Review

af2215 goat polyclonal anti human cd46 antibody r d systems (R&D Systems)

R&D Systems is a verified supplier

R&D Systems manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

R&D Systems af2215 goat polyclonal anti human cd46 antibody r d systems

Figure 2. HCMV Trimer and Pentamer Hit Validation (A and B) BLI analysis conﬁrmed binding of (A) HCMV trimer to PDGFRa and TGFbRIII, and of (B) pentamer to Nrp2, THBD, LILRB3, and <t>CD46,</t> respectively. Recombinant ECDs for the receptors identiﬁed as putative binding partners were captured onto protein A-coated sensors and as- sayed for binding to HCMV trimer or pentamer recombinant puriﬁed protein complexes tested at the indicated concentrations. (C) Summary of new binding partners identiﬁed for HCMV trimer and pentamer complexes, alongside their respective kinetic parameters, calculated by BLI using puriﬁed proteins and HCMV com- plexes. Representative results out of at least two independent assays are shown. Representative experimental ﬁttings are shown in Figure S3D. N.B., no binding detected by BLI.

Af2215 Goat Polyclonal Anti Human Cd46 Antibody R D Systems, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 80 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/goat+anti+cd46+polyclonal+antibody/Human%2FMouse%2FRat+Neuropilin-2+Antibody/pm30057110-469-14-20
Average 93 stars, based on 80 article reviews

af2215 goat polyclonal anti human cd46 antibody r d systems - by Bioz Stars, 2026-09

93/100 stars

Images

1) Product Images from "An Unbiased Screen for Human Cytomegalovirus Identifies Neuropilin-2 as a Central Viral Receptor."

Article Title: An Unbiased Screen for Human Cytomegalovirus Identifies Neuropilin-2 as a Central Viral Receptor.

Journal: Cell

doi: 10.1016/j.cell.2018.06.028

Figure Legend Snippet: Figure 2. HCMV Trimer and Pentamer Hit Validation (A and B) BLI analysis conﬁrmed binding of (A) HCMV trimer to PDGFRa and TGFbRIII, and of (B) pentamer to Nrp2, THBD, LILRB3, and CD46, respectively. Recombinant ECDs for the receptors identiﬁed as putative binding partners were captured onto protein A-coated sensors and as- sayed for binding to HCMV trimer or pentamer recombinant puriﬁed protein complexes tested at the indicated concentrations. (C) Summary of new binding partners identiﬁed for HCMV trimer and pentamer complexes, alongside their respective kinetic parameters, calculated by BLI using puriﬁed proteins and HCMV com- plexes. Representative results out of at least two independent assays are shown. Representative experimental ﬁttings are shown in Figure S3D. N.B., no binding detected by BLI.

Techniques Used: Biomarker Discovery, Binding Assay, Recombinant

Figure 3. Functional Validation of the Newly Identiﬁed HCMV Receptors Using Competition Studies and Lentiviral Overexpression (A) ARPE-19, MRC-9, and HUVECs were infected for 48 hr with the VR1814 virus that had been pre-incubated with different concentrations of soluble re- combinant ligands, including Nrp2, CD46, THBD, TGFbRIII, and PDGFRa proteins, or an anti-Nrp antibody. The percentage of infected cells was plotted against antibody and ligands concentration. Shown is the IC50 mean ± SEM of four independent experiments, calculated by nonlinear regression (Figures S5D–S5F). (B and C) Nrp2, CD46, THBD, and TGFbRIII receptors were overexpressed in ARPE-19 (B) and MRC-9 (C) using lentiviral vectors and then infected with the VR1814 virus. Overexpression of Nrp2 increased VR1814 viral infection in ARPE-19 epithelial, whereas no effect was observed in MRC-9 ﬁbroblasts. Shown is the mean ± SEM of four independent experiments. Statistical signiﬁcance was evaluated by t test (Mann-Whitney test). ****p < 0.0001. See also Figure S4.

Figure Legend Snippet: Figure 3. Functional Validation of the Newly Identiﬁed HCMV Receptors Using Competition Studies and Lentiviral Overexpression (A) ARPE-19, MRC-9, and HUVECs were infected for 48 hr with the VR1814 virus that had been pre-incubated with different concentrations of soluble re- combinant ligands, including Nrp2, CD46, THBD, TGFbRIII, and PDGFRa proteins, or an anti-Nrp antibody. The percentage of infected cells was plotted against antibody and ligands concentration. Shown is the IC50 mean ± SEM of four independent experiments, calculated by nonlinear regression (Figures S5D–S5F). (B and C) Nrp2, CD46, THBD, and TGFbRIII receptors were overexpressed in ARPE-19 (B) and MRC-9 (C) using lentiviral vectors and then infected with the VR1814 virus. Overexpression of Nrp2 increased VR1814 viral infection in ARPE-19 epithelial, whereas no effect was observed in MRC-9 ﬁbroblasts. Shown is the mean ± SEM of four independent experiments. Statistical signiﬁcance was evaluated by t test (Mann-Whitney test). ****p < 0.0001. See also Figure S4.

Techniques Used: Functional Assay, Biomarker Discovery, Over Expression, Infection, Virus, Incubation, Concentration Assay, MANN-WHITNEY

Figure 4. Functional Validation of the Newly Identiﬁed HCMV Receptors Using CRISPR/Cas9 Knockout and siRNA Knockdown (A) HAP-1 wild-type (WT) or knockout (KO) cells for Nrp2, CD46, and TGFbRIII receptors were generated using CRISPR/Cas9 and infected with the VR1814 virus. THBD is not expressed in HAP-1 cells (Figure S6B). Nrp2 KO strongly inhibited viral entry. HAP-1 cells recovered susceptibility to infection when cells were transduced with lentiviral vector encoding Nrp2, following Nrp2 KO. Shown is the percentage of infected cells mean ± SEM. (B) Representative images of infection in HAP-1 WT or KO cells for individual receptors. Scale bar, 10 mm. Immunoﬂuorescence staining of HCMV pp72 protein is shown in red; DAPI nuclear stain is shown blue. (C) HUVEC WT or siRNA knockdown (KD) cells for Nrp2, CD46, and TGFbRIII were infected with VR1814 virus for 48 hr. Shown is the percentage of infected cells mean ± SEM. (D) Representative images of infection in HUVECs. Scale bar, 10 mm. (E) ARPE-19 WT or siRNA KD cells for Nrp2 were infected with VR1814 virus for 48 hr. Shown is the percentage of infected cells mean ± SEM. (F) MRC-9 WT, siRNA KD for Nrp2, or shRNA KD for PDGFRa were infected with VR1814 virus for 48 hr. Shown is the percentage of infected cells mean ± SEM.

Figure Legend Snippet: Figure 4. Functional Validation of the Newly Identiﬁed HCMV Receptors Using CRISPR/Cas9 Knockout and siRNA Knockdown (A) HAP-1 wild-type (WT) or knockout (KO) cells for Nrp2, CD46, and TGFbRIII receptors were generated using CRISPR/Cas9 and infected with the VR1814 virus. THBD is not expressed in HAP-1 cells (Figure S6B). Nrp2 KO strongly inhibited viral entry. HAP-1 cells recovered susceptibility to infection when cells were transduced with lentiviral vector encoding Nrp2, following Nrp2 KO. Shown is the percentage of infected cells mean ± SEM. (B) Representative images of infection in HAP-1 WT or KO cells for individual receptors. Scale bar, 10 mm. Immunoﬂuorescence staining of HCMV pp72 protein is shown in red; DAPI nuclear stain is shown blue. (C) HUVEC WT or siRNA knockdown (KD) cells for Nrp2, CD46, and TGFbRIII were infected with VR1814 virus for 48 hr. Shown is the percentage of infected cells mean ± SEM. (D) Representative images of infection in HUVECs. Scale bar, 10 mm. (E) ARPE-19 WT or siRNA KD cells for Nrp2 were infected with VR1814 virus for 48 hr. Shown is the percentage of infected cells mean ± SEM. (F) MRC-9 WT, siRNA KD for Nrp2, or shRNA KD for PDGFRa were infected with VR1814 virus for 48 hr. Shown is the percentage of infected cells mean ± SEM.

Techniques Used: Functional Assay, Biomarker Discovery, CRISPR, Knock-Out, Knockdown, Generated, Infection, Virus, Transduction, Plasmid Preparation, Staining, shRNA

Activation Assay:

Article Title: Differential Expression of Complement Markers in Normal and AMD Transmitochondrial Cybrids
Article Snippet: 7 , CD46 , 44 kDa , Goat Anti-CD46 Polyclonal antibody # AF2005 (RD Systems) , 1:1000 , Human , Dnk pAb to Goat IgG (HRP) ab97120 (ABCAM) , beta-actin antibody GTX 110564 (Genetex).

Binding Assay:

Membrane:

Lysis:

Control:

Marker:

Inhibition:

Variant Assay:

Western Blot:

Gene Expression:

Quantitation Assay:

Expressing:

Image Search Results

Journal: Cell

Article Title: An Unbiased Screen for Human Cytomegalovirus Identifies Neuropilin-2 as a Central Viral Receptor.

doi: 10.1016/j.cell.2018.06.028

Figure Lengend Snippet: Figure 2. HCMV Trimer and Pentamer Hit Validation (A and B) BLI analysis conﬁrmed binding of (A) HCMV trimer to PDGFRa and TGFbRIII, and of (B) pentamer to Nrp2, THBD, LILRB3, and CD46, respectively. Recombinant ECDs for the receptors identiﬁed as putative binding partners were captured onto protein A-coated sensors and as- sayed for binding to HCMV trimer or pentamer recombinant puriﬁed protein complexes tested at the indicated concentrations. (C) Summary of new binding partners identiﬁed for HCMV trimer and pentamer complexes, alongside their respective kinetic parameters, calculated by BLI using puriﬁed proteins and HCMV com- plexes. Representative results out of at least two independent assays are shown. Representative experimental ﬁttings are shown in Figure S3D. N.B., no binding detected by BLI.

Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Antibodies Goat polyclonal anti-human/mouse/rat Neuropilin-2 antibody R&D Systems Cat# AF2215 Goat polyclonal anti-human CD46 antibody R&D Systems Cat# AF2005 Mouse monoclonal anti-Thrombomodulin antibody Abcam Cat# ab33513 Goat polyclonal anti-TGFbRIII antibody Sigma Cat# T1940 Sheep polyclonal IgG R&D Cat# 5-001-A Goat polyclonal anti-CMV pp71 (vC-20) antibody Santa Cruz Biotechnology Cat# SC-33323 Mouse monoclonal anti-CMV pp72 (6E1) antibody Santa Cruz Biotechnology Cat# SC-69834 Rabbit anti-goat IgG (H+L) superclonal secondary antibody, Alex Fluor 594 ThermoFisher Cat# A27016 Donkey anti-sheep IgG (H+L) cross-adsorbed secondary antibody, Alexa Fluor 488 ThermoFisher Cat# A11015 F(ab’)2-goat anti-mouse IgG (H+L) cross-adsorbed secondary antibody, Alexa Fluor 594 ThermoFisher Cat# A11020 Alexa Fluor 647 AffiniPure Donkey Anti-Human IgG (H+L) Jackson Immunoresearch Cat# 709-605-149 Goat Anti-Human IgG, Fcg fragment specific Jackson Immunoresearch Cat# 109-155-008 3G16 Antibody Macagno et al., 2010 N/A anti-CD46 R&D systems AF2005 anti-Thrombomodulin Abcam clone 141C01 anti-TGFbRIII a Sigma T1940 Pan-Nrp Antibody Appleton et al., 2007 N/A MSL109 Ciferri et al., 2015a N/A anti-HCMV pp72/86, clone 5D2 Kabanova et al., 2016 N/A anti-PDGFRa for FACS BD Biosciences clone aR1 anti-PDGFRa for western blot clone C-9 Santa Cruz Biotechnology anti-alpha-Tubulin clone B-7 Santa Cruz Biotechnology Anti- Strep,Tag II Monoclonal Antibody Novagen 71591-3 Bacterial and Virus Strains HCMV clinical isolate VR1814 Virologia e Microbiologia, Fondazione IRCCS Policlinico N/A Chemicals, Peptides, and Recombinant Proteins Human LILRB3 R&D Systems Cat# 9159-T5-050 Human FCAR R&D Systems Cat# 3939-FA-050 Human Neuropilin-1 R&D Systems Cat# 3870-N1-025 Human Neuropilin-2 R&D Systems Cat# 2215-N2-025 Human TGFb1 R&D Systems Cat# 240-B-002 Human NELL1 R&D Systems Cat# 5487-NL-050 Nitrocefin Millipore Sigma Cat# 484400 D-desthiobiotin Millipore Sigma Cat# 71610 Lipofectamine 2000 Transfection Reagent ThermoFisher Cat# 11668-019 Lipofectamine RNAiMAX Transfection Reagent ThermoFisher Cat# 13778030 DMEM/F-12 ThermoFisher Cat# 11320033 GlutaMAX supplement ThermoFisher Cat# 35050061 Penicillin-Streptomycin ThermoFisher Cat# 10378016 (Continued on next page) Cell 174, 1–14.e1–e10, August 23, 2018 e1

Techniques: Biomarker Discovery, Binding Assay, Recombinant

Journal: Cell

Article Title: An Unbiased Screen for Human Cytomegalovirus Identifies Neuropilin-2 as a Central Viral Receptor.

doi: 10.1016/j.cell.2018.06.028

Figure Lengend Snippet: Figure 3. Functional Validation of the Newly Identiﬁed HCMV Receptors Using Competition Studies and Lentiviral Overexpression (A) ARPE-19, MRC-9, and HUVECs were infected for 48 hr with the VR1814 virus that had been pre-incubated with different concentrations of soluble re- combinant ligands, including Nrp2, CD46, THBD, TGFbRIII, and PDGFRa proteins, or an anti-Nrp antibody. The percentage of infected cells was plotted against antibody and ligands concentration. Shown is the IC50 mean ± SEM of four independent experiments, calculated by nonlinear regression (Figures S5D–S5F). (B and C) Nrp2, CD46, THBD, and TGFbRIII receptors were overexpressed in ARPE-19 (B) and MRC-9 (C) using lentiviral vectors and then infected with the VR1814 virus. Overexpression of Nrp2 increased VR1814 viral infection in ARPE-19 epithelial, whereas no effect was observed in MRC-9 ﬁbroblasts. Shown is the mean ± SEM of four independent experiments. Statistical signiﬁcance was evaluated by t test (Mann-Whitney test). ****p < 0.0001. See also Figure S4.

Techniques: Functional Assay, Biomarker Discovery, Over Expression, Infection, Virus, Incubation, Concentration Assay, MANN-WHITNEY

Journal: Cell

Article Title: An Unbiased Screen for Human Cytomegalovirus Identifies Neuropilin-2 as a Central Viral Receptor.

doi: 10.1016/j.cell.2018.06.028

Figure Lengend Snippet: Figure 4. Functional Validation of the Newly Identiﬁed HCMV Receptors Using CRISPR/Cas9 Knockout and siRNA Knockdown (A) HAP-1 wild-type (WT) or knockout (KO) cells for Nrp2, CD46, and TGFbRIII receptors were generated using CRISPR/Cas9 and infected with the VR1814 virus. THBD is not expressed in HAP-1 cells (Figure S6B). Nrp2 KO strongly inhibited viral entry. HAP-1 cells recovered susceptibility to infection when cells were transduced with lentiviral vector encoding Nrp2, following Nrp2 KO. Shown is the percentage of infected cells mean ± SEM. (B) Representative images of infection in HAP-1 WT or KO cells for individual receptors. Scale bar, 10 mm. Immunoﬂuorescence staining of HCMV pp72 protein is shown in red; DAPI nuclear stain is shown blue. (C) HUVEC WT or siRNA knockdown (KD) cells for Nrp2, CD46, and TGFbRIII were infected with VR1814 virus for 48 hr. Shown is the percentage of infected cells mean ± SEM. (D) Representative images of infection in HUVECs. Scale bar, 10 mm. (E) ARPE-19 WT or siRNA KD cells for Nrp2 were infected with VR1814 virus for 48 hr. Shown is the percentage of infected cells mean ± SEM. (F) MRC-9 WT, siRNA KD for Nrp2, or shRNA KD for PDGFRa were infected with VR1814 virus for 48 hr. Shown is the percentage of infected cells mean ± SEM.

Techniques: Functional Assay, Biomarker Discovery, CRISPR, Knock-Out, Knockdown, Generated, Infection, Virus, Transduction, Plasmid Preparation, Staining, shRNA

The classical pathway is triggered by interaction of C1 with immune or non-immune complexes leading to conformational changes in C1q, activation of C1r and C1s, and subsequent assembly of C3 convertase. The lectin pathway is activated by binding of mannose-binding lectin (MBL) to mannose residues on the pathogen surface, which activates the MBL-associated serine proteases (MASPs), followed by formation of C3 convertase. Spontaneous hydrolysis of C3 initiates the alternative complement pathway. All three pathways of the complement cascade converge on the classical C3 convertase, which cleaves and activates component C3, forming C3a and C3b. This triggers a series of further cleavage and activation events, leading to cleavage of C5 into C5a and C5b, and eventual formation of the membrane attack complex (MAC), consisting of C5b, C6, C7, C8, and C9. MAC is the terminal cytolytic complex of the complement pathway; it causes osmotic lysis of target cells by forming transmembrane channels that disrupt the phospholipid bilayer of target cells. The complement system is tightly regulated by the following complement control proteins: CFH, CFHR1, CFHR4, CFB, CD55, CD59, CD46, CFI, and CFP.

Journal: PLoS ONE

Article Title: Differential Expression of Complement Markers in Normal and AMD Transmitochondrial Cybrids

doi: 10.1371/journal.pone.0159828

Figure Lengend Snippet: The classical pathway is triggered by interaction of C1 with immune or non-immune complexes leading to conformational changes in C1q, activation of C1r and C1s, and subsequent assembly of C3 convertase. The lectin pathway is activated by binding of mannose-binding lectin (MBL) to mannose residues on the pathogen surface, which activates the MBL-associated serine proteases (MASPs), followed by formation of C3 convertase. Spontaneous hydrolysis of C3 initiates the alternative complement pathway. All three pathways of the complement cascade converge on the classical C3 convertase, which cleaves and activates component C3, forming C3a and C3b. This triggers a series of further cleavage and activation events, leading to cleavage of C5 into C5a and C5b, and eventual formation of the membrane attack complex (MAC), consisting of C5b, C6, C7, C8, and C9. MAC is the terminal cytolytic complex of the complement pathway; it causes osmotic lysis of target cells by forming transmembrane channels that disrupt the phospholipid bilayer of target cells. The complement system is tightly regulated by the following complement control proteins: CFH, CFHR1, CFHR4, CFB, CD55, CD59, CD46, CFI, and CFP.

Article Snippet: 7 , CD46 , 44 kDa , Goat Anti-CD46 Polyclonal antibody # AF2005 (RD Systems) , 1:1000 , Human , Dnk pAb to Goat IgG (HRP) ab97120 (ABCAM) , beta-actin antibody GTX 110564 (Genetex).

Techniques: Activation Assay, Binding Assay, Membrane, Lysis, Control

Journal: PLoS ONE

Article Title: Differential Expression of Complement Markers in Normal and AMD Transmitochondrial Cybrids

doi: 10.1371/journal.pone.0159828

Figure Lengend Snippet: Complement Markers’ Information.

Techniques: Marker, Activation Assay, Membrane, Lysis, Inhibition

Journal: PLoS ONE

Article Title: Differential Expression of Complement Markers in Normal and AMD Transmitochondrial Cybrids

doi: 10.1371/journal.pone.0159828

Figure Lengend Snippet: Complement Genes’ Information.

Techniques: Variant Assay

Complement Proteins’ Western Blotting Information.

Journal: PLoS ONE

Article Title: Differential Expression of Complement Markers in Normal and AMD Transmitochondrial Cybrids

doi: 10.1371/journal.pone.0159828

Figure Lengend Snippet: Complement Proteins’ Western Blotting Information.

Techniques: Western Blot

Journal: PLoS ONE

Article Title: Differential Expression of Complement Markers in Normal and AMD Transmitochondrial Cybrids

doi: 10.1371/journal.pone.0159828

Figure Lengend Snippet: Complement Gene Expression Data.

Techniques: Gene Expression

Decreased protein levels of CFH, CFHL1, CD55, CD59, CFI, and CD46, and increased levels of CFP, CFB, CFHR4, and CFHR1 protein in AMD cybrids. (A, C, E, G, I, K, M, O, Q, S) Representative Western blots of CFH, CFHL1, CD55, CD59, CFI, CFP, CFB, CD46, CFHR4, and CFHR1 respectively. (B, D, F, H, J, L, N, P, R, T) Graphs showing quantitation of CFH, CFHL1, CD55, CD59, CFI, CFP, CFB, CD46, CFHR4, and CFHR1 proteins in Older-Normal and AMD cybrids. * P < 0.05, ** P < 0.01. n = 4–5. Data were analyzed using Student’s T-test.

Journal: PLoS ONE

Article Title: Differential Expression of Complement Markers in Normal and AMD Transmitochondrial Cybrids

doi: 10.1371/journal.pone.0159828

Figure Lengend Snippet: Decreased protein levels of CFH, CFHL1, CD55, CD59, CFI, and CD46, and increased levels of CFP, CFB, CFHR4, and CFHR1 protein in AMD cybrids. (A, C, E, G, I, K, M, O, Q, S) Representative Western blots of CFH, CFHL1, CD55, CD59, CFI, CFP, CFB, CD46, CFHR4, and CFHR1 respectively. (B, D, F, H, J, L, N, P, R, T) Graphs showing quantitation of CFH, CFHL1, CD55, CD59, CFI, CFP, CFB, CD46, CFHR4, and CFHR1 proteins in Older-Normal and AMD cybrids. * P < 0.05, ** P < 0.01. n = 4–5. Data were analyzed using Student’s T-test.

Techniques: Western Blot, Quantitation Assay

Journal: PLoS ONE

Article Title: Differential Expression of Complement Markers in Normal and AMD Transmitochondrial Cybrids

doi: 10.1371/journal.pone.0159828

Figure Lengend Snippet: Complement Protein Expression Data.

Techniques: Expressing

Characterization of Ad35K++. ( a ) Polyacrylamide sodium dodecyl sulfate (SDS) gel analysis of Ad35K++. Five micrograms of protein samples were loaded in Laemmli buffer containing β-mercaptoethanol with or without boiling for 5 minutes. The right graphic shows a schematic of Ad35K++ in the various states: Native Ad35K++ contains three monomers comprising the C-terminal, affinity-enhanced fiber knob, which interacts with CD46 and a shaft motif required for trimerization. During production, the monomer spontaneously trimerizes. When boiled under denaturing and reducing conditions, the trimer dissociates into monomers. ( b ) Ad35K++ activity in the rituximab complement-dependent cytotoxicity assay using Raji cells. Raji cells were incubated with Ad35K++ (25 µg/ml) for 8 hours followed by rituximab (15 µg/ml). After 30 minutes, normal human serum (NHS) was added and viable cells were counted 3 hours later based on trypan blue exclusion. Controls included incubation with phosphate-buffered saline (PBS)/NHS or rituximab/NHS. The viability of PBS/NHS-treated cells was taken as 100%. N = 3 independent experiments. Rituximab/NHS versus Ad35K++/rituximab/NHS: P < 0.001.

Journal: Molecular Therapy. Methods & Clinical Development

Article Title: Preclinical safety, pharmacokinetics, pharmacodynamics, and biodistribution studies with Ad35K++ protein: a novel rituximab cotherapeutic

doi: 10.1038/mtm.2016.13

Figure Lengend Snippet: Characterization of Ad35K++. ( a ) Polyacrylamide sodium dodecyl sulfate (SDS) gel analysis of Ad35K++. Five micrograms of protein samples were loaded in Laemmli buffer containing β-mercaptoethanol with or without boiling for 5 minutes. The right graphic shows a schematic of Ad35K++ in the various states: Native Ad35K++ contains three monomers comprising the C-terminal, affinity-enhanced fiber knob, which interacts with CD46 and a shaft motif required for trimerization. During production, the monomer spontaneously trimerizes. When boiled under denaturing and reducing conditions, the trimer dissociates into monomers. ( b ) Ad35K++ activity in the rituximab complement-dependent cytotoxicity assay using Raji cells. Raji cells were incubated with Ad35K++ (25 µg/ml) for 8 hours followed by rituximab (15 µg/ml). After 30 minutes, normal human serum (NHS) was added and viable cells were counted 3 hours later based on trypan blue exclusion. Controls included incubation with phosphate-buffered saline (PBS)/NHS or rituximab/NHS. The viability of PBS/NHS-treated cells was taken as 100%. N = 3 independent experiments. Rituximab/NHS versus Ad35K++/rituximab/NHS: P < 0.001.

Article Snippet: The mouse anti-human CD46 monoclonal antibody (clone 344519) and the goat anti-human CD46 polyclonal antibody were from R&D Systems (Minneapolis, MN).

Techniques: SDS-Gel, Activity Assay, CDC Assay, Incubation, Saline

Journal: Molecular Therapy. Methods & Clinical Development

Article Title: Preclinical safety, pharmacokinetics, pharmacodynamics, and biodistribution studies with Ad35K++ protein: a novel rituximab cotherapeutic

doi: 10.1038/mtm.2016.13

Figure Lengend Snippet: Pharmacokinetics (PK) and biodistribution studies in CD46tg mice. ( a ) Ad35K++ serum clearance. Ad35K++ serum concentrations were measured by enzyme-linked immunosorbent assay. Left panel: Summary of data from six animals. Right panel: Semi-log plots of average serum concentrations versus time profile (used for calculating the PK values). ( b ) Ad35K++ concentration in tissues at 6 hours after intravenous injection into hCD46 transgenic mice. Shown are Ad35K++ concentrations normalized to total protein as measured using the Bradford assay. N = 3.

Article Snippet: The mouse anti-human CD46 monoclonal antibody (clone 344519) and the goat anti-human CD46 polyclonal antibody were from R&D Systems (Minneapolis, MN).

Techniques: Drug discovery, Enzyme-linked Immunosorbent Assay, Concentration Assay, Injection, Transgenic Assay, Bradford Assay

In vivo activity of Ad35K++ in the Raji tumor xenograft mouse model. Immunodeficient CB17-SCID/beige mice received human lymphoma Raji cells via tail vein injection. ( a ) Three cycles of treatment were given at days 8, 11, and 14 after Raji cell injection (see arrows). Treatment groups were: (i) phosphate-buffered saline (PBS), (ii) Ad35K++ (2 mg/kg), (iii) rituximab (2 mg/kg), (iv) Ad35K++ followed 10 hours later by rituximab (“Ad35K++ → rituximab”), and (v) Ad35K++ given together with rituximab (“Ad35K++ plus rituximab”). Kaplan-Meier survival analysis with days of onset of hind leg paralysis as endpoints. N = 5. ( b ) CD46 shedding after Ad35K++ injection. Mice with established Raji tumors were intravenously injected with Ad35K++ at 2 mg/kg on day 17 after Raji cell injection (see arrow). The control group received PBS. Serum samples before and after Ad35K++/PBS injection were collected and CD46 was measured by enzyme-linked immunosorbent assay using antibodies that recognize the extracellular domain of CD46. N = 5.

Journal: Molecular Therapy. Methods & Clinical Development

Article Title: Preclinical safety, pharmacokinetics, pharmacodynamics, and biodistribution studies with Ad35K++ protein: a novel rituximab cotherapeutic

doi: 10.1038/mtm.2016.13

Figure Lengend Snippet: In vivo activity of Ad35K++ in the Raji tumor xenograft mouse model. Immunodeficient CB17-SCID/beige mice received human lymphoma Raji cells via tail vein injection. ( a ) Three cycles of treatment were given at days 8, 11, and 14 after Raji cell injection (see arrows). Treatment groups were: (i) phosphate-buffered saline (PBS), (ii) Ad35K++ (2 mg/kg), (iii) rituximab (2 mg/kg), (iv) Ad35K++ followed 10 hours later by rituximab (“Ad35K++ → rituximab”), and (v) Ad35K++ given together with rituximab (“Ad35K++ plus rituximab”). Kaplan-Meier survival analysis with days of onset of hind leg paralysis as endpoints. N = 5. ( b ) CD46 shedding after Ad35K++ injection. Mice with established Raji tumors were intravenously injected with Ad35K++ at 2 mg/kg on day 17 after Raji cell injection (see arrow). The control group received PBS. Serum samples before and after Ad35K++/PBS injection were collected and CD46 was measured by enzyme-linked immunosorbent assay using antibodies that recognize the extracellular domain of CD46. N = 5.

Article Snippet: The mouse anti-human CD46 monoclonal antibody (clone 344519) and the goat anti-human CD46 polyclonal antibody were from R&D Systems (Minneapolis, MN).

Techniques: In Vivo, Activity Assay, Injection, Saline, Control, Enzyme-linked Immunosorbent Assay

Soluble CD46 serum levels in M. fascicularis . CD46 was measured by enzyme-linked immunosorbent assay with human CD46 extracellular domain (ECD)-specific antibodies that cross-react with macaque CD46. ( a ) Results from animals that were in the dose finding study which went for 7 days. ( b,c ) Results from animals that were in the 14-day efficacy study ( b ) and 6-hour biodistribution study ( c ). Ad35K++ doses are indicated in each graph.

Journal: Molecular Therapy. Methods & Clinical Development

Article Title: Preclinical safety, pharmacokinetics, pharmacodynamics, and biodistribution studies with Ad35K++ protein: a novel rituximab cotherapeutic

doi: 10.1038/mtm.2016.13

Figure Lengend Snippet: Soluble CD46 serum levels in M. fascicularis . CD46 was measured by enzyme-linked immunosorbent assay with human CD46 extracellular domain (ECD)-specific antibodies that cross-react with macaque CD46. ( a ) Results from animals that were in the dose finding study which went for 7 days. ( b,c ) Results from animals that were in the 14-day efficacy study ( b ) and 6-hour biodistribution study ( c ). Ad35K++ doses are indicated in each graph.

Article Snippet: The mouse anti-human CD46 monoclonal antibody (clone 344519) and the goat anti-human CD46 polyclonal antibody were from R&D Systems (Minneapolis, MN).

Techniques: Enzyme-linked Immunosorbent Assay

Flow cytometry on M. fascicularis PBMC. ( a ) CD46 levels were assessed based on the mean fluorescence intensity (MFI) after staining with a goat polyclonal anti-CD46 antibody followed by an anti-goat Alexa Fluor 488 antibody. The relative percentage of CD46 MFI compared to pretreatment controls is shown. ( b ) Percentage relative to pretreated controls of CD20-, CD4-, CD8-, and PD-1-positive PBMC subsets. Differences in the baseline levels of subsets between individual animals are common in NHPs.

Journal: Molecular Therapy. Methods & Clinical Development

Article Title: Preclinical safety, pharmacokinetics, pharmacodynamics, and biodistribution studies with Ad35K++ protein: a novel rituximab cotherapeutic

doi: 10.1038/mtm.2016.13

Figure Lengend Snippet: Flow cytometry on M. fascicularis PBMC. ( a ) CD46 levels were assessed based on the mean fluorescence intensity (MFI) after staining with a goat polyclonal anti-CD46 antibody followed by an anti-goat Alexa Fluor 488 antibody. The relative percentage of CD46 MFI compared to pretreatment controls is shown. ( b ) Percentage relative to pretreated controls of CD20-, CD4-, CD8-, and PD-1-positive PBMC subsets. Differences in the baseline levels of subsets between individual animals are common in NHPs.

Article Snippet: The mouse anti-human CD46 monoclonal antibody (clone 344519) and the goat anti-human CD46 polyclonal antibody were from R&D Systems (Minneapolis, MN).

Techniques: Flow Cytometry, Fluorescence, Staining

Effect of Ad35K++ on rituximab killing of CD20 cells in M. fascicularis . Ad35K++ (4 mg/kg) was injected 10 minutes after preinjection samples (pre) were collected. Rituximab (0.01 mg/kg) was injected 10 minutes after day 2 blood samples were collected. The upper graph shows CD46 levels on CD20 cells (red lines) and the percentage of CD20+ cells compared to baseline (blue line). The lower graphs show a similar analysis of CD4+ cells.

Journal: Molecular Therapy. Methods & Clinical Development

Article Title: Preclinical safety, pharmacokinetics, pharmacodynamics, and biodistribution studies with Ad35K++ protein: a novel rituximab cotherapeutic

doi: 10.1038/mtm.2016.13

Figure Lengend Snippet: Effect of Ad35K++ on rituximab killing of CD20 cells in M. fascicularis . Ad35K++ (4 mg/kg) was injected 10 minutes after preinjection samples (pre) were collected. Rituximab (0.01 mg/kg) was injected 10 minutes after day 2 blood samples were collected. The upper graph shows CD46 levels on CD20 cells (red lines) and the percentage of CD20+ cells compared to baseline (blue line). The lower graphs show a similar analysis of CD4+ cells.

Article Snippet: The mouse anti-human CD46 monoclonal antibody (clone 344519) and the goat anti-human CD46 polyclonal antibody were from R&D Systems (Minneapolis, MN).

Techniques: Injection

Review

af2215 goat polyclonal anti human cd46 antibody r d systems (R&D Systems)

Structured Review

Images

1) Product Images from "An Unbiased Screen for Human Cytomegalovirus Identifies Neuropilin-2 as a Central Viral Receptor."

Related Articles

Activation Assay:

Binding Assay:

Membrane:

Lysis:

Control:

Marker:

Inhibition:

Variant Assay:

Western Blot:

Gene Expression:

Quantitation Assay:

Expressing:

Similar Products

Image Search Results