TRAF3IP2 Antibody - BSA Free

Simple Western: TRAF3IP2 Antibody [NB100-56740]

Simple Western: TRAF3IP2 Antibody [NB100-56740] - Simple Western lane view shows a specific band for TRAF3IP2 in 0.5 mg/ml of Hek293 lysate. This experiment was performed under reducing conditions using the 12-230 kDa separation system.

Western Blot: TRAF3IP2 Antibody - BSA Free [NB100-56740] -

IL-18 inhibits miR-30a and miR-342 expression via stress-activated kinases. (A–C) IL-18 inhibits miR-30a and miR-342 expression via stress-activated kinases. Quiescent ASMCs were treated with inhibitors of either p38 MAPK (SB239063, 10 μM in DMSO for 1 h), ERK1/2 (SCH772984 10 μM in DMSO for 1 h) or JNK (SP600125, 20 μM in DMSO for 1 h) prior to IL-18 addition at 10 ng/mL for 30 min (experimental design in (A)). (B,C) Fresh DMSO (0.1%) served as a solvent control. miR-30a and miR-342 expressions were analyzed by TaqMan® Advanced miRNA assays, with U6 serving as a loading control. (B) * p < 0.001 vs. untreated, † p < at least 0.01 vs. IL-18 or IL-18+DMSO (n = 11), (C) * p < 0.01 vs. untreated, † p < at least 0.05 vs. IL-18 or IL-18+DMSO (n = 5). (D–F) miR-30a mimic inhibits IL-18-induced TRAF3IP2 expression. ASMC were transfected with miR-30a mimic (80 nM), made quiescent and then exposed to IL-18 at 10 ng/mL for 2 h (experimental design in (D)). TRAF3IP2 mRNA expression was analyzed by RT-qPCR (E) and its protein levels by Western blotting (F). (G–I) miR-342 mimic restores IL-18-induced RECK suppression. ASMCs were transfected with miR-342 mimic (80 nM), made quiescent and then exposed to IL-18 at 10 ng/mL for 6 h (experimental design in (G)). RECK mRNA expression was analyzed by RT-qPCR (H) and its protein levels by Western blotting (I). (F,I) While a representative immunoblot is shown, the intensities of immunoreactive bands from 4 independent experiments were semiquantified by densitometry and are summarized as mean +/- SEM on the right. (E,F,H,I) * p < 0.05, † at least p < 0.01 vs. untreated controls (n = 4). Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/39451191), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: TRAF3IP2 Antibody - BSA Free [NB100-56740] -

EF24 reverses IL-18-induced upregulation in TRAF3IP2 expression and RECK suppression. (A–C) EF24 blunts IL-18-induced TRAF3IP2 expression. Quiescent ASMCs were treated with EF24 (2.5 μM in DMSO for 1 h) prior to IL-18 addition at 10 ng/mL for 3 h (experimental design in (A)). DMSO alone (0.025%) served as a solvent control. TRAF3IP2 mRNA expression was analyzed by RT-qPCR (B) and its protein levels by Western blotting (C). (D–F) EF24 restores IL-18-induced RECK suppression. Quiescent ASMCs were treated with EF24 (2.5 μM in DMSO for 1 h) prior to IL-18 addition at 10 ng/mL for 6 h (experimental design in (D)). RECK mRNA expression was analyzed by RT-qPCR (E) and its protein levels by Western blotting (F). (C,F) While a representative immunoblot is shown, the intensities of immunoreactive bands from 3–4 independent experiments were semiquantified by densitometry and are summarized as mean +/- SEM on the right. (B,E) * p < at least 0.01 vs. Untreated; † p < at least 0.05 vs. IL-18 or IL-18+DMSO (n = 3–4), (C,F) * p < 0.05 vs. Untreated; † p < 0.05 vs. IL-18 or IL-18+DMSO. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/39451191), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: TRAF3IP2 Antibody - BSA Free [NB100-56740] -

TRAF3IP2 knockdown restores SMC marker expression and inhibits ASMC proinflammatory phenotype without affecting cell viability. (A–G) Silencing TRAF3IP2 restores IL-18-mediated suppression in SMC markers, but inhibits the expression of proinflammatory phenotype markers, without significantly modulating cell viability. ASMCs were transduced with adenoviral TRAF3IP2 shRNA (moi10 for 48 h), made quiescent and then treated with IL-18 (10 ng/mL for 48 h; experimental design in (A)). Expressions of the SMC markers ACTA2 (B,C) and MYH11 (D,E) were analyzed by both RT-qPCR (B,D) and Western blotting (C,E). The proinflammatory phenotype markers Galectin 3, Olr1, VCAM, CCL2, IL-6, IL-8, and TNF-alpha were analyzed by RT-qPCR using TaqMan™ probes (F). Cell viability was assessed by analyzing cleaved caspase-3 levels using a commercially available Caspase-3 (Cleaved) Human ELISA (G). H2O2 (100 μM for 18 h) served as a positive control and induced a significant increase in cleaved capase-3 levels. (C,E) While a representative immunoblot is shown, the intensities of immunoreactive bands from three independent experiments were semiquantified by densitometry and are summarized on the right. (B,D,F,G) * p < at least 0.01 vs. Untreated; † p < 0.01 vs. IL-18 or IL-18+GFP (n = 6 or 7). (C,E) * p < 0.05 vs. Untreated; † p < 0.05 vs. IL-18 or IL-18+GFP (n = 3). Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/39451191), licensed under a CC-BY license. Not internally tested by Novus Biologicals.