goat anti c3  (Valiant)

 
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    Name:
    Anti rat complement C3 goat antiserum to
    Description:
    Product is the lyophilized powder of goat antiserum to rat complement C3 and buffer salts
    Catalog Number:
    0855713
    Price:
    165.6
    Category:
    Life Sciences Antibodies Antisera
    Applications:
    Immunoassays, Immunoelectrophoresis, Immunodiffusion, Immunoprecipitation
    Size:
    2 mL
    		Buy from Supplier

    Structured Review

    Valiant goat anti c3
    Anti rat complement C3 goat antiserum to
    Product is the lyophilized powder of goat antiserum to rat complement C3 and buffer salts
    https://www.bioz.com/result/goat anti c3/product/Valiant
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    goat anti c3 - by Bioz Stars, 2021-03
    92/100 stars

    Images

    1) Product Images from "HIV Tat causes synapse loss in a mouse model of HIV-associated neurocognitive disorder that is independent of the classical complement cascade component C1q."

    Article Title: HIV Tat causes synapse loss in a mouse model of HIV-associated neurocognitive disorder that is independent of the classical complement cascade component C1q.

    Journal: Glia

    doi: 10.1002/glia.23511

    WT animals have elevated C3 activation in response to TAT exposure compared to mice with C1qa KO. Saline or HIV1-Tat was injected into the cortex of WT or C1qa-KO animals and the animals were processed for IHC 28 days later using anti-C3 antibodies. Images were taken at the injection site. Scale = 60μm. B) Quantification of C3 fluorescence intensity. Statistical Analysis: Two-Way ANOVA performed with independent variables: Injection treatment (Tat vs Saline; F (1,22) =11.56; p=0.003 - grey #) and Genotype (WT vs C1qa KO; F (1,22) =1.58; p=0.222). n=6–7 animals per group. No significant interaction between injection treatment and genotype was found (F (1,22) =1.55; p=0.226). ANOVA was followed by Holm’s-Sidak multiple comparison test (p
    Figure Legend Snippet: WT animals have elevated C3 activation in response to TAT exposure compared to mice with C1qa KO. Saline or HIV1-Tat was injected into the cortex of WT or C1qa-KO animals and the animals were processed for IHC 28 days later using anti-C3 antibodies. Images were taken at the injection site. Scale = 60μm. B) Quantification of C3 fluorescence intensity. Statistical Analysis: Two-Way ANOVA performed with independent variables: Injection treatment (Tat vs Saline; F (1,22) =11.56; p=0.003 - grey #) and Genotype (WT vs C1qa KO; F (1,22) =1.58; p=0.222). n=6–7 animals per group. No significant interaction between injection treatment and genotype was found (F (1,22) =1.55; p=0.226). ANOVA was followed by Holm’s-Sidak multiple comparison test (p

    Techniques Used: Activation Assay, Mouse Assay, Injection, Immunohistochemistry, Fluorescence

    2) Product Images from "Sialic acid is a critical fetal defense against maternal complement attack"

    Article Title: Sialic acid is a critical fetal defense against maternal complement attack

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI99945

    CVF decomplements the maternal serum and rescues the inflammatory phenotype of Cmas –/– implants. ( A ) C3 Western blot analysis. Serum of PBS- or CVF-treated pregnant mice at E8.5 was separated by SDS-PAGE and immunostained with anti-C3 antibody. C3 protein was only detectable in PBS-treated mice, but was depleted in CVF-treated pregnant mice. Anti-albumin staining was used as loading control. ( B ) C3 immunohistochemical staining of sagittal paraffin sections of E8.5 embryos within the uterus of PBS- or CVF-treated mice. In PBS-treated mothers, C3 reactivity was restricted to the EPC in control implants, but was expanded to the entire fetal-maternal interface in Cmas –/– embryos, with strong staining at the surface of TGCs. In implants of CVF-treated mothers, the C3 reactivity was abolished irrespective of the genotype. Insets show fetal TGCs. ( C ) Ly6G immunohistochemical staining for neutrophils on sagittal paraffin sections of E8.5 uteri from PBS- or CVF-treated mice. Ly6G-positive cells are sparsely distributed in proximity of control embryos of PBS-treated mothers. In contrast, the entire fetal-maternal boundary of Cmas –/– implants is infiltrated with Ly6G-positive cells in PBS-treated mice. CVF treatment does not change the phenotype of controls but reverts Ly6G staining of Cmas –/– implants to that of controls. ( D ) Quantification of Ly6G-positive cells (neutrophils) on sagittal paraffin sections of E8.5 uteri of PBS- or CVF-treated pregnant mice. Error bars indicate SD. Statistical analyses were performed by ANOVA with Newman-Keuls post test (*** P
    Figure Legend Snippet: CVF decomplements the maternal serum and rescues the inflammatory phenotype of Cmas –/– implants. ( A ) C3 Western blot analysis. Serum of PBS- or CVF-treated pregnant mice at E8.5 was separated by SDS-PAGE and immunostained with anti-C3 antibody. C3 protein was only detectable in PBS-treated mice, but was depleted in CVF-treated pregnant mice. Anti-albumin staining was used as loading control. ( B ) C3 immunohistochemical staining of sagittal paraffin sections of E8.5 embryos within the uterus of PBS- or CVF-treated mice. In PBS-treated mothers, C3 reactivity was restricted to the EPC in control implants, but was expanded to the entire fetal-maternal interface in Cmas –/– embryos, with strong staining at the surface of TGCs. In implants of CVF-treated mothers, the C3 reactivity was abolished irrespective of the genotype. Insets show fetal TGCs. ( C ) Ly6G immunohistochemical staining for neutrophils on sagittal paraffin sections of E8.5 uteri from PBS- or CVF-treated mice. Ly6G-positive cells are sparsely distributed in proximity of control embryos of PBS-treated mothers. In contrast, the entire fetal-maternal boundary of Cmas –/– implants is infiltrated with Ly6G-positive cells in PBS-treated mice. CVF treatment does not change the phenotype of controls but reverts Ly6G staining of Cmas –/– implants to that of controls. ( D ) Quantification of Ly6G-positive cells (neutrophils) on sagittal paraffin sections of E8.5 uteri of PBS- or CVF-treated pregnant mice. Error bars indicate SD. Statistical analyses were performed by ANOVA with Newman-Keuls post test (*** P

    Techniques Used: Western Blot, Mouse Assay, SDS Page, Staining, Immunohistochemistry

    Related Articles

    Staining:

    Article Title: Complement C3-Deficient Mice Fail to Display Age-Related Hippocampal Decline
    Article Snippet: Secondary Alexa Fluor-conjugated antibodies (Life Technologies) were added at 1:200 in 0.03% Triton X-100 with 10% goat serum for 2 h at room temperature (RT). .. For C3 staining, immunohistochemistry was performed using a goat anti-rat C3 antibody (1:200; MPBio Cappel) and buffers containing 1–5% BSA instead of goat serum ( ). .. Sections were mounted (Hard Set with DAPI; Vector Laboratories) and coverslipped.

    Immunohistochemistry:

    Article Title: Complement C3-Deficient Mice Fail to Display Age-Related Hippocampal Decline
    Article Snippet: Secondary Alexa Fluor-conjugated antibodies (Life Technologies) were added at 1:200 in 0.03% Triton X-100 with 10% goat serum for 2 h at room temperature (RT). .. For C3 staining, immunohistochemistry was performed using a goat anti-rat C3 antibody (1:200; MPBio Cappel) and buffers containing 1–5% BSA instead of goat serum ( ). .. Sections were mounted (Hard Set with DAPI; Vector Laboratories) and coverslipped.

    Incubation:

    Article Title: The mannose-binding lectin pathway is a significant contributor to reperfusion injury in the type 2 diabetic heart
    Article Snippet: Briefly, 2% rat serum (diluted with veronal-buffered saline with Ca++ and Mg++ (VBS++ )) was added to BSA–GlcNAc-coated 384-well microplates and incubated at 37°C for 30 min. .. The plates were washed and incubated with goat anti-rat C3 antibody (MP Biomedicals), followed by washing and detection with donkey anti-goat IRDye® 800 antibody (1:3,000; Rockland). ..

    Article Title: Contribution of Adipose-derived Factor D/Adipsin to Alternative Pathway Complement Activation: Lessons from Lipodystrophy
    Article Snippet: .. Goat anti-M C3 (MP Biomedicals), goat anti-Hu FB (CompTech), rabbit anti-M P , sheep anti-M FD (R & D) and rabbit anti-Hu FD (Abcam, Cambridge, MA) were incubated with the membranes for 2 h or overnight at 4° at RT. .. Secondary HRP-conjugated rabbit anti-goat IgG (Sigma-Aldrich), goat anti-rabbit IgG (GE Healthcare UK Limited), donkey anti-sheep IgG (R & D) or rabbit anti-human IgG (Jackson Immuno Research) was added for 1 h at 37°C.

    Article Title: Role of IgM and Angiotensin II Type I Receptor Autoantibodies in Local Complement Activation in Placental Ischemia-induced Hypertension in the Rat
    Article Snippet: Non-specific binding was blocked for 30 min with 10% donkey sera in PBS. .. The washed sections were incubated overnight at 4°C with goat anti-rat C3 (MP Biomedical 55713; Santa Ana, CA), rabbit anti-complement 5b-9 (EMD Millipore 204903; Darmstadt, Germany), goat anti-mouse Crry (Santa Cruz sc-25217; Dallas, TX) or rabbit anti-rat IgM (Rockland Immunochemicals 112-4107; Limerick, PA). .. Serial sections were incubated with appropriate isotype control antibodies.

    Article Title: Sialic acid is a critical fetal defense against maternal complement attack
    Article Snippet: .. Depletion of C3 in the serum of CVF-treated animals was confirmed by Western blot: 0.25 μl serum was separated by 12% SDS-PAGE under reducing conditions, transferred to PVDF membrane, and incubated with the primary antibodies goat anti-C3 (1:5,000, Cappel, MP Biomedicals) or goat anti-albumin (1:5,000, ab19194, Abcam) as a loading control. .. After incubation with anti-goat HRP-conjugated secondary antibody (1:15,000, sc-2020, Santa Cruz Biotechnology Inc.), detection was performed with enhanced chemoluminescence.

    Western Blot:

    Article Title: Sialic acid is a critical fetal defense against maternal complement attack
    Article Snippet: .. Depletion of C3 in the serum of CVF-treated animals was confirmed by Western blot: 0.25 μl serum was separated by 12% SDS-PAGE under reducing conditions, transferred to PVDF membrane, and incubated with the primary antibodies goat anti-C3 (1:5,000, Cappel, MP Biomedicals) or goat anti-albumin (1:5,000, ab19194, Abcam) as a loading control. .. After incubation with anti-goat HRP-conjugated secondary antibody (1:15,000, sc-2020, Santa Cruz Biotechnology Inc.), detection was performed with enhanced chemoluminescence.

    SDS Page:

    Article Title: Sialic acid is a critical fetal defense against maternal complement attack
    Article Snippet: .. Depletion of C3 in the serum of CVF-treated animals was confirmed by Western blot: 0.25 μl serum was separated by 12% SDS-PAGE under reducing conditions, transferred to PVDF membrane, and incubated with the primary antibodies goat anti-C3 (1:5,000, Cappel, MP Biomedicals) or goat anti-albumin (1:5,000, ab19194, Abcam) as a loading control. .. After incubation with anti-goat HRP-conjugated secondary antibody (1:15,000, sc-2020, Santa Cruz Biotechnology Inc.), detection was performed with enhanced chemoluminescence.

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    • goat anti c3  (Valiant)
    92
    Valiant goat anti c3
    WT animals have elevated C3 activation in response to TAT exposure compared to mice with C1qa KO. Saline or HIV1-Tat was injected into the cortex of WT or C1qa-KO animals and the animals were processed for IHC 28 days later using <t>anti-C3</t> antibodies. Images were taken at the injection site. Scale = 60μm. B) Quantification of C3 fluorescence intensity. Statistical Analysis: Two-Way ANOVA performed with independent variables: Injection treatment (Tat vs Saline; F (1,22) =11.56; p=0.003 - grey #) and Genotype (WT vs C1qa KO; F (1,22) =1.58; p=0.222). n=6–7 animals per group. No significant interaction between injection treatment and genotype was found (F (1,22) =1.55; p=0.226). ANOVA was followed by Holm’s-Sidak multiple comparison test (p
    Goat Anti C3, supplied by Valiant, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/goat anti c3/product/Valiant
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    goat anti c3 - by Bioz Stars, 2021-03
    92/100 stars
    		  Buy from Supplier
    anti goat c3  (Valiant)
    86
    Valiant anti goat c3
    WT animals have elevated C3 activation in response to TAT exposure compared to mice with C1qa KO. Saline or HIV1-Tat was injected into the cortex of WT or C1qa-KO animals and the animals were processed for IHC 28 days later using <t>anti-C3</t> antibodies. Images were taken at the injection site. Scale = 60μm. B) Quantification of C3 fluorescence intensity. Statistical Analysis: Two-Way ANOVA performed with independent variables: Injection treatment (Tat vs Saline; F (1,22) =11.56; p=0.003 - grey #) and Genotype (WT vs C1qa KO; F (1,22) =1.58; p=0.222). n=6–7 animals per group. No significant interaction between injection treatment and genotype was found (F (1,22) =1.55; p=0.226). ANOVA was followed by Holm’s-Sidak multiple comparison test (p
    Anti Goat C3, supplied by Valiant, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti goat c3/product/Valiant
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti goat c3 - by Bioz Stars, 2021-03
    86/100 stars
    		  Buy from Supplier

    Image Search Results


    WT animals have elevated C3 activation in response to TAT exposure compared to mice with C1qa KO. Saline or HIV1-Tat was injected into the cortex of WT or C1qa-KO animals and the animals were processed for IHC 28 days later using anti-C3 antibodies. Images were taken at the injection site. Scale = 60μm. B) Quantification of C3 fluorescence intensity. Statistical Analysis: Two-Way ANOVA performed with independent variables: Injection treatment (Tat vs Saline; F (1,22) =11.56; p=0.003 - grey #) and Genotype (WT vs C1qa KO; F (1,22) =1.58; p=0.222). n=6–7 animals per group. No significant interaction between injection treatment and genotype was found (F (1,22) =1.55; p=0.226). ANOVA was followed by Holm’s-Sidak multiple comparison test (p

    Journal: Glia

    Article Title: HIV Tat causes synapse loss in a mouse model of HIV-associated neurocognitive disorder that is independent of the classical complement cascade component C1q.

    doi: 10.1002/glia.23511

    Figure Lengend Snippet: WT animals have elevated C3 activation in response to TAT exposure compared to mice with C1qa KO. Saline or HIV1-Tat was injected into the cortex of WT or C1qa-KO animals and the animals were processed for IHC 28 days later using anti-C3 antibodies. Images were taken at the injection site. Scale = 60μm. B) Quantification of C3 fluorescence intensity. Statistical Analysis: Two-Way ANOVA performed with independent variables: Injection treatment (Tat vs Saline; F (1,22) =11.56; p=0.003 - grey #) and Genotype (WT vs C1qa KO; F (1,22) =1.58; p=0.222). n=6–7 animals per group. No significant interaction between injection treatment and genotype was found (F (1,22) =1.55; p=0.226). ANOVA was followed by Holm’s-Sidak multiple comparison test (p

    Article Snippet: We used the following antibodies in these experiments: rabbit anti-Iba1 at 1:1000 (Wako Biochemicals, 019–19741) rabbit anti-C1q (Abcam clone 4.8, KO verified in ( )), goat anti-C3 (MP Biomedicals 55730, KO verified in ( )), and guinea pig anti-piccolo (Synaptic Systems, 142104).

    Techniques: Activation Assay, Mouse Assay, Injection, Immunohistochemistry, Fluorescence

    CVF decomplements the maternal serum and rescues the inflammatory phenotype of Cmas –/– implants. ( A ) C3 Western blot analysis. Serum of PBS- or CVF-treated pregnant mice at E8.5 was separated by SDS-PAGE and immunostained with anti-C3 antibody. C3 protein was only detectable in PBS-treated mice, but was depleted in CVF-treated pregnant mice. Anti-albumin staining was used as loading control. ( B ) C3 immunohistochemical staining of sagittal paraffin sections of E8.5 embryos within the uterus of PBS- or CVF-treated mice. In PBS-treated mothers, C3 reactivity was restricted to the EPC in control implants, but was expanded to the entire fetal-maternal interface in Cmas –/– embryos, with strong staining at the surface of TGCs. In implants of CVF-treated mothers, the C3 reactivity was abolished irrespective of the genotype. Insets show fetal TGCs. ( C ) Ly6G immunohistochemical staining for neutrophils on sagittal paraffin sections of E8.5 uteri from PBS- or CVF-treated mice. Ly6G-positive cells are sparsely distributed in proximity of control embryos of PBS-treated mothers. In contrast, the entire fetal-maternal boundary of Cmas –/– implants is infiltrated with Ly6G-positive cells in PBS-treated mice. CVF treatment does not change the phenotype of controls but reverts Ly6G staining of Cmas –/– implants to that of controls. ( D ) Quantification of Ly6G-positive cells (neutrophils) on sagittal paraffin sections of E8.5 uteri of PBS- or CVF-treated pregnant mice. Error bars indicate SD. Statistical analyses were performed by ANOVA with Newman-Keuls post test (*** P

    Journal: The Journal of Clinical Investigation

    Article Title: Sialic acid is a critical fetal defense against maternal complement attack

    doi: 10.1172/JCI99945

    Figure Lengend Snippet: CVF decomplements the maternal serum and rescues the inflammatory phenotype of Cmas –/– implants. ( A ) C3 Western blot analysis. Serum of PBS- or CVF-treated pregnant mice at E8.5 was separated by SDS-PAGE and immunostained with anti-C3 antibody. C3 protein was only detectable in PBS-treated mice, but was depleted in CVF-treated pregnant mice. Anti-albumin staining was used as loading control. ( B ) C3 immunohistochemical staining of sagittal paraffin sections of E8.5 embryos within the uterus of PBS- or CVF-treated mice. In PBS-treated mothers, C3 reactivity was restricted to the EPC in control implants, but was expanded to the entire fetal-maternal interface in Cmas –/– embryos, with strong staining at the surface of TGCs. In implants of CVF-treated mothers, the C3 reactivity was abolished irrespective of the genotype. Insets show fetal TGCs. ( C ) Ly6G immunohistochemical staining for neutrophils on sagittal paraffin sections of E8.5 uteri from PBS- or CVF-treated mice. Ly6G-positive cells are sparsely distributed in proximity of control embryos of PBS-treated mothers. In contrast, the entire fetal-maternal boundary of Cmas –/– implants is infiltrated with Ly6G-positive cells in PBS-treated mice. CVF treatment does not change the phenotype of controls but reverts Ly6G staining of Cmas –/– implants to that of controls. ( D ) Quantification of Ly6G-positive cells (neutrophils) on sagittal paraffin sections of E8.5 uteri of PBS- or CVF-treated pregnant mice. Error bars indicate SD. Statistical analyses were performed by ANOVA with Newman-Keuls post test (*** P

    Article Snippet: Depletion of C3 in the serum of CVF-treated animals was confirmed by Western blot: 0.25 μl serum was separated by 12% SDS-PAGE under reducing conditions, transferred to PVDF membrane, and incubated with the primary antibodies goat anti-C3 (1:5,000, Cappel, MP Biomedicals) or goat anti-albumin (1:5,000, ab19194, Abcam) as a loading control.

    Techniques: Western Blot, Mouse Assay, SDS Page, Staining, Immunohistochemistry