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rabbit complement ma  (Cedarlane)


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    Cedarlane rabbit complement ma
    Rabbit Complement Ma, supplied by Cedarlane, used in various techniques. Bioz Stars score: 94/100, based on 101 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+complement/Rabbit+Complement+MA%2C+Lyophilized/us12590164-356-4-7
    Average 94 stars, based on 101 article reviews
    rabbit complement ma - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

    Control:

    Article Title: The Anti‐Human P2X7 Monoclonal Antibody (Clone L4) Can Mediate Complement‐Dependent Cytotoxicity of Human Leukocytes
    Article Snippet: Cells were washed twice with RPMI‐1640 medium containing 2 mM GlutaMAX and 0.1% bovine serum albumin (BSA; Amresco, Solon, USA; RPMI‐BSA). .. Then, 50 μL RPMI‐BSA, 50 μL of PBS, anti‐P2X7 or isotype control mAb (2 μg/mL), and 50 μL of rabbit complement (at a final dilution of 1:4) (Cedarlane Laboratories, Burlington, Canada) were added per well in triplicate. .. To determine maximal LDH release, 135 μL RPMI‐BSA and 15 μL 10x Lysis Solution (Promega, Madison, USA) were added to wells in triplicate (maximum release wells).

    Article Title: The Anti-Human P2X7 Monoclonal Antibody (Clone L4) Can Mediate Complement-Dependent Cytotoxicity of Human Leukocytes.
    Article Snippet: Cells were washed twice with RPMI-1640 medium containing 2 mM GlutaMAX and 0.1% bovine serum albumin (BSA; Amresco, Solon, USA; RPMI-BSA). .. Then, 50 μL RPMI-BSA, 50 μL of PBS, anti-P2X7 or isotype control mAb (2 μg/mL), and 50 μL of rabbit complement (at a final dilution of 1:4) (Cedarlane Laboratories, Burlington, Canada) were added 9 of 12 nloaded from https://onlinelibrary.w iley.com /doi/10.1002/eji.202451196 by IN A SP - N E PA L , W iley O nline L ibrary on [26/01/2025]. ..

    Isolation:

    Article Title: Impact of COVID-19 Vaccination and Infection on Anti-Triple-Knockout (TKO) Pig Antibody Production: A Study in Patients With End-Stage Liver Disease and Liver Transplant Recipients.
    Article Snippet: This study investigates the impact of COVID-19 vaccination, with a focus on inactivated vaccines, on the production of anti-tripleknockout (TKO) pig antibodies, crucial for xenotransplantation.Although it is known that vaccination influences anti-pig antibody production, the specific effects of COVID-19 vaccines, particularly inactivated forms, remain underexplored.. We analyzed serum samples from healthy individuals, patients with end-stage liver disease (ESLD), and liver transplant (LT) recipients to assess antibody binding to TKO pig cells.. Our findings reveal a significant difference in anti-TKO pig antibody levels among healthy controls, ESLD patients, and LT recipients.

    FACS:

    Article Title: Impact of COVID-19 Vaccination and Infection on Anti-Triple-Knockout (TKO) Pig Antibody Production: A Study in Patients With End-Stage Liver Disease and Liver Transplant Recipients.
    Article Snippet: This study investigates the impact of COVID-19 vaccination, with a focus on inactivated vaccines, on the production of anti-tripleknockout (TKO) pig antibodies, crucial for xenotransplantation.Although it is known that vaccination influences anti-pig antibody production, the specific effects of COVID-19 vaccines, particularly inactivated forms, remain underexplored.. We analyzed serum samples from healthy individuals, patients with end-stage liver disease (ESLD), and liver transplant (LT) recipients to assess antibody binding to TKO pig cells.. Our findings reveal a significant difference in anti-TKO pig antibody levels among healthy controls, ESLD patients, and LT recipients.

    Article Title: Evaluation of Complement-Dependent Cytotoxicity Assays for Gene-Edited Pig-to-Human Xenotransplantation.
    Article Snippet: Background: Gene-edited pigs for xenotransplantation usually contain one or more transgenes encoding human complement regulatory proteins (CRPs).. Because of species differences, human CRP(s) expressed in gene-edited pigs may have difficulty inhibiting the activation of exogenous rabbit complement added to a complement-dependent cytotoxicity (CDC) assay.. The use of human complement instead of rabbit complement in CDC experiments may more accurately reflect the actual regulatory activity

    Incubation:

    Article Title: Impact of COVID-19 Vaccination and Infection on Anti-Triple-Knockout (TKO) Pig Antibody Production: A Study in Patients With End-Stage Liver Disease and Liver Transplant Recipients.
    Article Snippet: This study investigates the impact of COVID-19 vaccination, with a focus on inactivated vaccines, on the production of anti-tripleknockout (TKO) pig antibodies, crucial for xenotransplantation.Although it is known that vaccination influences anti-pig antibody production, the specific effects of COVID-19 vaccines, particularly inactivated forms, remain underexplored.. We analyzed serum samples from healthy individuals, patients with end-stage liver disease (ESLD), and liver transplant (LT) recipients to assess antibody binding to TKO pig cells.. Our findings reveal a significant difference in anti-TKO pig antibody levels among healthy controls, ESLD patients, and LT recipients.

    Article Title: Productivity-enhanced antibody and method for producing same
    Article Snippet: .. To this was added rabbit complement MA (Cedarlane, Cat #CL3221) at a ratio of 1:4, and incubation was performed in a CO2 incubator at 37° C. for 2 hours. .. Subsequently, for the cells, the FACSVerse (BD Biosciences) machine was used to count a total of 10,000 cells, and analysis was performed with the FlowJo software (FIG. 15).

    Article Title: Evaluation of Complement-Dependent Cytotoxicity Assays for Gene-Edited Pig-to-Human Xenotransplantation.
    Article Snippet: Background: Gene-edited pigs for xenotransplantation usually contain one or more transgenes encoding human complement regulatory proteins (CRPs).. Because of species differences, human CRP(s) expressed in gene-edited pigs may have difficulty inhibiting the activation of exogenous rabbit complement added to a complement-dependent cytotoxicity (CDC) assay.. The use of human complement instead of rabbit complement in CDC experiments may more accurately reflect the actual regulatory activity

    Concentration Assay:

    Article Title: Impact of COVID-19 Vaccination and Infection on Anti-Triple-Knockout (TKO) Pig Antibody Production: A Study in Patients With End-Stage Liver Disease and Liver Transplant Recipients.
    Article Snippet: This study investigates the impact of COVID-19 vaccination, with a focus on inactivated vaccines, on the production of anti-tripleknockout (TKO) pig antibodies, crucial for xenotransplantation.Although it is known that vaccination influences anti-pig antibody production, the specific effects of COVID-19 vaccines, particularly inactivated forms, remain underexplored.. We analyzed serum samples from healthy individuals, patients with end-stage liver disease (ESLD), and liver transplant (LT) recipients to assess antibody binding to TKO pig cells.. Our findings reveal a significant difference in anti-TKO pig antibody levels among healthy controls, ESLD patients, and LT recipients.

    Single Cell:

    Article Title: Heterochromatic gene silencing controls CD4 + T cell susceptibility to regulatory T cell-mediated suppression in a murine allograft model
    Article Snippet: Bone marrow was isolated from C57BL/6 J (H2 b ) and B6D2F1 (H2 bd ) mice by centrifugation. .. The single-cell suspensions were then depleted from NK and T cells by complement-mediated lysis using rabbit complement (7,5%, Cedarlane) and antibody specific for Thy1.2 (AT83, hybridoma supernatant) and for the glycolipid asialo ganglioside-GM1 (Fujifilm Wako Chemicals). ..

    Lysis:

    Article Title: Heterochromatic gene silencing controls CD4 + T cell susceptibility to regulatory T cell-mediated suppression in a murine allograft model
    Article Snippet: Bone marrow was isolated from C57BL/6 J (H2 b ) and B6D2F1 (H2 bd ) mice by centrifugation. .. The single-cell suspensions were then depleted from NK and T cells by complement-mediated lysis using rabbit complement (7,5%, Cedarlane) and antibody specific for Thy1.2 (AT83, hybridoma supernatant) and for the glycolipid asialo ganglioside-GM1 (Fujifilm Wako Chemicals). ..



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    (A) Biofilm formation ability of commensal vs. inflammatory S. epidermidis strains. Biofilm positive strains were defined relative to a canonical biofilm-forming strain (Sep_1457). Numbers indicate strain counts per category and P-value and odds ratio calculated using Fisher’s exact test. (B-E) Survival ability in blood as measured by CFUs at 0, 2, and 24h of S. epidermidis strains (D) with respect to a bloodstream infection S. aureus strain (USA300LAC, (B)) with or without <t>complement</t> (+/-Comp) depletion (C, E). Points represent individual strains (or replicates for S. aureus) and boxes indicate IQR with median. Lines connect matched conditions. Significance was assessed by paired t-test with Bonferroni correction. (F-G) PCA plot of Staphylococcus cellular (F) or extracellular (G) metabolomes. Staphylococcus metabolomes were inferred by metabolic feature intensity within untargeted metabolomes. (H) Diagram of arginine metabolism pathway highlighting reactions catalyzed by arcA , argF , and argG . (I-K) Violin plots showing the metabolite abundance of arginine (I), carbamoyl-P (J), and argininosuccinate (K) in strains with or without arcA , argF , or argG. Points indicate normalized metabolite intensity; violins show distributions with embedded boxplots (median and IQR). Gene labels are black if acting on or downstream of the metabolite, grey otherwise. (L-N) Growth dynamics of inflammatory vs. commensal S. epidermidis strains in skin-like media with (+Arg) or without (-Arg) arginine. Maximum growth rate (L), maximum density (M), and area under the curve (AUC) (N) are derived from OD600 measurements every 0.5h over 10 hours at 37C. Points represent strains with paired conditions connected with lines. Statistical significance was determined by paired t -test followed by Bonferroni correction. (O-Q) Protein expression of cytokines IL-8 (O), CCL20 (P) and IL-36γ (Q) in the basal media of Staphylococcus -colonized RHE was measured by ELISA (n=3-4 replicates per strain in an independent experiment colonizing 3 inflammatory and 4 commensal S. epidermidis strains and S. aureus as a reference). Points represent individual replicates colored by cluster and boxes show IQR with median. (R) Model summarizing species- and strain-level effects of Staphylococcus on RHE. Species-level differences distinguish commensal and pathogenic effects, while strain-level variation within S. epidermidis identifies inflammatory strains that activate a proinflammatory transcriptional program including upstream regulators (e.g. NFKB), chemokines (e.g., CCL20), cytokines (e.g., IL36γ) and downstream antimicrobial effectors (e.g. LCN2). Inflammatory S. epidermidis also enhances skin barrier defensive genes, particularly members of the LCE and SPRR gene families, which contribute to both barrier integrity and antimicrobial defense, and are regulated by transcription factors such as MAFB. These effects are linked to differences in gene content (e.g., cell surface genes), transcriptional programs, metabolism (e.g., arginine pathway), and pathogen-like growth phenotypes. P-values: **** p ≤ 0.0001, *** 0.0001 < p ≤ 0.001, ** 0.001 < p ≤ 0.01, * 0.01 < p ≤ 0.05., ns p > 0.05.
    Rabbit Red Blood Cells With Complement, supplied by Innovative Research Inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    (A) Biofilm formation ability of commensal vs. inflammatory S. epidermidis strains. Biofilm positive strains were defined relative to a canonical biofilm-forming strain (Sep_1457). Numbers indicate strain counts per category and P-value and odds ratio calculated using Fisher’s exact test. (B-E) Survival ability in blood as measured by CFUs at 0, 2, and 24h of S. epidermidis strains (D) with respect to a bloodstream infection S. aureus strain (USA300LAC, (B)) with or without <t>complement</t> (+/-Comp) depletion (C, E). Points represent individual strains (or replicates for S. aureus) and boxes indicate IQR with median. Lines connect matched conditions. Significance was assessed by paired t-test with Bonferroni correction. (F-G) PCA plot of Staphylococcus cellular (F) or extracellular (G) metabolomes. Staphylococcus metabolomes were inferred by metabolic feature intensity within untargeted metabolomes. (H) Diagram of arginine metabolism pathway highlighting reactions catalyzed by arcA , argF , and argG . (I-K) Violin plots showing the metabolite abundance of arginine (I), carbamoyl-P (J), and argininosuccinate (K) in strains with or without arcA , argF , or argG. Points indicate normalized metabolite intensity; violins show distributions with embedded boxplots (median and IQR). Gene labels are black if acting on or downstream of the metabolite, grey otherwise. (L-N) Growth dynamics of inflammatory vs. commensal S. epidermidis strains in skin-like media with (+Arg) or without (-Arg) arginine. Maximum growth rate (L), maximum density (M), and area under the curve (AUC) (N) are derived from OD600 measurements every 0.5h over 10 hours at 37C. Points represent strains with paired conditions connected with lines. Statistical significance was determined by paired t -test followed by Bonferroni correction. (O-Q) Protein expression of cytokines IL-8 (O), CCL20 (P) and IL-36γ (Q) in the basal media of Staphylococcus -colonized RHE was measured by ELISA (n=3-4 replicates per strain in an independent experiment colonizing 3 inflammatory and 4 commensal S. epidermidis strains and S. aureus as a reference). Points represent individual replicates colored by cluster and boxes show IQR with median. (R) Model summarizing species- and strain-level effects of Staphylococcus on RHE. Species-level differences distinguish commensal and pathogenic effects, while strain-level variation within S. epidermidis identifies inflammatory strains that activate a proinflammatory transcriptional program including upstream regulators (e.g. NFKB), chemokines (e.g., CCL20), cytokines (e.g., IL36γ) and downstream antimicrobial effectors (e.g. LCN2). Inflammatory S. epidermidis also enhances skin barrier defensive genes, particularly members of the LCE and SPRR gene families, which contribute to both barrier integrity and antimicrobial defense, and are regulated by transcription factors such as MAFB. These effects are linked to differences in gene content (e.g., cell surface genes), transcriptional programs, metabolism (e.g., arginine pathway), and pathogen-like growth phenotypes. P-values: **** p ≤ 0.0001, *** 0.0001 < p ≤ 0.001, ** 0.001 < p ≤ 0.01, * 0.01 < p ≤ 0.05., ns p > 0.05.
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    (A) Biofilm formation ability of commensal vs. inflammatory S. epidermidis strains. Biofilm positive strains were defined relative to a canonical biofilm-forming strain (Sep_1457). Numbers indicate strain counts per category and P-value and odds ratio calculated using Fisher’s exact test. (B-E) Survival ability in blood as measured by CFUs at 0, 2, and 24h of S. epidermidis strains (D) with respect to a bloodstream infection S. aureus strain (USA300LAC, (B)) with or without <t>complement</t> (+/-Comp) depletion (C, E). Points represent individual strains (or replicates for S. aureus) and boxes indicate IQR with median. Lines connect matched conditions. Significance was assessed by paired t-test with Bonferroni correction. (F-G) PCA plot of Staphylococcus cellular (F) or extracellular (G) metabolomes. Staphylococcus metabolomes were inferred by metabolic feature intensity within untargeted metabolomes. (H) Diagram of arginine metabolism pathway highlighting reactions catalyzed by arcA , argF , and argG . (I-K) Violin plots showing the metabolite abundance of arginine (I), carbamoyl-P (J), and argininosuccinate (K) in strains with or without arcA , argF , or argG. Points indicate normalized metabolite intensity; violins show distributions with embedded boxplots (median and IQR). Gene labels are black if acting on or downstream of the metabolite, grey otherwise. (L-N) Growth dynamics of inflammatory vs. commensal S. epidermidis strains in skin-like media with (+Arg) or without (-Arg) arginine. Maximum growth rate (L), maximum density (M), and area under the curve (AUC) (N) are derived from OD600 measurements every 0.5h over 10 hours at 37C. Points represent strains with paired conditions connected with lines. Statistical significance was determined by paired t -test followed by Bonferroni correction. (O-Q) Protein expression of cytokines IL-8 (O), CCL20 (P) and IL-36γ (Q) in the basal media of Staphylococcus -colonized RHE was measured by ELISA (n=3-4 replicates per strain in an independent experiment colonizing 3 inflammatory and 4 commensal S. epidermidis strains and S. aureus as a reference). Points represent individual replicates colored by cluster and boxes show IQR with median. (R) Model summarizing species- and strain-level effects of Staphylococcus on RHE. Species-level differences distinguish commensal and pathogenic effects, while strain-level variation within S. epidermidis identifies inflammatory strains that activate a proinflammatory transcriptional program including upstream regulators (e.g. NFKB), chemokines (e.g., CCL20), cytokines (e.g., IL36γ) and downstream antimicrobial effectors (e.g. LCN2). Inflammatory S. epidermidis also enhances skin barrier defensive genes, particularly members of the LCE and SPRR gene families, which contribute to both barrier integrity and antimicrobial defense, and are regulated by transcription factors such as MAFB. These effects are linked to differences in gene content (e.g., cell surface genes), transcriptional programs, metabolism (e.g., arginine pathway), and pathogen-like growth phenotypes. P-values: **** p ≤ 0.0001, *** 0.0001 < p ≤ 0.001, ** 0.001 < p ≤ 0.01, * 0.01 < p ≤ 0.05., ns p > 0.05.
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    (A) Biofilm formation ability of commensal vs. inflammatory S. epidermidis strains. Biofilm positive strains were defined relative to a canonical biofilm-forming strain (Sep_1457). Numbers indicate strain counts per category and P-value and odds ratio calculated using Fisher’s exact test. (B-E) Survival ability in blood as measured by CFUs at 0, 2, and 24h of S. epidermidis strains (D) with respect to a bloodstream infection S. aureus strain (USA300LAC, (B)) with or without complement (+/-Comp) depletion (C, E). Points represent individual strains (or replicates for S. aureus) and boxes indicate IQR with median. Lines connect matched conditions. Significance was assessed by paired t-test with Bonferroni correction. (F-G) PCA plot of Staphylococcus cellular (F) or extracellular (G) metabolomes. Staphylococcus metabolomes were inferred by metabolic feature intensity within untargeted metabolomes. (H) Diagram of arginine metabolism pathway highlighting reactions catalyzed by arcA , argF , and argG . (I-K) Violin plots showing the metabolite abundance of arginine (I), carbamoyl-P (J), and argininosuccinate (K) in strains with or without arcA , argF , or argG. Points indicate normalized metabolite intensity; violins show distributions with embedded boxplots (median and IQR). Gene labels are black if acting on or downstream of the metabolite, grey otherwise. (L-N) Growth dynamics of inflammatory vs. commensal S. epidermidis strains in skin-like media with (+Arg) or without (-Arg) arginine. Maximum growth rate (L), maximum density (M), and area under the curve (AUC) (N) are derived from OD600 measurements every 0.5h over 10 hours at 37C. Points represent strains with paired conditions connected with lines. Statistical significance was determined by paired t -test followed by Bonferroni correction. (O-Q) Protein expression of cytokines IL-8 (O), CCL20 (P) and IL-36γ (Q) in the basal media of Staphylococcus -colonized RHE was measured by ELISA (n=3-4 replicates per strain in an independent experiment colonizing 3 inflammatory and 4 commensal S. epidermidis strains and S. aureus as a reference). Points represent individual replicates colored by cluster and boxes show IQR with median. (R) Model summarizing species- and strain-level effects of Staphylococcus on RHE. Species-level differences distinguish commensal and pathogenic effects, while strain-level variation within S. epidermidis identifies inflammatory strains that activate a proinflammatory transcriptional program including upstream regulators (e.g. NFKB), chemokines (e.g., CCL20), cytokines (e.g., IL36γ) and downstream antimicrobial effectors (e.g. LCN2). Inflammatory S. epidermidis also enhances skin barrier defensive genes, particularly members of the LCE and SPRR gene families, which contribute to both barrier integrity and antimicrobial defense, and are regulated by transcription factors such as MAFB. These effects are linked to differences in gene content (e.g., cell surface genes), transcriptional programs, metabolism (e.g., arginine pathway), and pathogen-like growth phenotypes. P-values: **** p ≤ 0.0001, *** 0.0001 < p ≤ 0.001, ** 0.001 < p ≤ 0.01, * 0.01 < p ≤ 0.05., ns p > 0.05.

    Journal: bioRxiv

    Article Title: Species and strain diversity in Staphylococcus drive divergent host responses in human skin

    doi: 10.64898/2026.04.30.720712

    Figure Lengend Snippet: (A) Biofilm formation ability of commensal vs. inflammatory S. epidermidis strains. Biofilm positive strains were defined relative to a canonical biofilm-forming strain (Sep_1457). Numbers indicate strain counts per category and P-value and odds ratio calculated using Fisher’s exact test. (B-E) Survival ability in blood as measured by CFUs at 0, 2, and 24h of S. epidermidis strains (D) with respect to a bloodstream infection S. aureus strain (USA300LAC, (B)) with or without complement (+/-Comp) depletion (C, E). Points represent individual strains (or replicates for S. aureus) and boxes indicate IQR with median. Lines connect matched conditions. Significance was assessed by paired t-test with Bonferroni correction. (F-G) PCA plot of Staphylococcus cellular (F) or extracellular (G) metabolomes. Staphylococcus metabolomes were inferred by metabolic feature intensity within untargeted metabolomes. (H) Diagram of arginine metabolism pathway highlighting reactions catalyzed by arcA , argF , and argG . (I-K) Violin plots showing the metabolite abundance of arginine (I), carbamoyl-P (J), and argininosuccinate (K) in strains with or without arcA , argF , or argG. Points indicate normalized metabolite intensity; violins show distributions with embedded boxplots (median and IQR). Gene labels are black if acting on or downstream of the metabolite, grey otherwise. (L-N) Growth dynamics of inflammatory vs. commensal S. epidermidis strains in skin-like media with (+Arg) or without (-Arg) arginine. Maximum growth rate (L), maximum density (M), and area under the curve (AUC) (N) are derived from OD600 measurements every 0.5h over 10 hours at 37C. Points represent strains with paired conditions connected with lines. Statistical significance was determined by paired t -test followed by Bonferroni correction. (O-Q) Protein expression of cytokines IL-8 (O), CCL20 (P) and IL-36γ (Q) in the basal media of Staphylococcus -colonized RHE was measured by ELISA (n=3-4 replicates per strain in an independent experiment colonizing 3 inflammatory and 4 commensal S. epidermidis strains and S. aureus as a reference). Points represent individual replicates colored by cluster and boxes show IQR with median. (R) Model summarizing species- and strain-level effects of Staphylococcus on RHE. Species-level differences distinguish commensal and pathogenic effects, while strain-level variation within S. epidermidis identifies inflammatory strains that activate a proinflammatory transcriptional program including upstream regulators (e.g. NFKB), chemokines (e.g., CCL20), cytokines (e.g., IL36γ) and downstream antimicrobial effectors (e.g. LCN2). Inflammatory S. epidermidis also enhances skin barrier defensive genes, particularly members of the LCE and SPRR gene families, which contribute to both barrier integrity and antimicrobial defense, and are regulated by transcription factors such as MAFB. These effects are linked to differences in gene content (e.g., cell surface genes), transcriptional programs, metabolism (e.g., arginine pathway), and pathogen-like growth phenotypes. P-values: **** p ≤ 0.0001, *** 0.0001 < p ≤ 0.001, ** 0.001 < p ≤ 0.01, * 0.01 < p ≤ 0.05., ns p > 0.05.

    Article Snippet: Rabbit red blood cells with complement (Innovative Research Inc.; #IRBRBC10ML) was aliquoted into 96-well plates (150 μL per well).

    Techniques: Infection, Derivative Assay, Expressing, Enzyme-linked Immunosorbent Assay