inhibitor sb239063  (MedChemExpress)

Journal: Scientific Reports

Article Title: PTPRK promotes resiniferatoxin-induced postherpetic neuralgia via activating DUSP1/p38 MAPK signaling pathway in dorsal root ganglia

doi: 10.1038/s41598-025-24233-y

Figure Lengend Snippet: SB239063 treatment reversed PTPRK overexpression-induced mechanical allodynia and inflammation in rat DRG tissues. A , PTPRK expression was analyzed by RT-qPCR after Lv-NC and Lv-PTPRK vectors transfection; B , Paw withdrawal thresholds and C , paw withdrawal latency in each group were quantified; ELISA was performed to assess the concentrations of D , TNF-α, E , IL-1β, and F , IL-4 in DRG tissues of each group; RT-qPCR was performed to analyze the mRNA levels of G , TNF-α, H , IL-1β, I , IL-4, J , BDNF, K , Nav1.3, L , Nav1.7, and M , TRPV1 in DRG tissues of each group. ( N = 5; ** p < 0.01 vs. the Lv-NC group; ## p < 0.01 vs. the Lv-PTPRK group).

Article Snippet: To inhibit p38 MAPK activation, the specific inhibitor SB239063 (10 mg/kg; HY-11068; purity: 99.61%; MedChem Express) was administered intraperitoneally once daily for 7 days.

Techniques: Over Expression, Expressing, Quantitative RT-PCR, Transfection, Enzyme-linked Immunosorbent Assay

Journal: Cell Reports Medicine

Article Title: Inhibition of MAPK p38α overcomes the cancer immunosurveillance defect caused by FPR1 loss-of-function mutation

doi: 10.1016/j.xcrm.2026.102683

Figure Lengend Snippet: Genetic and pharmaceutic screenings to identify gene targets for restoring the Fpr1 -deficient dendritic cell function (A and B) Schematic of the screening workflow using Fpr1-WT or Fpr1 −/− de-iniDCs or BMDCs for in vitro antigen presentation. Briefly, DCs were exposed to OVA antigen, washed, and co-cultured with B3Z T cell hybridomas; IL-2 production by B3Z cells was quantified by ELISA. The Cas9-expressing iniDCs were transfected with individual gRNAs to establish specific gene knockouts. (C–E) (C) Scatterplot of normalized IL-2 production (mean, n = 3 ) after individual gene knockout. Gene KOs significantly increasing IL-2 in WT, Fpr1 −/− , or both genotypes are labeled in green, blue, and red, respectively (multiple t test). L2 production (mean ± SEM, n = 4 ) after treatment of de-iniDCs (D) or BMDCs (E) with MAPK p38α inhibitors SB203580 or skepinone-L (10 or 30 μM). (F) Fpr1 −/− de-iniDCs were pretreated with ICCB library compounds and then subjected to antigen presentation assay. The log 2 fold change (FC) in IL-2 ( n = 3) and corresponding p values (by multiple t test) are shown as volcano plot. Red dots indicate hits (FC > 2, p < 0.01). (G) Heatmap of normalized IL-2 (mean, n = 5) for selected compounds at indicated concentrations in WT and Fpr1 −/− de-iniDCs. (H and I) Normalized IL-2 production (mean ± SEM, n = 4) for additional Fpr1 -WT and Fpr1 −/− de-iniDC clones treated with SB203580 or SB239063 (10 or 30 μM). Statistical significance was determined by two-way ANOVA with Dunnett’s multiple comparisons test vs. genotype-matched controls.

Article Snippet: SB239063 , MedChemExpress , Cat# HY-11068.

Techniques: Cell Function Assay, In Vitro, Immunopeptidomics, Cell Culture, Enzyme-linked Immunosorbent Assay, Expressing, Transfection, Gene Knockout, Labeling, Clone Assay