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R&D Systems
biotinylated il 36α antibodies Biotinylated Il 36α Antibodies, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/result/biotinylated il 36α antibodies/product/R&D Systems Average 94 stars, based on 1 article reviews
biotinylated il 36α antibodies - by Bioz Stars,
2026-03
94/100 stars
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Thermo Fisher
biotinylated hil-36α protein ![]() Biotinylated Hil 36α Protein, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/result/biotinylated hil-36α protein/product/Thermo Fisher Average 90 stars, based on 1 article reviews
biotinylated hil-36α protein - by Bioz Stars,
2026-03
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Image Search Results
Journal: Scientific Reports
Article Title: Small Molecule IL-36γ Antagonist as a Novel Therapeutic Approach for Plaque Psoriasis
doi: 10.1038/s41598-019-45626-w
Figure Lengend Snippet: IL-36γ is upregulated in psoriatic lesions and drives psoriasiform changes in 3D skin equivalents. ( A ) In situ hybridization images of psoriasis patient tissue isolated from a lesion (left) or non-lesional skin (right). Red spots represent RNA signal for the select probes; images representative of three patients are shown. ( B ) Differences between lesional and non-lesional RNA signals were quantified for each probe represented in. ( A ) Average of 3 patients is shown ± S.E.M. (*p < 0.05 in an unpaired, two-tailed t test; df = 4, t = 4.458 (IL-36α), 3.633 (IL-36γ), 4.289 (IL-36R), 3.027 (IL-36Ra)). ( C ) H&E (top) and loricrin (bottom) staining of fully differentiated 3D skin equivalents untreated or treated with 0.3 μg/mL hIL-36γ with or without the presence of 10 μg/mL of function blocking hIL-36Ra. Representative images at 32X magnification are shown. ( D ) Differences between RNA transcripts in treated and non-treated 3D skin equivalents were quantified for each probe using qRT-PCR. Average of 6 treated and 7 control is shown ± S.E.M. (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 using ANOVA with Dunnett’s post hoc test vs. hIL-36γ alone; (F; DF) = 38.58; 18 (S100A7), 114.3; 18 (DEFB4), 129.5; 18 (Elafin), 8.934; 18 (K16), 31.49; 18 (Involucrin), 10.96; 18 (K10)). ( E ) Differences between secreted CXCL1, IL-8 and IL-6 proteins in treated and non-treated 3D skin equivalents were quantified using immunoassays. Average of 6 treated (5 in CXCL1 and IL-8 NT column) and 7 control samples is shown ± S.E.M. (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 using ANOVA with Dunnett’s post hoc test vs. hIL-36γ alone; (F, DF) = 70.64; 17 (CXCL1), 72.23; 17 (IL-8), 49.54; 18 (IL-6)).
Article Snippet: The affinity resin was prepared using
Techniques: In Situ Hybridization, Isolation, Two Tailed Test, Staining, Blocking Assay, Quantitative RT-PCR
Journal: Scientific Reports
Article Title: Small Molecule IL-36γ Antagonist as a Novel Therapeutic Approach for Plaque Psoriasis
doi: 10.1038/s41598-019-45626-w
Figure Lengend Snippet: Effects of A-552 on hIL-36γ-induced CXCL1 release in mice. ( A ) hIL-36γ induced CXCL1 release in a dose dependent manner (mIL-36α was used as a positive control). ( B ) hIL-36γ-induced CXCL1 release was completely blocked by anti-mouse IL-36R antibody. ( C ) hIL-36γ-induced CXCL1 release was inhibited by A-552 in a dose-dependent manner. ( D ) A-553 had little effect on CXCL1 release induced by hIL-36γ. Average of 6 mice per group is shown ± S.E.M. (****p < 0.0001 using ANOVA with Dunnett’s post hoc test vs. Veh + hIL-36γ; (F; DF) = 46732; 17 ( B ), 78.41; 28 ( C ), 22.77; 34 ( D )).
Article Snippet: The affinity resin was prepared using
Techniques: Positive Control