acta2 rfpcherry tg mice  (Worthington Biochemical)


Bioz Verified Symbol Worthington Biochemical is a verified supplier
Bioz Manufacturer Symbol Worthington Biochemical manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 92
    Name:
    Ovalbumin
    Description:
    Major protein of egg white with a molecular weight of 45 kDa A lyophilized powder
    Catalog Number:
    ls003048
    Price:
    148
    Size:
    5 gm
    Source:
    Egg white
    Cas Number:
    9006.59.1
    Buy from Supplier


    Structured Review

    Worthington Biochemical acta2 rfpcherry tg mice
    TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions <t>Lyz2-EGFP-ki;Acta2-RFPcherry-Tg</t> mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). (E) Time-lapse IVM images ( Video S1 ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). (G) IVM images ( Video S2 ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p
    Major protein of egg white with a molecular weight of 45 kDa A lyophilized powder
    https://www.bioz.com/result/acta2 rfpcherry tg mice/product/Worthington Biochemical
    Average 92 stars, based on 115 article reviews
    Price from $9.99 to $1999.99
    acta2 rfpcherry tg mice - by Bioz Stars, 2020-10
    92/100 stars

    Images

    1) Product Images from "Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis"

    Article Title: Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis

    Journal: Immunity

    doi: 10.1016/j.immuni.2018.09.018

    TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). (E) Time-lapse IVM images ( Video S1 ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). (G) IVM images ( Video S2 ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p
    Figure Legend Snippet: TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). (E) Time-lapse IVM images ( Video S1 ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). (G) IVM images ( Video S2 ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p

    Techniques Used: Mouse Assay, In Vivo, Labeling, Blocking Assay, Injection, Transmission Electron Microscopy

    Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. (C) Time-lapse IVM images ( Video S3 ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). (H) Time-lapse confocal IVM images ( Video S4 ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.
    Figure Legend Snippet: Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. (C) Time-lapse IVM images ( Video S3 ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). (H) Time-lapse confocal IVM images ( Video S4 ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.

    Techniques Used: Mouse Assay, In Vivo, Labeling, Injection, Blocking Assay, Transmission Electron Microscopy, Inhibition

    2) Product Images from "Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis"

    Article Title: Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis

    Journal: Immunity

    doi: 10.1016/j.immuni.2018.09.018

    TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p
    Figure Legend Snippet: TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p

    Techniques Used: Mouse Assay, In Vivo, Labeling, Blocking Assay, Injection, Transmission Electron Microscopy

    Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.
    Figure Legend Snippet: Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.

    Techniques Used: Mouse Assay, In Vivo, Labeling, Injection, Blocking Assay, Transmission Electron Microscopy, Inhibition

    3) Product Images from "Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis"

    Article Title: Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis

    Journal: Immunity

    doi: 10.1016/j.immuni.2018.09.018

    CXCL1 and CXCL2 Are Differentially Expressed in TNF-Stimulated Tissues (A–E) WT mice were treated i.s. with PBS or TNF and cremaster muscles were IF stained for CXCL1 or CXCL2 and CD31 (ECs), α-SMA (pericytes), and MRP14 (neutrophils). Representative confocal images of venules showing CXCL1 (A) or CXCL2 (C) staining within EC and pericyte isosurface masks and quantifications of CXCL1 (B) and CXCL2 (D) in ECs or pericytes, in terms of MFIs (n = 4 mice per group) from 4 independent experiments. (E) Confocal abluminal and cross-sectional images (acquired along the dashed line and presented at 90° rotation) of a venule showing overall CXCL2 staining representative of 4 independent experiments. (F) Cxcl1 and Cxcl2 mRNA levels relative to Gapdh in circulating neutrophils 2–3 hr after i.s. PBS or TNF injection as determined by real-time PCR (n = 4–5 mice per group, 2 independent experiments). (G–J) Purified mouse bone marrow neutrophils were treated with PBS or TNF (1 nM, 1 hr) on uncoated (G, H), BSA-coated, or CXCL1-coated wells (I, J). CXCL1 and/or CXCL2 levels in lysates (G and I) and supernatants (H and J) as quantified by ELISA (n = 4–12) from 2–4 independent experiments. Means ± SEM, ∗ p
    Figure Legend Snippet: CXCL1 and CXCL2 Are Differentially Expressed in TNF-Stimulated Tissues (A–E) WT mice were treated i.s. with PBS or TNF and cremaster muscles were IF stained for CXCL1 or CXCL2 and CD31 (ECs), α-SMA (pericytes), and MRP14 (neutrophils). Representative confocal images of venules showing CXCL1 (A) or CXCL2 (C) staining within EC and pericyte isosurface masks and quantifications of CXCL1 (B) and CXCL2 (D) in ECs or pericytes, in terms of MFIs (n = 4 mice per group) from 4 independent experiments. (E) Confocal abluminal and cross-sectional images (acquired along the dashed line and presented at 90° rotation) of a venule showing overall CXCL2 staining representative of 4 independent experiments. (F) Cxcl1 and Cxcl2 mRNA levels relative to Gapdh in circulating neutrophils 2–3 hr after i.s. PBS or TNF injection as determined by real-time PCR (n = 4–5 mice per group, 2 independent experiments). (G–J) Purified mouse bone marrow neutrophils were treated with PBS or TNF (1 nM, 1 hr) on uncoated (G, H), BSA-coated, or CXCL1-coated wells (I, J). CXCL1 and/or CXCL2 levels in lysates (G and I) and supernatants (H and J) as quantified by ELISA (n = 4–12) from 2–4 independent experiments. Means ± SEM, ∗ p

    Techniques Used: Mouse Assay, Staining, Injection, Real-time Polymerase Chain Reaction, Purification, Enzyme-linked Immunosorbent Assay

    Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. (C) Time-lapse IVM images ( Video S3 ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). (H) Time-lapse confocal IVM images ( Video S4 ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.
    Figure Legend Snippet: Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. (C) Time-lapse IVM images ( Video S3 ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). (H) Time-lapse confocal IVM images ( Video S4 ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.

    Techniques Used: Mouse Assay, In Vivo, Labeling, Injection, Blocking Assay, Transmission Electron Microscopy, Inhibition

    TNF-Induced Neutrophil Migration Is Dependent on Both CXCL1 and CXCL2 WT mice pre-treated intrascrotally (i.s.) with control (ctr) or blocking mAbs or Cxcr2 −/− mice were subjected to i.s. injections of PBS or TNF. The cremaster muscles were immunostained for MRP14 (neutrophils) and α-SMA (pericytes) and analyzed for neutrophil infiltration by confocal microscopy. (A) and (C) are representative images and (B), (D), and (E) show quantifications (n = 4–10 mice per group) from 5–6 independent experiments. Means ± SEM, ∗∗∗ p
    Figure Legend Snippet: TNF-Induced Neutrophil Migration Is Dependent on Both CXCL1 and CXCL2 WT mice pre-treated intrascrotally (i.s.) with control (ctr) or blocking mAbs or Cxcr2 −/− mice were subjected to i.s. injections of PBS or TNF. The cremaster muscles were immunostained for MRP14 (neutrophils) and α-SMA (pericytes) and analyzed for neutrophil infiltration by confocal microscopy. (A) and (C) are representative images and (B), (D), and (E) show quantifications (n = 4–10 mice per group) from 5–6 independent experiments. Means ± SEM, ∗∗∗ p

    Techniques Used: Migration, Mouse Assay, Blocking Assay, Confocal Microscopy

    4) Product Images from "Presentation of Toxoplasma gondii Antigens via the Endogenous Major Histocompatibility Complex Class I Pathway in Nonprofessional and Professional Antigen-Presenting Cells ▿"

    Article Title: Presentation of Toxoplasma gondii Antigens via the Endogenous Major Histocompatibility Complex Class I Pathway in Nonprofessional and Professional Antigen-Presenting Cells ▿

    Journal:

    doi: 10.1128/IAI.00954-07

    MHC-I presentation of OVA by hematopoietic and nonhematopoietic cells infected with OVA transgenic T. gondii . DCs, MΦ, fibroblasts, or astrocytes were cultivated without (top panels) or with (bottom panels) IFN-γ and TNF-α, followed
    Figure Legend Snippet: MHC-I presentation of OVA by hematopoietic and nonhematopoietic cells infected with OVA transgenic T. gondii . DCs, MΦ, fibroblasts, or astrocytes were cultivated without (top panels) or with (bottom panels) IFN-γ and TNF-α, followed

    Techniques Used: Infection, Transgenic Assay

    Related Articles

    Infection:

    Article Title: Presentation of Toxoplasma gondii Antigens via the Endogenous Major Histocompatibility Complex Class I Pathway in Nonprofessional and Professional Antigen-Presenting Cells ▿
    Article Snippet: .. When primed, cells were cultivated in the presence of 100 U/ml recombinant murine IFN-γ and 10 U/ml tumor necrosis factor alpha (TNF-α) for 4 h, followed by the addition of 10 μl of antigen or parasites (0.1 μg/ml OVA amino acid 257 to 264 [OVA257-264 ] peptide SIINFEKL [ M r , 1,088; 92 pM; Invitrogen], 500 μg/ml soluble OVA [Worthington, Lakewood, NJ], live T. gondii tachyzoites at a multiplicity of infection [MOI] of 0.5, or heat-killed tachyzoites [treated 20 min at 56°C] at an MOI of 5) and incubation for an additional 16 h. Plates were spun and washed twice in RPMI medium without phenol red (Gibco), and 105 B3Z CD8+ T cells were added to 100 μl of RPMI (supplemented with 10% fetal bovine serum, 2 mM glutamine, 1 mM sodium pyruvate, 0.5 μM 2-mercaptoethanol, 100 U/ml penicillin, and 100 μg/ml streptomycin; without phenol red) and incubated for 16 h. β-Galactosidase activity was detected by adding chlorophenol red-β- d -galactopyranoside (CPRG; Calbiochem, San Diego, CA) at a final concentration of 100 μM for 16 h, and absorbance was measured at 562 nm. .. B3Z cell activation was expressed as the increase ( n -fold) in absorbance, relative to values obtained in the absence of antigen or parasites.

    Mouse Assay:

    Article Title: Tolerance induction in memory CD4 T cells is partial and reversible
    Article Snippet: .. Immunisations and infections TRACE mice were given Dox+ chow (Envigo) for a total of 7 days starting two days prior to immunisation with 40μg of ovalbumin (OVA) protein (Worthington) conjugated to 20μm polyethylene carboxylate beads (Polysciences Inc.) with 20μg of polyinosinic:polycytidinic acid (InvivoGen) and 20μg of anti-CD40 (BioXcell) s.c in the scruff. ..

    Article Title: Sustained cross‐presentation capacity of murine splenic dendritic cell subsets in vivo
    Article Snippet: .. After 30 min of antibody circulation, mice were injected intravenously with 5 μg Ovalbumin (OVA, Worthington Biochemical Corporation) or OVA conjugated with Alexa Fluor 647 (Life Technologies). .. As control antibody, polyclonal rabbit anti‐human papilloma virus (HPV) E6 IgG were generated in our lab by vaccinating New Zealand rabbits with recombinant E6 protein.

    Article Title: Protease-activated receptor 2 activation of myeloid dendritic cells regulates allergic airway inflammation
    Article Snippet: .. For sensitization and challenge experiments, mice (6-8 weeks old) were anesthetized with ketamine (45 mg/kg)/xylazine (8 mg/kg) prior to inhalation of PBS (40 μl), LPS-free ovalbumin (OVA; 100 μg/mouse; Worthington Biochem Corp, Lakewood NJ), OVA (100 μg) plus enriched protease (0.5 units), or OVA (100 μg) plus LPS (0.1 μg/mouse; Sigma Chemical Corp, St. Louis MO #055:B5) on day 0, 14, and 21 [ ]. .. For the adoptive transfer of bone marrow-derived DCs (BMDC), 40 μl of BMDC (1 × 106 cells) suspension was administered via instillation into the airways of anesthetized mice.

    Concentration Assay:

    Article Title: Presentation of Toxoplasma gondii Antigens via the Endogenous Major Histocompatibility Complex Class I Pathway in Nonprofessional and Professional Antigen-Presenting Cells ▿
    Article Snippet: .. When primed, cells were cultivated in the presence of 100 U/ml recombinant murine IFN-γ and 10 U/ml tumor necrosis factor alpha (TNF-α) for 4 h, followed by the addition of 10 μl of antigen or parasites (0.1 μg/ml OVA amino acid 257 to 264 [OVA257-264 ] peptide SIINFEKL [ M r , 1,088; 92 pM; Invitrogen], 500 μg/ml soluble OVA [Worthington, Lakewood, NJ], live T. gondii tachyzoites at a multiplicity of infection [MOI] of 0.5, or heat-killed tachyzoites [treated 20 min at 56°C] at an MOI of 5) and incubation for an additional 16 h. Plates were spun and washed twice in RPMI medium without phenol red (Gibco), and 105 B3Z CD8+ T cells were added to 100 μl of RPMI (supplemented with 10% fetal bovine serum, 2 mM glutamine, 1 mM sodium pyruvate, 0.5 μM 2-mercaptoethanol, 100 U/ml penicillin, and 100 μg/ml streptomycin; without phenol red) and incubated for 16 h. β-Galactosidase activity was detected by adding chlorophenol red-β- d -galactopyranoside (CPRG; Calbiochem, San Diego, CA) at a final concentration of 100 μM for 16 h, and absorbance was measured at 562 nm. .. B3Z cell activation was expressed as the increase ( n -fold) in absorbance, relative to values obtained in the absence of antigen or parasites.

    Article Title: Heat-Induced Structural Changes Affect OVA-Antigen Processing and Reduce Allergic Response in Mouse Model of Food Allergy
    Article Snippet: .. Ovalbumin Preparation For i.p . sensitization, OVA (Worthington, Lakewood, NJ, USA) and heated OVA (h-OVA; prepared by exposure of OVA to 70°C for 10 minutes, enabling accurate and reproducible dosing) were dissolved in phosphate-buffer saline (PBS) to a final concentration of 300 µg/ml containing 5 mg/ml of alum adjuvant (Sigma, Steinheim, Germany). .. For oral administration, OVA and h-OVA were dissolved in PBS to a final concentration of 100 mg/ml.

    Incubation:

    Article Title: Presentation of Toxoplasma gondii Antigens via the Endogenous Major Histocompatibility Complex Class I Pathway in Nonprofessional and Professional Antigen-Presenting Cells ▿
    Article Snippet: .. When primed, cells were cultivated in the presence of 100 U/ml recombinant murine IFN-γ and 10 U/ml tumor necrosis factor alpha (TNF-α) for 4 h, followed by the addition of 10 μl of antigen or parasites (0.1 μg/ml OVA amino acid 257 to 264 [OVA257-264 ] peptide SIINFEKL [ M r , 1,088; 92 pM; Invitrogen], 500 μg/ml soluble OVA [Worthington, Lakewood, NJ], live T. gondii tachyzoites at a multiplicity of infection [MOI] of 0.5, or heat-killed tachyzoites [treated 20 min at 56°C] at an MOI of 5) and incubation for an additional 16 h. Plates were spun and washed twice in RPMI medium without phenol red (Gibco), and 105 B3Z CD8+ T cells were added to 100 μl of RPMI (supplemented with 10% fetal bovine serum, 2 mM glutamine, 1 mM sodium pyruvate, 0.5 μM 2-mercaptoethanol, 100 U/ml penicillin, and 100 μg/ml streptomycin; without phenol red) and incubated for 16 h. β-Galactosidase activity was detected by adding chlorophenol red-β- d -galactopyranoside (CPRG; Calbiochem, San Diego, CA) at a final concentration of 100 μM for 16 h, and absorbance was measured at 562 nm. .. B3Z cell activation was expressed as the increase ( n -fold) in absorbance, relative to values obtained in the absence of antigen or parasites.

    Activity Assay:

    Article Title: Presentation of Toxoplasma gondii Antigens via the Endogenous Major Histocompatibility Complex Class I Pathway in Nonprofessional and Professional Antigen-Presenting Cells ▿
    Article Snippet: .. When primed, cells were cultivated in the presence of 100 U/ml recombinant murine IFN-γ and 10 U/ml tumor necrosis factor alpha (TNF-α) for 4 h, followed by the addition of 10 μl of antigen or parasites (0.1 μg/ml OVA amino acid 257 to 264 [OVA257-264 ] peptide SIINFEKL [ M r , 1,088; 92 pM; Invitrogen], 500 μg/ml soluble OVA [Worthington, Lakewood, NJ], live T. gondii tachyzoites at a multiplicity of infection [MOI] of 0.5, or heat-killed tachyzoites [treated 20 min at 56°C] at an MOI of 5) and incubation for an additional 16 h. Plates were spun and washed twice in RPMI medium without phenol red (Gibco), and 105 B3Z CD8+ T cells were added to 100 μl of RPMI (supplemented with 10% fetal bovine serum, 2 mM glutamine, 1 mM sodium pyruvate, 0.5 μM 2-mercaptoethanol, 100 U/ml penicillin, and 100 μg/ml streptomycin; without phenol red) and incubated for 16 h. β-Galactosidase activity was detected by adding chlorophenol red-β- d -galactopyranoside (CPRG; Calbiochem, San Diego, CA) at a final concentration of 100 μM for 16 h, and absorbance was measured at 562 nm. .. B3Z cell activation was expressed as the increase ( n -fold) in absorbance, relative to values obtained in the absence of antigen or parasites.

    Affinity Purification:

    Article Title: Neutralizing Human Fab Fragments against Measles Virus Recovered by Phage Display
    Article Snippet: .. The antigenic specificity of affinity-purified Fab fragments was evaluated by analyses of the reactivities to tetanus toxoid (SBL Vaccin, Stockholm, Sweden), ovalbumin (Worthington Biochemical Corp., Lakewood, N.J.), and BSA. .. The antigens (10 μg ml−1 ) were applied directly to microtiter plates, and the ELISA was performed as described above.

    Recombinant:

    Article Title: Presentation of Toxoplasma gondii Antigens via the Endogenous Major Histocompatibility Complex Class I Pathway in Nonprofessional and Professional Antigen-Presenting Cells ▿
    Article Snippet: .. When primed, cells were cultivated in the presence of 100 U/ml recombinant murine IFN-γ and 10 U/ml tumor necrosis factor alpha (TNF-α) for 4 h, followed by the addition of 10 μl of antigen or parasites (0.1 μg/ml OVA amino acid 257 to 264 [OVA257-264 ] peptide SIINFEKL [ M r , 1,088; 92 pM; Invitrogen], 500 μg/ml soluble OVA [Worthington, Lakewood, NJ], live T. gondii tachyzoites at a multiplicity of infection [MOI] of 0.5, or heat-killed tachyzoites [treated 20 min at 56°C] at an MOI of 5) and incubation for an additional 16 h. Plates were spun and washed twice in RPMI medium without phenol red (Gibco), and 105 B3Z CD8+ T cells were added to 100 μl of RPMI (supplemented with 10% fetal bovine serum, 2 mM glutamine, 1 mM sodium pyruvate, 0.5 μM 2-mercaptoethanol, 100 U/ml penicillin, and 100 μg/ml streptomycin; without phenol red) and incubated for 16 h. β-Galactosidase activity was detected by adding chlorophenol red-β- d -galactopyranoside (CPRG; Calbiochem, San Diego, CA) at a final concentration of 100 μM for 16 h, and absorbance was measured at 562 nm. .. B3Z cell activation was expressed as the increase ( n -fold) in absorbance, relative to values obtained in the absence of antigen or parasites.

    Injection:

    Article Title: Sustained cross‐presentation capacity of murine splenic dendritic cell subsets in vivo
    Article Snippet: .. After 30 min of antibody circulation, mice were injected intravenously with 5 μg Ovalbumin (OVA, Worthington Biochemical Corporation) or OVA conjugated with Alexa Fluor 647 (Life Technologies). .. As control antibody, polyclonal rabbit anti‐human papilloma virus (HPV) E6 IgG were generated in our lab by vaccinating New Zealand rabbits with recombinant E6 protein.

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 92
    Worthington Biochemical jervøe storm pm
    Jervøe Storm Pm, supplied by Worthington Biochemical, 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/jervøe storm pm/product/Worthington Biochemical
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    jervøe storm pm - by Bioz Stars, 2020-10
    92/100 stars
      Buy from Supplier

    91
    Worthington Biochemical kenealy pm
    Kenealy Pm, supplied by Worthington Biochemical, used in various techniques. Bioz Stars score: 91/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/kenealy pm/product/Worthington Biochemical
    Average 91 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    kenealy pm - by Bioz Stars, 2020-10
    91/100 stars
      Buy from Supplier

    91
    Worthington Biochemical jervoe storm pm
    Jervoe Storm Pm, supplied by Worthington Biochemical, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/jervoe storm pm/product/Worthington Biochemical
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    jervoe storm pm - by Bioz Stars, 2020-10
    91/100 stars
      Buy from Supplier

    Image Search Results