protein expression  (R&D Systems)

Journal: Science advances

Article Title: Caspase-1-dependent pyroptosis converts αSMA + CAFs into collagen-III high iCAFs to fuel chemoresistant cancer stem cells.

doi: 10.1126/sciadv.adt8697

Figure Lengend Snippet: Fig. 4. Tumor cell pyroptosis skews CAFs toward iCAFs in a CCR6-dependent mechanism. (A) Representative image illustrating a cytokine protein array (i.e., Proteome Profiler Human XL Cytokine Array Kit, R&D Systems) probed with the supernatant collected from WT and Casp1 KO T24 cancer cells after 48 hours of gemcitabine treat- ment. Red, blue, and green boxes highlighting the individual cytokines or chemokines with the most differential expression (i.e., reduction) in Casp1 KO versus WT Gem- treated supernatant. (B) Bar graph quantifying the intensity of three cytokines differentially released in WT and Casp1 KO supernatant, i.e., CXCL5, CXCL10, and CCL20. (C) ELISA quantification of CXCL5, CXCL10, and CCL20 protein concentration in the supernatants collected from gemcitabine-treated WT and Casp1 KO T24 blad- der cancer cells. (D) Flow cytometry assessing the percentage of αSMAhigh/+ CAFs and αSMA−PDGFβ+ iCAFs treated with CM from Gem-treated T24 cells with anti-CXCR2 neutralizing Ab, (anti-CXCR2 Ab, blocking receptor downstream to CXCL5), anti-CXCL10 neutralizing Ab, anti-CCL20 neutralizing ab, and CCR6i (blocking receptor down- stream to CCL20). (E) Violin dot plot quantifying the relative changes in the percentage of αSMA−PDGFβ+ iCAFs upon CM-Gem ± chemokine or chemokine receptor neutralizing Ab treatments.

Article Snippet: Tumor cell pyroptosis skews CAFs toward iCAFs in a CCR6- dependent mechanism. (A) Representative image illustrating a cytokine protein array (i.e., Proteome Profiler human Xl cytokine Array Kit, R&d Systems) probed with the supernatant collected from Wt and casp1 KO t24 cancer cells after 48 hours of gemcitabine treatment.

Techniques: Protein Array, Quantitative Proteomics, Enzyme-linked Immunosorbent Assay, Protein Concentration, Flow Cytometry, Blocking Assay

Journal: Acta neuropathologica communications

Article Title: Downregulation of STAT3 transcription factor reverses synaptotoxic phenotype of reactive astrocytes associated with prion diseases.

doi: 10.1186/s40478-025-02028-6

Figure Lengend Snippet: Fig. 6 Reactive microglia and astrocytes secrete pro-inflammatory factors. Analysis of media conditioned by reactive microglia and astrocytes isolated from 22L-Cre+/− and non-infected, adult Cre+/− mice using cytokine/chemokine profiling array. A, B. Representative array images of mouse cytokines in media conditioned by reactive microglia (A) and astrocytes (B). C. Quantification cytokines secreted by microglia and astrocytes from 22L-Cre+/− and Cre+/− animals. D. Venn diagram illustrating an overlap in secreted molecules between reactive astrocytes and microglia. Factors upregulated or down regulated in reactive versus homeostatic states are shown using bold and thin fonts, respectively. Data represent mean ± SE, ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05 and ‘ns’ is non-significant by two-tailed, unpaired t-test, N = 3 independent experiments, where conditioned media were obtained from three independent cultures, each originating from an individual animal

Article Snippet: Recombinant mouse IL-6, proteome profiler array- mouse cytokine array panel A (R&D Systems, Minneapolis, MN); Bicinchoninicacid (BCA) protein assay kit, 70 μm nylon mesh filter, 0.22 μm filter, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide), polyvinylidenefluoride (PVDF) membrane (Millipore, Temecula, CA); protease/phosphatase inhibitor (Cell Signaling Technology, Danvers, MA).

Techniques: Isolation, Infection, Two Tailed Test