neutrophils were challenged with LPS (1 μg/mL) or pre-treated with p38i (10 µM), P38(αβ)i (10 µM) prior to LPS challenge (n = 4). e , f Different time points after LPS (1 μg/mL) stimulation of neutrophils, the phosphorylation of p38, p38α, MSK1, MK2 and expression of PD-L1 were observed. g Western blot results of the phosphorylation of MSK1 in neutrophils which stimulated with LPS (1 μg/mL) in 12 and 24 h. P38i (10 µM), P38(αβ)i (10 µM) or MK2i (20 µM) was preloaded. h Western blot results of PD-L1 expression in neutrophils which stimulated with LPS (1 μg/mL) in 12 h. p38i (10 µM), p38(αβ)i (10 µM), MSK1i (25 µM), MK2i (20 µM) were preloaded. i inhibitors. # p < 0.05, ## p < 0.01 and ### p < 0.001, compared with control group; *p < 0.05, **p < 0.01 and ***p < 0.001, compared with LPS group. Data are mean ± SEM

Journal: Critical Care

Article Title: Identification and characterization of neutrophil heterogeneity in sepsis

doi: 10.1186/s13054-021-03481-0

Figure Lengend Snippet: Sepsis induces neutrophil differentiation is mediated by p38α-MSK1/-MK2 pathway. a Gene chip showed activation of MAPK and p38α pathways at 0.5 h and 1 h after LPS (1 μg/mL) stimulation. b , c q-PCR results for PD-L1 mRNA expression. Neutrophils were challenged with LPS (1 μg/mL) or pre-treated with p38i (10 μM), MSK1i (25 μM) or MK2i (20 μM) prior to LPS challenge (n = 4). d q-PCR results for PD-L1 mRNA expression. Neutrophils were challenged with LPS (1 μg/mL) or pre-treated with p38i (10 µM), P38(αβ)i (10 µM) prior to LPS challenge (n = 4). e , f Different time points after LPS (1 μg/mL) stimulation of neutrophils, the phosphorylation of p38, p38α, MSK1, MK2 and expression of PD-L1 were observed. g Western blot results of the phosphorylation of MSK1 in neutrophils which stimulated with LPS (1 μg/mL) in 12 and 24 h. P38i (10 µM), P38(αβ)i (10 µM) or MK2i (20 µM) was preloaded. h Western blot results of PD-L1 expression in neutrophils which stimulated with LPS (1 μg/mL) in 12 h. p38i (10 µM), p38(αβ)i (10 µM), MSK1i (25 µM), MK2i (20 µM) were preloaded. i inhibitors. # p < 0.05, ## p < 0.01 and ### p < 0.001, compared with control group; *p < 0.05, **p < 0.01 and ***p < 0.001, compared with LPS group. Data are mean ± SEM

Article Snippet: All of inhibitors (P38i, P38(αβ)i, MSK1i, MK2i) were obtained from ApexBio (USA).

Techniques: Activation Assay, Expressing, Phospho-proteomics, Western Blot, Control