pstat3  (Cell Signaling Technology Inc)

Journal: Cell reports

Article Title: Therapeutic activation of IL-22-producing innate lymphoid cells enhances host defenses to Clostridioides difficile infection

doi: 10.1016/j.celrep.2025.115438

Figure Lengend Snippet: Cohoused C57BL/6 and Il22 −/− mice were treated with R848 or H 2 O and large intestine epithelial fractions were collected 3 h later. (A) STAT3 phosphorylation was determined by immunoblot. (B) STAT3 activation was quantified by dividing the integrated densities of pSTAT3 by STAT3 ( n = 3–4 per group). (C) Antibiotic-treated Villin Cre Stat3 fl/fl mice ( Stat3 ΔIEC ) and Stat3 fl/fl ( Stat3 flox ) controls were treated with R848 or H 2 O and infected with C. difficile , and disease severity was assessed at day 2 p.i. Data combined from two experiments ( n = 10 per group). (D) Frequency of proliferating intestinal stem cells following R848 treatment. Cohoused C57BL/6 and Il22 −/− mice were treated with R848 or H 2 O and received EdU by intraperitoneal injection 12 h later. Intestinal stem cell proliferation was measured by EdU incorporation 2 h later ( n = 4–5 per group). FACS plots gated on live, EpCam + , CD45 neg , CD44 hi , CD24 lo , c-Kit neg cells to identify intestinal stem cells. (E–G) Antibiotic-treated C57BL/6 mice were treated with R848 or H 2 O and infected with C. difficile , and intestinal barrier integrity was assessed. (E) Epithelial cells (live, CD45 neg , Epcam + ) were collected at day 2 p.i., and viability was measured by flow cytometry ( n = 3–7 per group). (F) Mice received 20 mg of FITC-dextran by oral gavage at day 2 p.i., and intestinal permeability was assessed by measuring serum levels of FITC-dextran 4 h later. Data combined from two experiments ( n = 4–10 per group). (G) Concentrations of albumin in cecal contents were compared at day 2 p.i. Data combined from four experiments ( n = 8–20). Data are presented as mean ± SEM. Statistical significance calculated by (B, C, and G) two-way ANOVA with Šídák’s correction, (D and E) multiple t test with Holm-Šidák correction, and (F) Kruskal-Wallis test with Dunn’s correction. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. See also – .

Article Snippet: Anti-mouse pSTAT3 (Tyr705), Rabbit , Cell Signaling , Cat# 9145; RRID: AB_2491009.

Techniques: Phospho-proteomics, Western Blot, Activation Assay, Infection, Injection, Flow Cytometry, Permeability

Journal: Cell Reports Medicine

Article Title: A patient-derived T cell lymphoma biorepository uncovers pathogenetic mechanisms and host-related therapeutic vulnerabilities

doi: 10.1016/j.xcrm.2025.102029

Figure Lengend Snippet:

Article Snippet: anti-pSTAT3 (clone M9C6) , Cell Signaling Technology , 4113; RRID: AB_2198588.

Techniques: Transduction, Recombinant, Saline, Software, Sterility, Transferring, Ointment

Journal: Frontiers in Pharmacology

Article Title: Cinnamic acid alleviates hypertensive left ventricular hypertrophy by antagonizing the vasopressor activity and the pro-cardiac hypertrophic signaling of angiotensin II

doi: 10.3389/fphar.2025.1555991

Figure Lengend Snippet: Cinnamic acid dampens cardiomyocyte STAT3 and ERK1/2 activation in response to ang II. After 30-min incubation with vehicle or cinnamic acid, NRCMs were exposed to ang II for 12 h (A) or 5 min (B) . (A) The levels of pSTAT3 and STAT3. (B) The levels of pERK1/2 and ERK1/2. α-tubulin was included for normalization purposes. n = 4 per group. **P < 0.01. Ang II, angiotensin II; CA, cinnamic acid; VC, vehicle control.

Article Snippet: The membranes were blocked with 5% BSA for 1 h at room temperature and incubated overnight at 4°C with primary antibodies including monoclonal mouse anti-STAT3 antibody (1:1000, 9139, Cell Signaling Technology, United States), monoclonal mouse anti-phosphorylated-STAT3 (pSTAT3) antibody (1:2000, 4,113, Cell Signaling Technology, United States), polyclonal rabbit anti-ERK1/2 antibody (1:1000, 9102, Cell Signaling Technology, United States), monoclonal mouse anti-phosphorylated ERK1/2 (pERK1/2) antibody (1:2000, 9106, Cell Signaling Technology, United States) or monoclonal mouse anti-alpha tubulin (α-tubulin) antibody (1:4500, ab7291, Abcam, United States).

Techniques: Activation Assay, Incubation, Control

Journal: Frontiers in Pharmacology

Article Title: Cinnamic acid alleviates hypertensive left ventricular hypertrophy by antagonizing the vasopressor activity and the pro-cardiac hypertrophic signaling of angiotensin II

doi: 10.3389/fphar.2025.1555991

Figure Lengend Snippet: Cinnamic acid dampens cardiomyocyte STAT3 and ERK1/2 activation in response to IL-6 stimulation. After 30-min incubation with vehicle or cinnamic acid, H9c2 cells were exposed to IL-6 for 15 min (n = 4 per group). The levels of pSTAT3 and STAT3 (A) as well as pERK1/2 and ERK1/2 (B) were then analyzed. α-tubulin was included for normalization purposes. *P < 0.05, **P < 0.01, ***P < 0.001. CA, cinnamic acid.

Article Snippet: The membranes were blocked with 5% BSA for 1 h at room temperature and incubated overnight at 4°C with primary antibodies including monoclonal mouse anti-STAT3 antibody (1:1000, 9139, Cell Signaling Technology, United States), monoclonal mouse anti-phosphorylated-STAT3 (pSTAT3) antibody (1:2000, 4,113, Cell Signaling Technology, United States), polyclonal rabbit anti-ERK1/2 antibody (1:1000, 9102, Cell Signaling Technology, United States), monoclonal mouse anti-phosphorylated ERK1/2 (pERK1/2) antibody (1:2000, 9106, Cell Signaling Technology, United States) or monoclonal mouse anti-alpha tubulin (α-tubulin) antibody (1:4500, ab7291, Abcam, United States).

Techniques: Activation Assay, Incubation