mapk erk pathway activator ro 67 7476  (MedChemExpress)

Journal: Translational Oncology

Article Title: Zeaxanthin targets TOP2A to regulate autophagy and suppress lung cancer progression via the MAPK/ERK pathway

doi: 10.1016/j.tranon.2025.102658

Figure Lengend Snippet: Zea modulates MAPK/ERK signaling to inhibit LC progression. A: Analysis of gene expression differences pre- and post-Zea treatment; B: Heat map analysis of TOP 50 DEGs; C: GO functional enrichment of differentially expressed genes; D: KEGG pathway enrichment of differentially expressed genes; E: WB analysis of MAPK/ERK pathway proteins. A549 cells: NC, Zea, Zea + Ro 67–7476. F: Cell viability measured by CCK-8; G: Cell proliferation assessed by colony formation; H: Cell migration analyzed by Transwell; I: Cell apoptosis detected by flow cytometry; J: WB of autophagy-related proteins; K: IF analysis of autophagosomes and lysosomes, with LC3 for autophagosomes and LAMP1 for lysosomes. ** P < 0.01, *** P < 0.001. The data is presented as mean ± standard deviation, and inter-group comparisons are conducted using ANOVA and Tukey’s post hoc test.

Article Snippet: We also wondered whether the impact of Zea on LC cells was associated with the MAPK/ERK signaling, so we treated A549 cells with Zea and subsequently added MAPK/ERK pathway activator Ro 67–7476 (MCE, USA) to activate this pathway.

Techniques: Gene Expression, Functional Assay, CCK-8 Assay, Migration, Flow Cytometry, Standard Deviation

Journal: Translational Oncology

Article Title: Zeaxanthin targets TOP2A to regulate autophagy and suppress lung cancer progression via the MAPK/ERK pathway

doi: 10.1016/j.tranon.2025.102658

Figure Lengend Snippet: Zea targets TOP2A to enhance autophagy via the MAPK/ERK pathway and impedes LC progression. A549 cells: oe-NC, oe-TOP2A, A: TOP2A mRNA level detected by qRT-PCR A549 cells: oe-NC, oe-TOP2A, oe-NC + Zea, oe-TOP2A + Zea. B: WB analysis of TOP2A, MAPK/ERK pathway proteins (p-ERK1/2, ERK1/2, p-MEK, MEK), and autophagy-related proteins (LC3-I, LC3-II, Beclin 1); C: IF detection of autophagosome and lysosome formation; D: CCK-8 assay of cell viability; E: Colony formation assay of cell proliferation; F: Transwell assay of cell migration; G: Flow cytometry analysis of cell apoptosis. ** P < 0.01, *** P < 0.001. The data is presented as mean ± standard deviation, and inter-group comparisons are conducted using ANOVA and Tukey’s post hoc test.

Article Snippet: We also wondered whether the impact of Zea on LC cells was associated with the MAPK/ERK signaling, so we treated A549 cells with Zea and subsequently added MAPK/ERK pathway activator Ro 67–7476 (MCE, USA) to activate this pathway.

Techniques: Quantitative RT-PCR, CCK-8 Assay, Colony Assay, Transwell Assay, Migration, Flow Cytometry, Standard Deviation

Journal: Translational Oncology

Article Title: Zeaxanthin targets TOP2A to regulate autophagy and suppress lung cancer progression via the MAPK/ERK pathway

doi: 10.1016/j.tranon.2025.102658

Figure Lengend Snippet: In vivo evidence that Zea targets TOP2A to influence the MAPK/ERK pathway and autophagy to mitigate LC progression. Animal groups: oe-NC, oe-TOP2A, oe-NC + Zea, oe-TOP2A + Zea. A: Tumor images from the mouse model; B: Weight of mouse tumor tissues; C: Volume of mouse tumor tissues; D: HE staining images of mouse tumor tissues; E: IHC detection of TOP2A and KI67 expression levels in tumor tissues; F: WB analysis of MAPK/ERK pathway proteins (p-ERK1/2, ERK1/2, p-MEK, MEK) and autophagy-related proteins (LC3-I, LC3-II, Beclin 1); G: IF detection of autophagosome and lysosome colocalization. *** P < 0.001. The data is presented as mean ± standard deviation, and inter-group comparisons are conducted using ANOVA and Tukey’s post hoc test.

Article Snippet: We also wondered whether the impact of Zea on LC cells was associated with the MAPK/ERK signaling, so we treated A549 cells with Zea and subsequently added MAPK/ERK pathway activator Ro 67–7476 (MCE, USA) to activate this pathway.

Techniques: In Vivo, Staining, Expressing, Standard Deviation

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: PTPRK activated the DUSP1/p38 MAPK signaling pathway in PHN. A , Western blot was performed to analyze the protein levels of DUSP1, p-p38 MAPK, and p38 MAPK in DRG tissues of each group; B , The protein levels of PTPRK, DUSP1, p-p38 MAPK, and p38 MAPK in Lv-NC and Lv-PTPRK groups were detected via Western blot. ( N = 5).

Article Snippet: Conversely, to activate the p38 MAPK pathway, rats were injected with anisomycin (2.5 mg/kg; HY-18982; purity: 99.82%; MedChem Express), a known inducer of p38 phosphorylation , once daily for 7 days.

Techniques: Western Blot

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: p38 MAPK signaling pathway activation promoted mechanical allodynia and inflammation in rat DRG tissues. A , Paw withdrawal thresholds and B , paw withdrawal latency in each group were quantified; ELISA was performed to assess the concentrations of C , TNF-α, D , IL-1β, and E , IL-4 in DRG tissues of each group; RT-qPCR was performed to analyze the mRNA levels of F , TNF-α, G , IL-1β, H , IL-4, I , BDNF, J , Nav1.3, K , Nav1.7, and L , TRPV1 in DRG tissues of each group. ( N = 5; ** p < 0.01 vs. the RTX-PHN + Lv-shNC group; # p < 0.05, ## p < 0.01 vs. the RTX-PHN + Lv-shPTPRK group).

Article Snippet: Conversely, to activate the p38 MAPK pathway, rats were injected with anisomycin (2.5 mg/kg; HY-18982; purity: 99.82%; MedChem Express), a known inducer of p38 phosphorylation , once daily for 7 days.

Techniques: Activation Assay, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR

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: PTPRK overexpression promoted inflammation via activating DUSP1/p38 MAPK signaling pathway in rat DRG cells. A , PTPRK expression was analyzed by RT-qPCR after empty and PTPRK overexpression vectors transfection; B , The protein levels of PTPRK, DUSP1, p-p38 MAPK, and p38 MAPK in each group were detected though Western blot; ELISA was performed to assess the concentrations of C , TNF-α, D , IL-1β, and E , IL-4 in DRG cells of each group; RT-qPCR was performed to analyze the mRNA levels of F , TNF-α, G , IL-1β, H , IL-4, I , BDNF, J , Nav1.3, K , Nav1.7, and L , TRPV1 in DRG cells of each group. ( N = 3; ** p < 0.01 vs. the vector group; ## p < 0.01 vs. the PTPRK group).

Article Snippet: Conversely, to activate the p38 MAPK pathway, rats were injected with anisomycin (2.5 mg/kg; HY-18982; purity: 99.82%; MedChem Express), a known inducer of p38 phosphorylation , once daily for 7 days.

Techniques: Over Expression, Expressing, Quantitative RT-PCR, Transfection, Western Blot, Enzyme-linked Immunosorbent Assay, Plasmid Preparation

Journal: medRxiv

Article Title: Psychiatric disorders converge on common pathways but diverge in cellular context, spatial distribution, and directionality of genetic effects

doi: 10.1101/2025.07.11.25331381

Figure Lengend Snippet: ( a )-( c ) Histograms display the distribution of gene set size when stratified the pathway clusters by ( a ) S-A axis, ( b ) 12 cell types, and ( c ) both S-A axis and cell types. Vertical dashed line indicates our 50 genes cut-off for gene sets to be included in the analysis. ( d ) Venn diagrams show the number of genes intersected between the major pathway gene sets (Chromatin regulation, MAPK signaling, Calcium signaling, and Synaptic transmission), Postnatal Excitatory Neurons, and Sensorimotor or Association genes.

Article Snippet: SCZ-DUP associations in cell-signaling (MAPK, cell-cycle) and metabolic pathways were concentrated in postnatal excitatory neurons and neurovascular cells.

Techniques: Transmission Assay