Journal: Poultry Science

Article Title: Gut microbiota-derived taurolithocholic acid modulates myofiber-type switching via p38 MAPK/PGC-1α signaling underlying breed differences between Arbor Acres and Taoyuan chickens

doi: 10.1016/j.psj.2026.106914

Figure Lengend Snippet: TLCA regulates mitochondrial biogenesis and altered myofiber type composition through the p38 MAPK/PGC-1α signaling pathway. A Cell viability of cells treated with different concentrations of TLCA for 24 h (n = 10). B & F The mRNA expression of MYH1A and MYH7B (n = 6). C & G Intracellular enzymatic activities of succinate dehydrogenase (SDH) and lactate dehydrogenase (LDH), ATP content and mitochondrial DNA (mtDNA) content (n = 6). D & H The mRNA expression of HK1, GPI, PGAM1, PGK1, PYGL, PGC-1α, NRF1 and TFAM (n = 6). E The protein expression of PGC-1α, p38 MAPK and phosphorylation p38 MAPK (n = 3). I The protein expression of PGC-1α (n = 3). Data were shown as mean ± SD; *Represents significant difference when compared with 0 μM TLCA or CON group, and # represents significant difference when compared with TLCA group. *& # P < 0.05, ⁎⁎ & ## P < 0.01, ⁎⁎⁎ & ### P < 0.001.

Article Snippet: The differentiation medium containing TLCA and p38 MAPK inhibitor SB203580 (152121-47-6, MedChemExpress, Shanghai, China) was added to CPMs after 4 days of differentiation, and the cells were collected after 24 h.

Techniques: Expressing, Phospho-proteomics

Journal: iScience

Article Title: Targeting USP14 enhances immunotherapy response by reprogramming tumor-associated macrophages in colon cancer

doi: 10.1016/j.isci.2026.115362

Figure Lengend Snippet: Identification of the mechanism underlying IU1-mediated reprogramming of M2 macrophages (A and B) Verification of the efficiency of i.v. injection of clodronate liposome (Clo) in depleting TAMs of the blood (A) and the TME (B). (C and D) Statistics of tumor size monitored for 21 days in MC38 tumor-bearing mice after various indicated treatments. (E) Statistic of the percentage of CTLs in the TME after the indicated treatment. (F) Volcano plots of the differentially expressed genes between the PBS and the IU1 group. Red dots show significantly up-regulated genes in the IU1 group, and green dots show significantly down-regulated genes. (G) Heatmap illustrates the differentially expressed M1-and M2-related genes in TAMs in the IU1 group and the PBS group based on RNA sequencing results. (H) KEGG analysis identifies the 17 most enriched pathways based on the differentially expressed genes of the two groups. (I) Western blotting of p -JNK, p -ERK, p-p38, and GAPDH in IL-4/13-BMDM M2 cells treated with IU1 at the indicated time points. (J) RT-PCR to verify the typical M1/M2 polarization-related genes in M2 macrophages after treatment with IU1. (K) Flow cytometry analysis of CD206 expression on the IL-4/13-induced BMDM M2 cells from various indicated treatments. Treatments indicated: DMSO stimulation, IU1 (10 μM) stimulation, IU1 (10 μM) stimulation in the presence of inhibitors of p38 (SB203580, 10 μM), JNK (SP600125, 10 μM), Erk1/2 (U0126-EtOH, 10 μM). Statistical analysis was performed using one-way ANOVA with Tukey’s multiple comparison test. Data are presented as the mean ± SEM. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001, and ns: not significant.

Article Snippet: SB203580 , MedChemExpress , HY-10256.

Techniques: Injection, RNA Sequencing, Western Blot, Reverse Transcription Polymerase Chain Reaction, Flow Cytometry, Expressing, Comparison

Journal: Oncology Reports

Article Title: Sphingosine-1-phosphate receptor 1 enhances olfactory receptor 51E1-mediated inhibition of proliferation via Src/JNK signaling in prostate cancer cells

doi: 10.3892/or.2026.9103

Figure Lengend Snippet: Co-expression of S1PR1 amplifies OR51E1-Src-JNK signaling and suppression of proliferation. (A and B) Inhibitor profiling reveals signaling pathways involved in NA-induced reduction of LNCaP cell viability. LNCaP cells were preincubated for 1 h with (A) canonical OR pathway inhibitors (SQ-22536, 100 µM; H-89, 3 µM; ESI-09, 3 µM; SU6656, 10 µM) or with (B) other, less well-characterized pathway inhibitors (SU6656, 10 µM; Dasatinib, 10 nM; SP600125, 3 µM; SB203580, 3 µM; U0126, 10 µM; AG-490, 10 µM), followed by treatment with NA for 48 h. SQ-22536 and SU6656 were included in both panels for comparison. Cell viability was measured using the CCK-8 assay. Data represent the mean ± SEM of at least three independent experiments. Statistical analysis was performed using an unpaired Student's t-test. Hash symbols (#) indicate statistical significance between vehicle- and NA-treated cells, whereas asterisks (*) indicate statistical significance between cells treated with NA alone and those co-treated with NA and the indicated inhibitors. (C) Western blot analysis of JNK activation in LNCaP and LNCaP-S1PR1 cells treated with NA for 1 h. Protein levels of p-JNK and total JNK were analyzed. (D) Effect of Src inhibition on NA-induced JNK activation. LNCaP cells were pretreated with the Src inhibitor SU6656 (10 µM) for 1 h and then treated with NA for 1 h. Protein levels of p-JNK and total JNK were assessed. Band intensities were quantified using ImageJ software. Data represent the mean ± SEM of three independent experiments. Statistical significance was determined using an unpaired Student's t-test. (E) Effect of Src inhibition on NA-mediated suppression of proliferation. LNCaP and LNCaP-S1PR1 cells were pretreated with SU6656 for 1 h, and cell viability was measured using the CCK-8 assay after NA treatment. Data represent the mean ± SEM of at least three independent experiments and were analyzed using two-way ANOVA with Tukey's multiple comparison test. (F) Effect of Src inhibition on NA-induced apoptosis. LNCaP and LNCaP-S1PR1 cells were pretreated with dasatinib (100 nM) for 1 h and then treated with NA. Apoptosis was assessed using annexin V/PI staining. Data represent the mean ± SEM of three independent experiments and were analyzed using two-way ANOVA with Tukey's multiple comparison test. ### P<0.001 and #### P<0.0001; *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. S1PR1, sphingosine-1-phosphate receptor 1; OR51E1, olfactory receptor 51E1; NA, nonanoic acid; CCK-8, Cell Counting Kit-8; p-, phosphorylated; PI, propidium iodide; ns, not significant.

Article Snippet: For pathway inhibitor experiments, cells were pre-treated for 1 h with the indicated pathway inhibitors (SQ-22536, 100 μM (cat. no. 568500; MilliporeSigma; PubChem ID 5270); SU6656, 10 μM (cat. no. 572635; MilliporeSigma; PubChem ID 5312137); dasatinib, 10 nM (cat. no. CDS023389; MilliporeSigma; PubChem ID 3062316); SP600125, 10 μM (cat. no. HY-12041; MilliporeSigma; PubChem ID NSC75890); SB203580, 10 μM (cat. no. S1076; Selleck Chemicals; PubChem ID 176155); U0126, 1 μM (cat. no. HY-12031A; MilliporeSigma; PubChem ID 3006531); AG490, 10 μM (cat. no. HY-12000; MilliporeSigma; PubChem ID 5328779), followed by incubation with or without NA for 48 h. Subsequently, 10 μl of CCK-8 reagent was added to each well and incubated for 4 h at 37°C.

Techniques: Expressing, Protein-Protein interactions, Comparison, CCK-8 Assay, Western Blot, Activation Assay, Inhibition, Software, Staining, Olfactory, Cell Counting