rabbit anti phospho p38mapk  (Cell Signaling Technology Inc)

Journal: Scientific Reports

Article Title: The hydroxamate based HDAC inhibitor WMJ-J-09 induces colorectal cancer cell death by targeting tubulin and downregulating survivin

doi: 10.1038/s41598-025-04714-w

Figure Lengend Snippet: LKB1-p38 MAPK signaling contributed to WMJ-J-09-mediated p21 and survivin regulation. ( A ) Immunoblot result of p38MAPK phosphorylation in HCT116 cells exposed to WMJ-J-09. ( B , C ) Immunoblot result of p21 ( B ) and survivin ( C ) expression in WMJ-J-09-stimulated HCT116 cells with or without p38 inhibitor III ( D ) Immunoblot result of LKB1 phosphorylation in HCT116 cells exposed to WMJ-J-09 for indicated periods. ( E ) Immunoblot results from the effects of LKB1 siRNA or negative control siRNA on p38MAPK and p53 phosphorylation elicited by WMJ-J-09. ( F ) Immunoblot result of the effects of LKB1 siRNA or negative control siRNA on WMJ-J-09-modulated p21 and survivin expression in HCT116 cells. Each band intensity was quantified, and total α-tubulin levels normalized the fold changes of LKB1, p21, and survivin; total p53 levels normalized that of p53 phosphorylation; total p38MAPK levels normalized that of p38MAPK phosphorylation; total LKB1 levels normalized that of LKB1 phosphorylation. Error bars, mean ± S.E.M. (shown only for independent replicate experiments with n ≥ 4). One-way ANOVA followed by Tukey’s post-hoc test assessed statistical significance (*p < 0.05 compared to the control group).

Article Snippet: Antibodies against α-tubulin Lys40 acetylation, p53, p53 Lys379 acetylation, p53 Ser15 phosphorylation, p38MAPK Thr180/Tyr182 phosphorylation, p38MAPK, LKB1, LKB1 Ser428 phosphorylation, PARP, cleaved caspase 3 (active form) and survivin were from Cell Signaling (Danvers, MA, U.S.A.).

Techniques: Western Blot, Phospho-proteomics, Expressing, Negative Control, Control

Journal: Pharmaceutical Biology

Article Title: Integrated pharmacoanalysis, bioinformatics analysis, and experimental validation to identify the ingredients and mechanisms of Xiao-Luo-Wan in uterine fibroids treatment

doi: 10.1080/13880209.2025.2485905

Figure Lengend Snippet: Molecular docking models of XLW components that bind to potential targets in 3-dimensional stereoimages. Molecular docking pattern diagrams of (A) TRIM9 and buergerinin B, (B) TRIM9 and cedrol, (C) TRIM9 and ent-15B-16-epoxy-kauan-17-ol, (D) NF-κB p65 and buergerinin B, (E) NF-κB p65 and cedrol, (F) NF-κB p65 and ent-15B-16-epoxy-kauan-17-ol, (G) p38MAPK and buergerinin B, (H) p38MAPK and cedrol, and (I) p38MAPK and ent-15B-epoxy-kauan-17-ol.

Article Snippet: Next, the membranes were blocked with Tris-buffered saline containing 5% nonfat milk for 1 h and incubated with primary antibodies against Ki-67 (1:5000; Abcam, Cat#: 92742, RRID:AB_10562976), Caspase9 (1:1000; CST, Cat#: 9508, RRID:AB_2068620), TRIM9 (1:1000; CST, Cat#: 47990, RRID: AB_3668999), NF-κB p65 (1:1000; CST, Cat#: 8242, RRID:AB_10859369), p-p38MAPK (1:1000; CST, Cat#: 9211, RRID:AB_331641) and β-actin (1:1000; CST, Cat#: 4967, RRID:AB_330288) overnight at 4 °C.

Techniques:

Journal: Pharmaceutical Biology

Article Title: Integrated pharmacoanalysis, bioinformatics analysis, and experimental validation to identify the ingredients and mechanisms of Xiao-Luo-Wan in uterine fibroids treatment

doi: 10.1080/13880209.2025.2485905

Figure Lengend Snippet: The 3 components with the highest affinity for candidate protein targets.

Article Snippet: Next, the membranes were blocked with Tris-buffered saline containing 5% nonfat milk for 1 h and incubated with primary antibodies against Ki-67 (1:5000; Abcam, Cat#: 92742, RRID:AB_10562976), Caspase9 (1:1000; CST, Cat#: 9508, RRID:AB_2068620), TRIM9 (1:1000; CST, Cat#: 47990, RRID: AB_3668999), NF-κB p65 (1:1000; CST, Cat#: 8242, RRID:AB_10859369), p-p38MAPK (1:1000; CST, Cat#: 9211, RRID:AB_331641) and β-actin (1:1000; CST, Cat#: 4967, RRID:AB_330288) overnight at 4 °C.

Techniques:

Journal: Pharmaceutical Biology

Article Title: Integrated pharmacoanalysis, bioinformatics analysis, and experimental validation to identify the ingredients and mechanisms of Xiao-Luo-Wan in uterine fibroids treatment

doi: 10.1080/13880209.2025.2485905

Figure Lengend Snippet: Effects of XLW decoction-treated serum on the (A) mRNA and (B) protein expression of TRIM9, NF-κB and p-p38MAPK in UMCs. * p < 0.05 compared with the control. # p < 0.05 compared with RU-486. RU-486: mifepristone; XLW-L: 20% XLW drug-containing serum; XLW-M: 30% XLW drug-containing serum; XLW-H: 40% XLW drug-containing serum.

Article Snippet: Next, the membranes were blocked with Tris-buffered saline containing 5% nonfat milk for 1 h and incubated with primary antibodies against Ki-67 (1:5000; Abcam, Cat#: 92742, RRID:AB_10562976), Caspase9 (1:1000; CST, Cat#: 9508, RRID:AB_2068620), TRIM9 (1:1000; CST, Cat#: 47990, RRID: AB_3668999), NF-κB p65 (1:1000; CST, Cat#: 8242, RRID:AB_10859369), p-p38MAPK (1:1000; CST, Cat#: 9211, RRID:AB_331641) and β-actin (1:1000; CST, Cat#: 4967, RRID:AB_330288) overnight at 4 °C.

Techniques: Expressing, Control

Journal: Translational Lung Cancer Research

Article Title: Targeting of arachidonic acid-modulated autophagy to enhance the sensitivity of ROS1 + or ALK + non-small cell lung cancer to crizotinib therapy

doi: 10.21037/tlcr-2025-105

Figure Lengend Snippet: Downregulation of MAPK/p-STAT3/PTGS2 drove metabolic reprogramming in crizotinib-resistant cells. (A) UMAP plots based on the top 5 principal components of all single-cell transcriptomes after quality control, color-coded by treatment group (ALK TKI-sensitive or TKI-resistant) or by subsets identified through unsupervised dimensionality reduction and clustering. The analysis revealed two TKI-sensitive clusters (SensC1 and SensC2) and six TKI-resistant clusters (ResiC1–ResiC6). (B) Differentially expressed genes in each subset, with the top 5 genes per subset being shown (see A for color codes). (C) Mean pathway activity scores for different cell subsets. (D) Human phospho-kinase array analysis was performed to evaluate signaling pathways in HCC78 and HCC78CR cells treated with 2 µM of crizotinib for 24 hours. The green arrow indicates the puncta of p-STAT3 (S727). (E) HCC78 and HCC78CR cells were treated with the 1 µM crizotinib for 24 hours. The protein levels of p-P38MAPK (T180/T182) and p-STAT3 (S727) were detected via western blotting. β-actin was used as the loading control. The gray value ratios of phosphorylated to total proteins are shown on the right. (F) Volcano plot of RNA-sequencing analysis comparing gene expression profiles between parental and resistant HCC78 cells. (G) KEGG pathway enrichment analysis of differentially expressed genes between parental and resistant HCC78 cells. (H) CNET mapping of four differential signaling pathways (lL-17 signaling pathway, cytokine-cytokine receptor interaction, NF-κB signaling pathway, and regulation of lipolysis in adipocytes). (I) UMAP and dot plots showing the expression levels of EPCAM and PTGS2 in each subset in ALK-TKI-sensitive and TKI-resistant tumors. (J) Unsupervised transcriptional trajectory analysis of different cell subsets generated using R package Monocle2, colored by pseudotime, cell subsets, and PTGS2 expression levels, respectively, in ALK TKI-sensitive and TKI-resistant tumors. (K) The levels of PTGS2 mRNA in HCC78CR and H3122CR cells, as compared to their corresponding parental cells, were measured using RT-qPCR. Data are presented as the mean ± SD. (E) Brown-Forsythe and Welch ANOVA tests and (K) Unpaired two-sided Student’s t -test. ns: no significance. *, P<0.05; **, P<0.01; ***, P<0.001; ****, P<0.0001. ANOVA, analysis of variance; ALK, anaplastic lymphoma kinase; Cri, crizotinib; CNET, computational network; CR, crizotinib resistance; EPCAM, epithelial cell adhesion molecule; KEGG, Kyoto Encyclopedia of Genes and Genomes; p38MAPK, mitogen-activated protein kinase; p-p38MAPK(T180/182), phosphorylation of mitogen-activated protein kinase on T180 and T182; STAT3, signal transducer and activator of transcription 3; p-STAT3(S727), phosphorylation of signal transducer and activator of transcription 3 on S727; no-diff, no difference; PTGS2, prostaglandin endoperoxide synthase 2; SD, standard deviation; TKI, tyrosine kinase inhibitor; UMAP, uniform manifold approximation and projection; WT, wild type.

Article Snippet: The primary antibodies used were LAMP1 [cat. no. 9091; Cell Signaling Technology (CST), Danvers, MA, USA], LC3B (cat. no. 83506; CST), p-p38MAPK (Thr180/Tyr182) (cat. no. 4511; CST), p38 MAPK (cat. no. 8690; CST), p-STAT3 (S727) (cat. no. 9134; CST), STAT3 (cat. no. 9139; CST), p-IRE1 (S724) (cat no. AP1442; ABclonal, Woburn, MA, USA), IRE1 (cat no. A17940; ABclonal), sXBP1 (cat no. A17007; ABclonal), p-PERK (T982) (cat no. AP0886; ABclonal), and PERK (cat. no. A18196; ABclonal). β-actin, HRP-conjugated goat anti-rabbit, and goat anti-mouse secondary antibodies were obtained from Boster Bio (Pleasanton, CA, USA).

Techniques: Control, Activity Assay, Protein-Protein interactions, Western Blot, RNA Sequencing, Gene Expression, Expressing, Generated, Quantitative RT-PCR, Phospho-proteomics, Standard Deviation