recombinant mouse scd163 (R&D Systems)
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Recombinant Mouse Scd163, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/recombinant+mouse+scd163/Recombinant+Mouse+CD163+Protein%2C+CF/pm26242746-407-0-4
Average 92 stars, based on 4 article reviews
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1) Product Images from "CD163 interacts with TWEAK to regulate tissue regeneration after ischaemic injury."
Article Title: CD163 interacts with TWEAK to regulate tissue regeneration after ischaemic injury.
Journal: Nature communications
doi: 10.1038/ncomms8792
Figure Legend Snippet: Figure 4 | TWEAK activates canonical NF-jB signalling and Notch activation and mediates the response of CD163 / mice to HLI. (a) Analysis of plasma from WT and CD163 / mice before and after femoral ligation for TWEAK and sCD163 levels by ELISA (n ¼ 5 per group). (b) Laser doppler analysis of CD163 / mice 3, 7, 14, 21 and 28 days after femoral ligation administered an isotype control or TWEAK blocking antibody (n ¼ 5 per group). (c) Immunoblotting of CD163 / IL at 14 days after femoral ligation with administration of isotype control or TWEAK blocking antibody (n ¼ 5 per group) with graphs showing quantitation of densitometry for phosphorylated/total p65 and NICD below. (d) Immunostaining for VE-cadherin (green) and b- dystroglycan (red) in CD163 / limbs with 14 day administration of TWEAK (5 or 25 mg kg 1 day 1) or saline (control) (n ¼ 5 per group). Scale bars, 100 mm. The graphs show the number of VE-cadherin positive cells/myofibre and the average muscle fibre area. (e) Immunoblotting of CD163 / limbs with 14 day administration of TWEAK (5 or 25 mg kg 1 day 1) or saline (control) (n ¼ 5 per group) with graphs showing quantitation of densitometry for phosphorylated p65/total p65, p52 and NICD. All bars show mean±s.e.m. *Po0.05 versus WT in a; versus CD163 / control in b,c and e. Po0.05 versus other groups in d,e. Comparisons between groups were achieved using a two-sided student’s t-test. For multiple group comparisons, we utilized a one-way ANOVA. If the variance ratio test (F-test) was significant, a more detailed post hoc analysis of differences between groups was made using a Tukey–Kramer honest significance difference test.
Techniques Used: Activation Assay, Clinical Proteomics, Ligation, Enzyme-linked Immunosorbent Assay, Control, Blocking Assay, Western Blot, Quantitation Assay, Immunostaining, Saline
Figure Legend Snippet: Figure 6 | sCD163 inhibits the effect of TWEAK on tissue regeneration. (a) TWEAK (100 ng ml 1) was added to VEGFR1, Fn14 or CD163-coated wells. Bound protein was measured by ELISA using an antibody to detect TWEAK. (b) Fn14 or CD163 were coated onto 96-well plates and incubated with increasing doses of untagged TWEAK. Bound protein was measured by ELISA. (c) Immunoblotting of MDEC stimulated with TWEAK at 200 ng ml 1
Techniques Used: Enzyme-linked Immunosorbent Assay, Incubation, Western Blot
Figure Legend Snippet: Figure 7 | CD163-TWEAK interaction controls skeletal muscle recovery after ischaemic injury. After ischaemic injury, macrophages secrete TWEAK which induces tissue canonical NF-KB/Notch mediated myogenic progenitor cell proliferation. TWEAK’s biological activity is tightly regulated by sCD163 binding which limits serum TWEAK levels and leads to resolution of canonical NF-kB/Notch activation at the site of injury, allowing for cell differentiation. In the absence of sCD163 (as seen in CD163-deficient mice), TWEAK levels are systemically elevated and TWEAK’s biological effect is unopposed leading to prolonged activation of NF-kB and Notch signalling which causes greater myogenic progenitor cell proliferation-induced myogenesis not limited to the site of injury.
Techniques Used: Activity Assay, Binding Assay, Activation Assay, Cell Differentiation
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