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Danaher Inc recombinant fst protein
Overexpression of <t>FST</t> reduces cardiac fibrosis by inhibiting the activation of the TGF-β–Smad3 pathway in vivo and in vitro . Quantitative real-time PCR analysis of TGF-β1, activin A, and TGF-β3 mRNA transcription [ (A–C) , n ≥4] and p -Smad3 and Smad3 protein expression in each group [ (D) , n = 4]. In vitro , NIH3T3 cells were treated with or without high glucose (30 mM), <t>recombinant</t> FST protein (10 ng/ml), and TGF-β1 (20 μM). Protein expression of COL1, COL3, p -Smad3, and Smad3 with different treatments [ (E–G) , n = 3]. * p < 0.05; ** p < 0.01; *** p <0.001.
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Image Search Results


Journal: Cell reports

Article Title: Single-cell analysis of early chick hypothalamic development reveals that hypothalamic cells are induced from prethalamic-like progenitors

doi: 10.1016/j.celrep.2021.110251

Figure Lengend Snippet:

Article Snippet: Explants were either treated with recombinant FST (7.5 μg/mL, Cat no. 769-FS-025, R&D Systems) or anti-FST antibody (20 μg/mL, AF669, R&D Systems) for 42 h, and processed for in situ hybridization chain reaction (HCR).

Techniques: Recombinant, Affinity Purification, Multiplex Assay, Hybridization, Amplification, Software

Overexpression of FST reduces cardiac fibrosis by inhibiting the activation of the TGF-β–Smad3 pathway in vivo and in vitro . Quantitative real-time PCR analysis of TGF-β1, activin A, and TGF-β3 mRNA transcription [ (A–C) , n ≥4] and p -Smad3 and Smad3 protein expression in each group [ (D) , n = 4]. In vitro , NIH3T3 cells were treated with or without high glucose (30 mM), recombinant FST protein (10 ng/ml), and TGF-β1 (20 μM). Protein expression of COL1, COL3, p -Smad3, and Smad3 with different treatments [ (E–G) , n = 3]. * p < 0.05; ** p < 0.01; *** p <0.001.

Journal: Frontiers in Pharmacology

Article Title: Follistatin Attenuates Myocardial Fibrosis in Diabetic Cardiomyopathy via the TGF-β–Smad3 Pathway

doi: 10.3389/fphar.2021.683335

Figure Lengend Snippet: Overexpression of FST reduces cardiac fibrosis by inhibiting the activation of the TGF-β–Smad3 pathway in vivo and in vitro . Quantitative real-time PCR analysis of TGF-β1, activin A, and TGF-β3 mRNA transcription [ (A–C) , n ≥4] and p -Smad3 and Smad3 protein expression in each group [ (D) , n = 4]. In vitro , NIH3T3 cells were treated with or without high glucose (30 mM), recombinant FST protein (10 ng/ml), and TGF-β1 (20 μM). Protein expression of COL1, COL3, p -Smad3, and Smad3 with different treatments [ (E–G) , n = 3]. * p < 0.05; ** p < 0.01; *** p <0.001.

Article Snippet: After starvation in serum-free medium for 24 h, the NIH3T3 cells were incubated in DMEM containing 5.5 mmol/L glucose, 33 mmol/L glucose (high glucose, HG), HG plus 10 ng/ml recombinant FST protein (human recombinant follistatin, BioVision, #4708), or HG plus 10 ng/ml recombinant FST protein and 20 μM TGF-β1 (MedChemExpress, United States).

Techniques: Over Expression, Activation Assay, In Vivo, In Vitro, Real-time Polymerase Chain Reaction, Expressing, Recombinant