pz1 agonist yoda1  (Tocris)

Journal: iScience

Article Title: Mechanical activation of PIEZO1 drives AP-1–dependent PTGS2/PGE2 signaling and corneal inflammation

doi: 10.1016/j.isci.2026.115396

Figure Lengend Snippet: Mechanical stretching activates AP-1 signaling via the PIEZO1-Ca 2+ pathway (A) Flow cytometry measurement of the mean fluorescence intensity of Ca 2+ in cells from different treatment groups (Control, Stretch, Stretch+GsMTx4) using Fluo-4 AM probe staining. (B) Quantitative analysis of the mean fluorescence intensity of Ca 2+ in the Control, Stretch, and Stretch+GsMTx4 groups ( n = 3). (C) Analysis of calcium concentration in the control, stretch, and stretch+GsMTx4 groups (μg/mL, n = 4). (D) Real-time imaging of calcium-fluorescent live cells under different treatment conditions (Con, Con+Yoda1, and Ca 2+ free+Yoda1 groups) (scale bars, 77 μm). (E and F) Mean fluorescence intensity curves for the Con, Con+Yoda1, and Ca 2+ free+Yoda1 groups over time (black arrows indicate the starting points for the addition of different drugs), with a total recording time of 10 min ( n = 6). (G) Western blotting analysis was performed to detect the expression of phosphorylated AP-1 proteins in the Control, Stretch, and Stretch+ Ca 2+ free groups, with β-actin serving as a loading control. (H, I) Relative protein levels of p -JUN and p -FOS were quantified ( n = 3). Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 (one-way ANOVA).

Article Snippet: Yoda1 , MedChemExpress , CAT#HY-18723.

Techniques: Flow Cytometry, Fluorescence, Control, Staining, Concentration Assay, Imaging, Western Blot, Expressing

Journal: iScience

Article Title: Mechanical activation of PIEZO1 drives AP-1–dependent PTGS2/PGE2 signaling and corneal inflammation

doi: 10.1016/j.isci.2026.115396

Figure Lengend Snippet: Activation of PIEZO1 regulates human corneal fibroblast function through the Ca 2+ /PTGS2 axis (A) Changes in PTGS2 mRNA levels following Yoda1 treatment (10 μM) ( n = 3). (B and C) Immunofluorescence staining and quantification of mean fluorescence intensity for PTGS2 protein in the control, Yoda1, and Yoda1+Ca 2+ free groups ( n = 3; scale bars, 50 μm). (D) Cell scratch assay for the Con, Yoda1 (10 μM), and Yoda1+Celecoxib (10 μM) groups (scale bars, 50 μm). (E) Quantitative analysis of scratch area (n = 3–5). (F) Immunofluorescence staining of COL1 protein in the Con, stretch, and stretch+celecoxib groups (scale bars, 50 μm). (G) Quantification of COL1 fluorescence intensity ( n = 4). (H) EdU fluorescent staining of the Con, stretch, and stretch+celecoxib groups (scale bars, 100 μm). (I) Quantitative analysis of EdU mean fluorescence intensity ( n = 5). Data are presented as mean ± SD. ∗∗ p < 0.01 and ∗∗∗ p < 0.001, ns = not significant (Student’s t test or one-way ANOVA).

Article Snippet: Yoda1 , MedChemExpress , CAT#HY-18723.

Techniques: Activation Assay, Immunofluorescence, Staining, Fluorescence, Control, Wound Healing Assay

Journal: iScience

Article Title: Ether phospholipids modulate somatosensory responses by tuning multiple receptor functions in Drosophila

doi: 10.1016/j.isci.2026.115209

Figure Lengend Snippet: ePLs modify dPIEZO activity in Drosophila cells (A–C) Representative Fura-2 imaging data for dPIEZO in control S2R+ cells and cells supplemented with 100 μM 18-AG. A, Typical ratiometric images before (Basal, at 60 s) and after the application of 10 μM Yoda1 (Yoda1, at 360 s) or 5 μM ionomycin (Ionomycin, at 540 s) in dPIEZO expressing cells (left) and dPIEZO expressing cells supplemented with 100 μM 18-AG (right). B, C, Representative Ca 2+ level traces in dPIEZO expressing cells (B), and 18-AG supplemented dPIEZO expressing cells (C). Red traces indicate Yoda1 responding cells (Δratio > 2). (D, E) Proportion of cells responding to Yoda1 (Δratio > 2) (D) and maximum Δratio response to Yoda1 normalized by the ionomycin response (E) in mock-transfected cells (control; n = 10, 18-AG; n = 10) and dPIEZO expressing cells (control, n = 10, 18-AG, n = 10). Each point represents a biological replicate; 25–40 cells were analyzed in each assay. Data are presented as mean ± SEM. ∗ p < 0.05 and ∗∗ p < 0.01; Tukey’s test. (F, G) Representative traces of patch-clamp recordings of mechanical stimuli-evoked dPIEZO activation without (F) or with (G) 100 μM 18-AG. (H) Quantification of the peak current density. Data are presented as mean ± SEM. ∗∗ p < 0.01; Mann-Whitney U test. (I) Proportion of responding cells (current size > 5 pA).

Article Snippet: Yoda1 , Tocris , 5586.

Techniques: Activity Assay, Imaging, Control, Expressing, Transfection, Patch Clamp, Activation Assay, MANN-WHITNEY

Journal: bioRxiv

Article Title: Epilepsy-associated potassium channel KCNT1 is required for multiciliated cell development in Xenopus

doi: 10.64898/2026.03.31.710877

Figure Lengend Snippet: (A) Inhibition of KCNT1 and Piezo signaling with KCNT1 antagonist, VU0606170 (20 µM), and Piezo signaling antagonist, GsMTx4 (5 µM), further exacerbates loss of motile cilia compared to KCNT1 antagonist (20 µM) alone. X. laevis embryos were treated from NF stage 6 to 38 and stained with acetylated-α-tubulin (cilia, magenta) and phalloidin (actin, grey). Embryo images were randomized and scored blinded to condition. Scale bars = 500 µm. (B) Quantification of data shown in A as a percentage of embryos with no cilia phenotype vs. mild, moderate or severe cilia phenotype. Fisher’s exact test was used to calculate significance using raw counts of individual embryos. **** = p < 0.0001, ns = no statistically significant difference. (C) Partial rescue of loss of cilia phenotype from KCNT1 inhibition (20 µM VU0606170) by co-treatment with a Piezo1 agonist, Yoda1 (110 µM), compared to KCNT1 antagonist alone (20 µM). Scale bars = 500 µm. (D) Quantification of data shown in C as a percentage of embryos with no cilia phenotype vs. mild, moderate or severe cilia phenotype. Fisher’s exact test was used to calculate significance using raw counts of individual embryos. **** = p < 0.0001, *** = 0.0009, ns = no statistically significant difference.

Article Snippet: KCNT1 antagonist (VU0606170, ProbeChem PC-73240), additional KCNT1 antagonist (Compound 31, Enamine EN300-27781598), Piezo1 antagonist (GsMTx4, MedChemExpress HY-P1410), and Piezo1 agonist (Yoda1, Sigma SML1558) were resuspended in DMSO at 10 mM, 10 mM, 5 mM, and 10 mM, respectively.

Techniques: Inhibition, Staining