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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: Subcutaneous administration of anti-CD38 antibodies
    Article Snippet: .. Rabbit complement (2-15 ul; #CL 3441 CedarLane Laboratories), was added to each well except control wells. .. CytoTox-Glo reagent (Promega, G7571/G7573) was used to detect cytotoxicity by luminescence.

    Article Title: Anti-CD38 binding domains
    Article Snippet: .. 50 μL of anti-CD38 antibody (9 μg/ml), control IgG1 antibody (9 μg/ml), or media alone was added to each well and left to incubate at room temperature (RT) for 10 min. Varying amounts (2-15 μL) of purified rabbit complement (Cat #CL 3441 Cedarlane Laboratories, Canada) was added to each well except control wells. .. After one-hour incubation at 37° C., the plate was brought to room temperature, 100 μL of cell titer CytoTox GloTM reagent (Promega G7571/G7573) was added to each well, the plate was shaken for 5 to 7 minutes, and luminescence was read on an EnVision® (Perkin Elmer) luminescence plate reader.

    Article Title: Methods and materials for assessing response to plasmablast- and plasma cell-depleting therapies
    Article Snippet: .. 50 μL of 2× anti-CD38 antibody, control IgG antibody, or media alone was added to each well and left to incubate at room temperature for 10 min. Varying amounts (2-15 μL) of purified rabbit complement (cat #CL 3441 Cedarlane Laboratories, Canada), depending upon the cell line was added to each well except control wells. .. After one hour incubation at 37° C., plates were brought to room temperature, 100 μL of cell titer CytoTox GloTM reagent (Promega G7571/G7573) was added per well, the plate shaken for 5 to 7 min and luminescence read on an EnVision® (Perkin Elmer) luminescence plate reader.

    Purification:

    Article Title: Anti-CD38 binding domains
    Article Snippet: .. 50 μL of anti-CD38 antibody (9 μg/ml), control IgG1 antibody (9 μg/ml), or media alone was added to each well and left to incubate at room temperature (RT) for 10 min. Varying amounts (2-15 μL) of purified rabbit complement (Cat #CL 3441 Cedarlane Laboratories, Canada) was added to each well except control wells. .. After one-hour incubation at 37° C., the plate was brought to room temperature, 100 μL of cell titer CytoTox GloTM reagent (Promega G7571/G7573) was added to each well, the plate was shaken for 5 to 7 minutes, and luminescence was read on an EnVision® (Perkin Elmer) luminescence plate reader.

    Article Title: Methods and materials for assessing response to plasmablast- and plasma cell-depleting therapies
    Article Snippet: .. 50 μL of 2× anti-CD38 antibody, control IgG antibody, or media alone was added to each well and left to incubate at room temperature for 10 min. Varying amounts (2-15 μL) of purified rabbit complement (cat #CL 3441 Cedarlane Laboratories, Canada), depending upon the cell line was added to each well except control wells. .. After one hour incubation at 37° C., plates were brought to room temperature, 100 μL of cell titer CytoTox GloTM reagent (Promega G7571/G7573) was added per well, the plate shaken for 5 to 7 min and luminescence read on an EnVision® (Perkin Elmer) luminescence plate reader.

    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.

    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: Proteins comprising CD3 antigen binding domains and uses thereof
    Article Snippet: .. Antibodies were added to target cells and incubated for 30 minutes at 37° C. After incubation, 15-20% (stock concentration) of rabbit complement (Cedarlane cat. #CL3441-S) and heat inactivated complement was added to the wells respectively in a volume of 25 μl/well. .. The mixture was incubated for 4-12 hours at 37° C. Target cell lysis was detected by addition of 100 μl of CellTitre-Glo (Promega cat. #G9242) reagent followed by incubation for 10 minutes at room temperature.

    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.

    Article Title: Proteins comprising CD3 antigen binding domains and uses thereof
    Article Snippet: .. Antibodies were added to target cells and incubated for 30 minutes at 37° C. After incubation, 15-20% (stock concentration) of rabbit complement (Cedarlane cat. #CL3441-S) and heat inactivated complement was added to the wells respectively in a volume of 25 μl/well. .. The mixture was incubated for 4-12 hours at 37° C. Target cell lysis was detected by addition of 100 μl of CellTitre-Glo (Promega cat. #G9242) reagent followed by incubation for 10 minutes at room temperature.



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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