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recombinant human c3a c5a (Complement Technology Inc)

Name: recombinant human c3a c5a
Brand: Complement Technology Inc
Rating: 90 (1 reviews)

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Complement Technology Inc recombinant human c3a c5a
RNA interference suppresses local complement activation. BALF collected from Figure 1 were analyzed for C3a (A) and <t>C5a</t> (B) levels in the lung by ELISA. Values: Means ± SEM. (n=5-7 per group). One-way ANOVA, Newman-Keuls (A, B). Compared to bleomycin: ***: p<0.001; **: p<0.01; *: p<0.05. Results are representative of three independent experiments.

RNA interference suppresses local complement activation. BALF collected from Figure 1 were analyzed for C3a (A) and <t>C5a</t> (B) levels in the lung by ELISA. Values: Means ± SEM. (n=5-7 per group). One-way ANOVA, Newman-Keuls (A, B). Compared to bleomycin: ***: p<0.001; **: p<0.01; *: p<0.05. Results are representative of three independent experiments.

Recombinant Human C3a C5a, supplied by Complement Technology Inc, 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/recombinant human c3a c5a/product/Complement Technology Inc
Average 90 stars, based on 1 article reviews

recombinant human c3a c5a - by Bioz Stars, 2026-03

90/100 stars

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1) Product Images from "Potential Mechanisms Underlying TGF-β-mediated Complement Activation in Lung Fibrosis"

Article Title: Potential Mechanisms Underlying TGF-β-mediated Complement Activation in Lung Fibrosis

Journal: Cellular & molecular medicine: open access

doi:

RNA interference suppresses local complement activation. BALF collected from Figure 1 were analyzed for C3a (A) and C5a (B) levels in the lung by ELISA. Values: Means ± SEM. (n=5-7 per group). One-way ANOVA, Newman-Keuls (A, B). Compared to bleomycin: ***: p<0.001; **: p<0.01; *: p<0.05. Results are representative of three independent experiments.

Figure Legend Snippet: RNA interference suppresses local complement activation. BALF collected from Figure 1 were analyzed for C3a (A) and C5a (B) levels in the lung by ELISA. Values: Means ± SEM. (n=5-7 per group). One-way ANOVA, Newman-Keuls (A, B). Compared to bleomycin: ***: p<0.001; **: p<0.01; *: p<0.05. Results are representative of three independent experiments.

Techniques Used: Activation Assay, Enzyme-linked Immunosorbent Assay

Figure Legend Snippet: miRNA regulation in response to TGF-β, C3a and C5a for 24 h in normal primary human SAECs.

Techniques Used:

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Representative images from immunofluorescent double staining of factor H-related protein 3 (FHR-3 in red) and complement activation (C3d in green) in tissues obtained from (A) living donor kidneys (n=8), (B) acute tubular necrosis (ATN) (n=6), (C) Banff IA (n=6), (D) Banff IB (n=6), (E) Banff IIA (n=6), (F) Banff IIB (n=6), and (G) chronic rejection (CR) (n=6). Nuclei were counterstained with DAPI.

Journal: medRxiv

Article Title: Factor H-related protein 3 (FHR-3) deposition in kidney allografts – localization and correlation with complement activation

doi: 10.1101/2023.10.24.23297478

Figure Lengend Snippet: Representative images from immunofluorescent double staining of factor H-related protein 3 (FHR-3 in red) and complement activation (C3d in green) in tissues obtained from (A) living donor kidneys (n=8), (B) acute tubular necrosis (ATN) (n=6), (C) Banff IA (n=6), (D) Banff IB (n=6), (E) Banff IIA (n=6), (F) Banff IIB (n=6), and (G) chronic rejection (CR) (n=6). Nuclei were counterstained with DAPI.

Article Snippet: In the experiments, we used recombinant human C3a (Hycult Biotech), recombinant human C5a (Hycult Biotech), and a combination of the two to stimulate the podocytes.

Techniques: Double Staining, Activation Assay

Different staining patterns of factor H-related protein 3 (FHR-3 in red) and complement activation (C3d in green) in transplanted kidneys. Nuclei were counterstained with DAPI. Representative images of (A) tubular FHR-3 staining (arrows) in acute tubular necrosis (ATN), (B) vascular FHR-3 staining (arrows) in T-cell-mediated rejection with severe tubulitis (Banff IB), and (C) low-intensity FHR-3 staining in Bowman’s capsule (arrows) and tubules (arrows) in chronic rejection (CR). Exemplary images of double staining for FHR-3 (red) and C3d (green) in transplanted kidneys revealing (C) predominant positive glomerular staining for FHR-3, (D) glomerular co-localization of FHR-3 and C3d, and (E) predominant positive glomerular staining for C3d.

Journal: medRxiv

Article Title: Factor H-related protein 3 (FHR-3) deposition in kidney allografts – localization and correlation with complement activation

doi: 10.1101/2023.10.24.23297478

Figure Lengend Snippet: Different staining patterns of factor H-related protein 3 (FHR-3 in red) and complement activation (C3d in green) in transplanted kidneys. Nuclei were counterstained with DAPI. Representative images of (A) tubular FHR-3 staining (arrows) in acute tubular necrosis (ATN), (B) vascular FHR-3 staining (arrows) in T-cell-mediated rejection with severe tubulitis (Banff IB), and (C) low-intensity FHR-3 staining in Bowman’s capsule (arrows) and tubules (arrows) in chronic rejection (CR). Exemplary images of double staining for FHR-3 (red) and C3d (green) in transplanted kidneys revealing (C) predominant positive glomerular staining for FHR-3, (D) glomerular co-localization of FHR-3 and C3d, and (E) predominant positive glomerular staining for C3d.

Article Snippet: In the experiments, we used recombinant human C3a (Hycult Biotech), recombinant human C5a (Hycult Biotech), and a combination of the two to stimulate the podocytes.

Techniques: Staining, Activation Assay, Double Staining

(A) Quantification of staining intensity of factor H-related protein 3 (FHR-3) and complement activation (C3d) by double immunofluorescent in living donor kidneys, acute tubular necrosis (ATN), Banff IA, Banff IB, Banff IIA, Banff IIB, and chronic rejection (CR). Each biopsy was scored by two independent observers in a blinded fashion. (B) The correlation between the staining intensity of FHR-3 and C3d using the Spearman Rank correlation coefficient (r represents the spearman’s rho). The dashed blue lines show the 95% confidence interval for the regression line (blue).

Journal: medRxiv

Article Title: Factor H-related protein 3 (FHR-3) deposition in kidney allografts – localization and correlation with complement activation

doi: 10.1101/2023.10.24.23297478

Figure Lengend Snippet: (A) Quantification of staining intensity of factor H-related protein 3 (FHR-3) and complement activation (C3d) by double immunofluorescent in living donor kidneys, acute tubular necrosis (ATN), Banff IA, Banff IB, Banff IIA, Banff IIB, and chronic rejection (CR). Each biopsy was scored by two independent observers in a blinded fashion. (B) The correlation between the staining intensity of FHR-3 and C3d using the Spearman Rank correlation coefficient (r represents the spearman’s rho). The dashed blue lines show the 95% confidence interval for the regression line (blue).

Article Snippet: In the experiments, we used recombinant human C3a (Hycult Biotech), recombinant human C5a (Hycult Biotech), and a combination of the two to stimulate the podocytes.

Techniques: Staining, Activation Assay

FIGURE 5. C3a-induced IL-6 release in human gingival epithelial cells. (A) Human immortalized gingival keratinocytes (HIGKs) were stimulated, or not, with heat-killed P. gingivalis (MOI of 10:1), C3a, or C5a and combinations thereof (at the indicated concentrations). Culture media were collected after a 24-h incubation and assayed for IL-6 by ELISA. (B) HIGKs were stimulated for 24 h with heat-killed P. gingivalis (MOI of 10:1) or Pam3Cys lipopeptide (1 mg/ml) and C3aR expression was measured by FACS. Representative histogram (left) and bar graphs for mean fluorescence intensity (MFI) of C3aR expression (right). (C) HIGKs were stimulated, or not, with C3a (500 ng/ml), Pam3Cys (1 mg/ml), or both, and IL-6 was measured in collected culture supernatants after a 24-h incubation. (D) HIGKs were stimulated for 24 h, or not, with P. gingivalis (MOI of 10:1) alone or with C3a (500 ng/ml), in the presence or absence of 10 mg/ml anti-TLR2 neutralizing Ab or isotype control (IC), which were added 2 h prior to stimulation. IL-6 release was assayed by ELISA. (E) HIGKs were pretreated with PD98059 (10 mM; MEK/ERK inhibitor), SP600125 (50mM; JNK inhibitor), SB202190 (20mM; p38 MAPK inhibitor), or SN50 (50mM, NF-kB inhibi- tor). After 1 h, Pam3Cys (1 mg/ml) was added in the cultures and C3aR expression (MFI) was determined by FACS after a 24-h incubation. (F) HIGKs were stimulated with Pam3Cys (1 mg/ml) for the indicated time lengths. Total protein was extracted and immunoblot analysis was performed with specific Abs against phosphorylated and total ERK1/2, JNK, and p38 MAPK as well as against GAPDH (loading control). (G) HIGKs were pretreated with Pam3Cys (1 mg/ml) for 4 h and then exposed to PD98059 (10 mM; MEK/ERK inhibitor), SP600125 (50mM; JNK inhibitor), SB202190 (20mM; p38 MAPK inhibitor), or SN50 (50mM, NF-kB inhibitor). After 1 h, C3a (500 ng/ml) was added in the cultures. Culture media were collected after 24 h and assayed for IL-6 by ELISA. Data are means ± SD (n 5 6 cultures per group). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 (A, D, E, and G, one-way ANOVA and a Tukey’s test; B and C, Dunnett’s multiple comparison tests).

Journal: Journal of immunology (Baltimore, Md. : 1950)

Article Title: Complement Is Required for Microbe-Driven Induction of Th17 and Periodontitis.

doi: 10.4049/jimmunol.2200338

Figure Lengend Snippet: FIGURE 5. C3a-induced IL-6 release in human gingival epithelial cells. (A) Human immortalized gingival keratinocytes (HIGKs) were stimulated, or not, with heat-killed P. gingivalis (MOI of 10:1), C3a, or C5a and combinations thereof (at the indicated concentrations). Culture media were collected after a 24-h incubation and assayed for IL-6 by ELISA. (B) HIGKs were stimulated for 24 h with heat-killed P. gingivalis (MOI of 10:1) or Pam3Cys lipopeptide (1 mg/ml) and C3aR expression was measured by FACS. Representative histogram (left) and bar graphs for mean fluorescence intensity (MFI) of C3aR expression (right). (C) HIGKs were stimulated, or not, with C3a (500 ng/ml), Pam3Cys (1 mg/ml), or both, and IL-6 was measured in collected culture supernatants after a 24-h incubation. (D) HIGKs were stimulated for 24 h, or not, with P. gingivalis (MOI of 10:1) alone or with C3a (500 ng/ml), in the presence or absence of 10 mg/ml anti-TLR2 neutralizing Ab or isotype control (IC), which were added 2 h prior to stimulation. IL-6 release was assayed by ELISA. (E) HIGKs were pretreated with PD98059 (10 mM; MEK/ERK inhibitor), SP600125 (50mM; JNK inhibitor), SB202190 (20mM; p38 MAPK inhibitor), or SN50 (50mM, NF-kB inhibi- tor). After 1 h, Pam3Cys (1 mg/ml) was added in the cultures and C3aR expression (MFI) was determined by FACS after a 24-h incubation. (F) HIGKs were stimulated with Pam3Cys (1 mg/ml) for the indicated time lengths. Total protein was extracted and immunoblot analysis was performed with specific Abs against phosphorylated and total ERK1/2, JNK, and p38 MAPK as well as against GAPDH (loading control). (G) HIGKs were pretreated with Pam3Cys (1 mg/ml) for 4 h and then exposed to PD98059 (10 mM; MEK/ERK inhibitor), SP600125 (50mM; JNK inhibitor), SB202190 (20mM; p38 MAPK inhibitor), or SN50 (50mM, NF-kB inhibitor). After 1 h, C3a (500 ng/ml) was added in the cultures. Culture media were collected after 24 h and assayed for IL-6 by ELISA. Data are means ± SD (n 5 6 cultures per group). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 (A, D, E, and G, one-way ANOVA and a Tukey’s test; B and C, Dunnett’s multiple comparison tests).

Article Snippet: The cells were seeded into 96-well plates at a density of 2 × 105 cells per well for 18 h and then challenged with heat-killed (65◦C, 1 h) P. gingivalis at a multiplicity of infection (MOI) of 10:1, in the presence or absence of different concentrations of recombinant human C3a or C5a (catalog no. 3677-C3-025 or 2037- C5-025/CF, R&D Systems) or the synthetic microbial lipopeptide Pam3Cys (catalog no. tlrl-pms, InvivoGen, San Diego, CA).

Techniques: Incubation, Enzyme-linked Immunosorbent Assay, Expressing, Fluorescence, Control, Western Blot, Comparison

Journal: Cellular & molecular medicine: open access

Article Title: Potential Mechanisms Underlying TGF-β-mediated Complement Activation in Lung Fibrosis

doi:

Figure Lengend Snippet: RNA interference suppresses local complement activation. BALF collected from Figure 1 were analyzed for C3a (A) and C5a (B) levels in the lung by ELISA. Values: Means ± SEM. (n=5-7 per group). One-way ANOVA, Newman-Keuls (A, B). Compared to bleomycin: ***: p<0.001; **: p<0.01; *: p<0.05. Results are representative of three independent experiments.

Article Snippet: These studies used recombinant human C3a and C5a (100 nM; Complement Technology, Inc., Tyler, TX), platelet-derived TGF-β1 (2 ng/ml; Roche Diagnostics, Germany).

Techniques: Activation Assay, Enzyme-linked Immunosorbent Assay

Journal: Cellular & molecular medicine: open access

Article Title: Potential Mechanisms Underlying TGF-β-mediated Complement Activation in Lung Fibrosis

doi:

Figure Lengend Snippet: miRNA regulation in response to TGF-β, C3a and C5a for 24 h in normal primary human SAECs.

Article Snippet: These studies used recombinant human C3a and C5a (100 nM; Complement Technology, Inc., Tyler, TX), platelet-derived TGF-β1 (2 ng/ml; Roche Diagnostics, Germany).

Techniques:

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1) Product Images from "Potential Mechanisms Underlying TGF-β-mediated Complement Activation in Lung Fibrosis"

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