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Genentech inc recombinant soluble cd4 (scd4)

Binding of HIV-1 and <t>HIV-1-CD4</t> complexes to CAP coated wells. Suspensions (50 μl) of purified HIV-1 IIIB (6.8 × 10 9 virus particles/ml) and of HIV-1 BaL (2.5 × 10 9 virus particles/ml), respectively, in 0.1 M sodium acetate pH 7.0 were mixed with 5 μg of <t>sCD4</t> and incubated for 30 min at 20°C. sCD4 was not added to control virus preparations. The suspensions were cooled on ice and polyethylene glycol 6000 (PEG) was added to a final concentration of 3% to separate HIV-1 from sCD4 (which does not precipitate in 3% PEG). After 90 min at 4°C, the mixtures were centrifuged at 10,000 rpm, the supernatant fluids removed and the pellets washed once with 3% PEG in PBS containing 10 mg/ml BSA. The pellets were resuspended in sodium acetate buffer pH 7.0 containing 25 μg/ml BSA, and serial dilutions (indicated on the abscissa) were added to CAP coated and control wells, respectively. After incubation for 5 h at 4°C, the supernatant fluids were removed, the wells washed, and the bound virus quantitated by ELISA for p24 antigen. The amount of HIV-1 IIIB and HIV-1 BaL bound to control wells was ≤ 2.1% and ≤ 13%, respectively, of that bound to CAP coated wells. All experiments were done at least in triplicate.

Recombinant Soluble Cd4 (Scd4), supplied by Genentech inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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recombinant soluble cd4 (scd4) - by Bioz Stars, 2026-07

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1) Product Images from "Anti-HIV-1 activity of cellulose acetate phthalate: Synergy with soluble CD4 and induction of "dead-end" gp41 six-helix bundles"

Article Title: Anti-HIV-1 activity of cellulose acetate phthalate: Synergy with soluble CD4 and induction of "dead-end" gp41 six-helix bundles

Journal: BMC Infectious Diseases

doi: 10.1186/1471-2334-2-6

Binding of HIV-1 and HIV-1-CD4 complexes to CAP coated wells. Suspensions (50 μl) of purified HIV-1 IIIB (6.8 × 10 9 virus particles/ml) and of HIV-1 BaL (2.5 × 10 9 virus particles/ml), respectively, in 0.1 M sodium acetate pH 7.0 were mixed with 5 μg of sCD4 and incubated for 30 min at 20°C. sCD4 was not added to control virus preparations. The suspensions were cooled on ice and polyethylene glycol 6000 (PEG) was added to a final concentration of 3% to separate HIV-1 from sCD4 (which does not precipitate in 3% PEG). After 90 min at 4°C, the mixtures were centrifuged at 10,000 rpm, the supernatant fluids removed and the pellets washed once with 3% PEG in PBS containing 10 mg/ml BSA. The pellets were resuspended in sodium acetate buffer pH 7.0 containing 25 μg/ml BSA, and serial dilutions (indicated on the abscissa) were added to CAP coated and control wells, respectively. After incubation for 5 h at 4°C, the supernatant fluids were removed, the wells washed, and the bound virus quantitated by ELISA for p24 antigen. The amount of HIV-1 IIIB and HIV-1 BaL bound to control wells was ≤ 2.1% and ≤ 13%, respectively, of that bound to CAP coated wells. All experiments were done at least in triplicate.

Figure Legend Snippet: Binding of HIV-1 and HIV-1-CD4 complexes to CAP coated wells. Suspensions (50 μl) of purified HIV-1 IIIB (6.8 × 10 9 virus particles/ml) and of HIV-1 BaL (2.5 × 10 9 virus particles/ml), respectively, in 0.1 M sodium acetate pH 7.0 were mixed with 5 μg of sCD4 and incubated for 30 min at 20°C. sCD4 was not added to control virus preparations. The suspensions were cooled on ice and polyethylene glycol 6000 (PEG) was added to a final concentration of 3% to separate HIV-1 from sCD4 (which does not precipitate in 3% PEG). After 90 min at 4°C, the mixtures were centrifuged at 10,000 rpm, the supernatant fluids removed and the pellets washed once with 3% PEG in PBS containing 10 mg/ml BSA. The pellets were resuspended in sodium acetate buffer pH 7.0 containing 25 μg/ml BSA, and serial dilutions (indicated on the abscissa) were added to CAP coated and control wells, respectively. After incubation for 5 h at 4°C, the supernatant fluids were removed, the wells washed, and the bound virus quantitated by ELISA for p24 antigen. The amount of HIV-1 IIIB and HIV-1 BaL bound to control wells was ≤ 2.1% and ≤ 13%, respectively, of that bound to CAP coated wells. All experiments were done at least in triplicate.

Techniques Used: Binding Assay, Purification, Incubation, Concentration Assay, Enzyme-linked Immunosorbent Assay

Synergism between CAP and sCD4 for virucidal activity against HIV-1 IIIB. sCD4 was added to 50 μl of HIV-1 IIIB (6.8 × 10 9 virus particles/ml) in PBS. After 30 min at 20°C, CAP was added to final concentrations between 0 and 1250 μg/ml and the mixtures were incubated for 5 min at 37°C. CAP at the same concentrations described above was also added to virus not pretreated with sCD4. Virus suspensions were put on ice and PEG was added to a final concentration of 3% to separate HIV-1 from CAP and sCD4. After 90 min at 4°C, the mixtures were centrifuged at 10,000 rpm, the supernatant fluids removed and the pellets washed twice with 3% PEG in PBS containing 10 mg/ml BSA. The final washed pellets were resuspended in tissue culture medium, and serial 2-fold dilutions in the same medium were added to MT-2 cells. Infection was monitored by ELISA for p24 antigen. The gray horizontal line corresponds to virus inactivation (80.2 ± 1.3% of residual infectivity) caused by treatment with sCD4 in the absence of CAP. All experiments were done at least in triplicate.

Figure Legend Snippet: Synergism between CAP and sCD4 for virucidal activity against HIV-1 IIIB. sCD4 was added to 50 μl of HIV-1 IIIB (6.8 × 10 9 virus particles/ml) in PBS. After 30 min at 20°C, CAP was added to final concentrations between 0 and 1250 μg/ml and the mixtures were incubated for 5 min at 37°C. CAP at the same concentrations described above was also added to virus not pretreated with sCD4. Virus suspensions were put on ice and PEG was added to a final concentration of 3% to separate HIV-1 from CAP and sCD4. After 90 min at 4°C, the mixtures were centrifuged at 10,000 rpm, the supernatant fluids removed and the pellets washed twice with 3% PEG in PBS containing 10 mg/ml BSA. The final washed pellets were resuspended in tissue culture medium, and serial 2-fold dilutions in the same medium were added to MT-2 cells. Infection was monitored by ELISA for p24 antigen. The gray horizontal line corresponds to virus inactivation (80.2 ± 1.3% of residual infectivity) caused by treatment with sCD4 in the absence of CAP. All experiments were done at least in triplicate.

Techniques Used: Activity Assay, Incubation, Concentration Assay, Infection, Enzyme-linked Immunosorbent Assay

Treatment of HIV-1 with CAP enhances the expression of binding sites for mAb NC-1. Purified HIV-1 IIIB (6.8 × 10 9 virus particles) and HIV-1 BaL (2.5 × 10 9 virus particles), respectively, each in 100 μl PBS were incubated for 30 min at 20°C in the presence (5 μg) or absence of sCD4. Each sample was divided into two equal portions. CAP in 0.1 M acetate pH 6.0 was added to one aliquot (final concentration 5 mg/ml). An equivalent amount of acetate without CAP was added to the second aliquot. After incubation for 5 min at 37°C, the suspensions were cooled on ice and PEG was added to a final concentration of 3% to separate HIV-1 from sCD4 and CAP. After 90 min at 4°C, the mixtures were centrifuged at 10,000 rpm, the supernatant fluids removed and the pellets washed once with 3% PEG in PBS containing 10 mg/ml BSA. The final washed pelleted viruses were suspended in PBS containing 100 μg/ml of each BSA and gelatin, and dilutions (indicated on the abscissa) in the same buffer were added to mAb NC-1 coated and control wells. After 5 h at 4°C, the wells were washed and bound virus was quantitated by ELISA for p24 antigen. The amount of HIV-1 IIIB and HIV-1 BaL, respectively, bound to control wells was ≤ 2.1% and ≤ 6.1% of that bound to mAb NC-1 coated wells. All experiments were done at least in triplicate.

Figure Legend Snippet: Treatment of HIV-1 with CAP enhances the expression of binding sites for mAb NC-1. Purified HIV-1 IIIB (6.8 × 10 9 virus particles) and HIV-1 BaL (2.5 × 10 9 virus particles), respectively, each in 100 μl PBS were incubated for 30 min at 20°C in the presence (5 μg) or absence of sCD4. Each sample was divided into two equal portions. CAP in 0.1 M acetate pH 6.0 was added to one aliquot (final concentration 5 mg/ml). An equivalent amount of acetate without CAP was added to the second aliquot. After incubation for 5 min at 37°C, the suspensions were cooled on ice and PEG was added to a final concentration of 3% to separate HIV-1 from sCD4 and CAP. After 90 min at 4°C, the mixtures were centrifuged at 10,000 rpm, the supernatant fluids removed and the pellets washed once with 3% PEG in PBS containing 10 mg/ml BSA. The final washed pelleted viruses were suspended in PBS containing 100 μg/ml of each BSA and gelatin, and dilutions (indicated on the abscissa) in the same buffer were added to mAb NC-1 coated and control wells. After 5 h at 4°C, the wells were washed and bound virus was quantitated by ELISA for p24 antigen. The amount of HIV-1 IIIB and HIV-1 BaL, respectively, bound to control wells was ≤ 2.1% and ≤ 6.1% of that bound to mAb NC-1 coated wells. All experiments were done at least in triplicate.

Techniques Used: Expressing, Binding Assay, Purification, Incubation, Concentration Assay, Enzyme-linked Immunosorbent Assay

Binding of biotinyl-gp120, biotinyl-sCD4 and biotinyl-gp120-sCD4 complexes to CAP coated wells. Graded quantities of biotinyl-gp120 (indicated on the abscissa) and of biotinyl-gp120-sCD4 complexes were added to CAP coated and control wells. The complexes were prepared by mixing 1 μg of biotinyl-gp120 with 500 ng of sCD4 for 30 min at 20°C in PBS. To determine the effect of sCD4/gp120 ratios on gp120 binding to CAP, constant amounts (500 ng) of biotinyl-gp120 were mixed with graded quantities of sCD4 (0 to 1,000 ng) (insert) and the mixtures were further handled as described above. Binding of biotinyl-gp120 did not increase at sCD4/biotinyl-gp120 weight ratios >1 (data not shown). In control experiments, graded quantities of biotinyl-sCD4 in the absence of gp120 were added to the wells. After incubation at 4°C overnight, the wells were washed and bound biotinylated proteins were detected from subsequent binding of HRP-streptavidin. Absorbance corresponding to biotinylated proteins bound to control wells was in the range of 0–0.026 and was substracted from the absorbance corresponding to biotinylated proteins bound to CAP coated wells.

Figure Legend Snippet: Binding of biotinyl-gp120, biotinyl-sCD4 and biotinyl-gp120-sCD4 complexes to CAP coated wells. Graded quantities of biotinyl-gp120 (indicated on the abscissa) and of biotinyl-gp120-sCD4 complexes were added to CAP coated and control wells. The complexes were prepared by mixing 1 μg of biotinyl-gp120 with 500 ng of sCD4 for 30 min at 20°C in PBS. To determine the effect of sCD4/gp120 ratios on gp120 binding to CAP, constant amounts (500 ng) of biotinyl-gp120 were mixed with graded quantities of sCD4 (0 to 1,000 ng) (insert) and the mixtures were further handled as described above. Binding of biotinyl-gp120 did not increase at sCD4/biotinyl-gp120 weight ratios >1 (data not shown). In control experiments, graded quantities of biotinyl-sCD4 in the absence of gp120 were added to the wells. After incubation at 4°C overnight, the wells were washed and bound biotinylated proteins were detected from subsequent binding of HRP-streptavidin. Absorbance corresponding to biotinylated proteins bound to control wells was in the range of 0–0.026 and was substracted from the absorbance corresponding to biotinylated proteins bound to CAP coated wells.

Techniques Used: Binding Assay, Incubation

Figure Legend Snippet: Synergism between CAP and sCD4 in inhibiting infection by HIV-1 IIIB.

Techniques Used: Infection

Figure Legend Snippet: Synergism between CAP and sCD4 in inhibiting infection by HIV-1 BaL.

Techniques Used: Infection

Induction of gp41 six-helix bundles by HIV-1 treatment with sCD4, CAP, CCR5 S-peptide and heat. HIV-1 IIIB and HIV-1 BaL, respectively, were treated with CAP and sCD4 as described in the legend for Fig. or exposed to 60°C for 10 min. HIV-1 BaL was also treated with the S-peptide and a control non-sulfated peptide from CCR5 as described in the legend for Fig. . The treated virus preparations and untreated control virus were treated with lysis buffer (see Methods) for 30 min at 20°C. CAP in lysis buffer (0.078 to 10 mg/ml) was also tested; the results for a 5 mg/ml concentration are shown (identical results were obtained for all other concentrations). The lysates were tested by a sandwich ELISA for the gp41 six-helix bundle (see Methods). All experiments were done at least in triplicate.

Figure Legend Snippet: Induction of gp41 six-helix bundles by HIV-1 treatment with sCD4, CAP, CCR5 S-peptide and heat. HIV-1 IIIB and HIV-1 BaL, respectively, were treated with CAP and sCD4 as described in the legend for Fig. or exposed to 60°C for 10 min. HIV-1 BaL was also treated with the S-peptide and a control non-sulfated peptide from CCR5 as described in the legend for Fig. . The treated virus preparations and untreated control virus were treated with lysis buffer (see Methods) for 30 min at 20°C. CAP in lysis buffer (0.078 to 10 mg/ml) was also tested; the results for a 5 mg/ml concentration are shown (identical results were obtained for all other concentrations). The lysates were tested by a sandwich ELISA for the gp41 six-helix bundle (see Methods). All experiments were done at least in triplicate.

Techniques Used: Lysis, Concentration Assay, Sandwich ELISA

Electrostatic potential maps of gp120 and the gp120-CD4 complex. Electrostatic potentials are shown for the solvent accessible surfaces. (A) The electrostatic potential map on gp120. Blue indicates electropositive areas whereas red represents electronegative areas. (B) After CD4 binds to gp120, the electropositive surface area (blue) increases markedly while the most negatively charged (red) area on gp120 (arrow) becomes blocked by sCD4.

Figure Legend Snippet: Electrostatic potential maps of gp120 and the gp120-CD4 complex. Electrostatic potentials are shown for the solvent accessible surfaces. (A) The electrostatic potential map on gp120. Blue indicates electropositive areas whereas red represents electronegative areas. (B) After CD4 binds to gp120, the electropositive surface area (blue) increases markedly while the most negatively charged (red) area on gp120 (arrow) becomes blocked by sCD4.

Techniques Used:

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Journal: BMC Infectious Diseases

Article Title: Anti-HIV-1 activity of cellulose acetate phthalate: Synergy with soluble CD4 and induction of "dead-end" gp41 six-helix bundles

doi: 10.1186/1471-2334-2-6

Figure Lengend Snippet: Binding of HIV-1 and HIV-1-CD4 complexes to CAP coated wells. Suspensions (50 μl) of purified HIV-1 IIIB (6.8 × 10 9 virus particles/ml) and of HIV-1 BaL (2.5 × 10 9 virus particles/ml), respectively, in 0.1 M sodium acetate pH 7.0 were mixed with 5 μg of sCD4 and incubated for 30 min at 20°C. sCD4 was not added to control virus preparations. The suspensions were cooled on ice and polyethylene glycol 6000 (PEG) was added to a final concentration of 3% to separate HIV-1 from sCD4 (which does not precipitate in 3% PEG). After 90 min at 4°C, the mixtures were centrifuged at 10,000 rpm, the supernatant fluids removed and the pellets washed once with 3% PEG in PBS containing 10 mg/ml BSA. The pellets were resuspended in sodium acetate buffer pH 7.0 containing 25 μg/ml BSA, and serial dilutions (indicated on the abscissa) were added to CAP coated and control wells, respectively. After incubation for 5 h at 4°C, the supernatant fluids were removed, the wells washed, and the bound virus quantitated by ELISA for p24 antigen. The amount of HIV-1 IIIB and HIV-1 BaL bound to control wells was ≤ 2.1% and ≤ 13%, respectively, of that bound to CAP coated wells. All experiments were done at least in triplicate.

Article Snippet: Recombinant soluble CD4 (sCD4) was from Genentech Inc., South San Francisco, CA.

Techniques: Binding Assay, Purification, Incubation, Concentration Assay, Enzyme-linked Immunosorbent Assay

Journal: BMC Infectious Diseases

Article Title: Anti-HIV-1 activity of cellulose acetate phthalate: Synergy with soluble CD4 and induction of "dead-end" gp41 six-helix bundles

doi: 10.1186/1471-2334-2-6

Figure Lengend Snippet: Synergism between CAP and sCD4 for virucidal activity against HIV-1 IIIB. sCD4 was added to 50 μl of HIV-1 IIIB (6.8 × 10 9 virus particles/ml) in PBS. After 30 min at 20°C, CAP was added to final concentrations between 0 and 1250 μg/ml and the mixtures were incubated for 5 min at 37°C. CAP at the same concentrations described above was also added to virus not pretreated with sCD4. Virus suspensions were put on ice and PEG was added to a final concentration of 3% to separate HIV-1 from CAP and sCD4. After 90 min at 4°C, the mixtures were centrifuged at 10,000 rpm, the supernatant fluids removed and the pellets washed twice with 3% PEG in PBS containing 10 mg/ml BSA. The final washed pellets were resuspended in tissue culture medium, and serial 2-fold dilutions in the same medium were added to MT-2 cells. Infection was monitored by ELISA for p24 antigen. The gray horizontal line corresponds to virus inactivation (80.2 ± 1.3% of residual infectivity) caused by treatment with sCD4 in the absence of CAP. All experiments were done at least in triplicate.

Article Snippet: Recombinant soluble CD4 (sCD4) was from Genentech Inc., South San Francisco, CA.

Techniques: Activity Assay, Incubation, Concentration Assay, Infection, Enzyme-linked Immunosorbent Assay

Journal: BMC Infectious Diseases

Article Title: Anti-HIV-1 activity of cellulose acetate phthalate: Synergy with soluble CD4 and induction of "dead-end" gp41 six-helix bundles

doi: 10.1186/1471-2334-2-6

Figure Lengend Snippet: Treatment of HIV-1 with CAP enhances the expression of binding sites for mAb NC-1. Purified HIV-1 IIIB (6.8 × 10 9 virus particles) and HIV-1 BaL (2.5 × 10 9 virus particles), respectively, each in 100 μl PBS were incubated for 30 min at 20°C in the presence (5 μg) or absence of sCD4. Each sample was divided into two equal portions. CAP in 0.1 M acetate pH 6.0 was added to one aliquot (final concentration 5 mg/ml). An equivalent amount of acetate without CAP was added to the second aliquot. After incubation for 5 min at 37°C, the suspensions were cooled on ice and PEG was added to a final concentration of 3% to separate HIV-1 from sCD4 and CAP. After 90 min at 4°C, the mixtures were centrifuged at 10,000 rpm, the supernatant fluids removed and the pellets washed once with 3% PEG in PBS containing 10 mg/ml BSA. The final washed pelleted viruses were suspended in PBS containing 100 μg/ml of each BSA and gelatin, and dilutions (indicated on the abscissa) in the same buffer were added to mAb NC-1 coated and control wells. After 5 h at 4°C, the wells were washed and bound virus was quantitated by ELISA for p24 antigen. The amount of HIV-1 IIIB and HIV-1 BaL, respectively, bound to control wells was ≤ 2.1% and ≤ 6.1% of that bound to mAb NC-1 coated wells. All experiments were done at least in triplicate.

Article Snippet: Recombinant soluble CD4 (sCD4) was from Genentech Inc., South San Francisco, CA.

Techniques: Expressing, Binding Assay, Purification, Incubation, Concentration Assay, Enzyme-linked Immunosorbent Assay

Journal: BMC Infectious Diseases

Article Title: Anti-HIV-1 activity of cellulose acetate phthalate: Synergy with soluble CD4 and induction of "dead-end" gp41 six-helix bundles

doi: 10.1186/1471-2334-2-6

Figure Lengend Snippet: Binding of biotinyl-gp120, biotinyl-sCD4 and biotinyl-gp120-sCD4 complexes to CAP coated wells. Graded quantities of biotinyl-gp120 (indicated on the abscissa) and of biotinyl-gp120-sCD4 complexes were added to CAP coated and control wells. The complexes were prepared by mixing 1 μg of biotinyl-gp120 with 500 ng of sCD4 for 30 min at 20°C in PBS. To determine the effect of sCD4/gp120 ratios on gp120 binding to CAP, constant amounts (500 ng) of biotinyl-gp120 were mixed with graded quantities of sCD4 (0 to 1,000 ng) (insert) and the mixtures were further handled as described above. Binding of biotinyl-gp120 did not increase at sCD4/biotinyl-gp120 weight ratios >1 (data not shown). In control experiments, graded quantities of biotinyl-sCD4 in the absence of gp120 were added to the wells. After incubation at 4°C overnight, the wells were washed and bound biotinylated proteins were detected from subsequent binding of HRP-streptavidin. Absorbance corresponding to biotinylated proteins bound to control wells was in the range of 0–0.026 and was substracted from the absorbance corresponding to biotinylated proteins bound to CAP coated wells.

Article Snippet: Recombinant soluble CD4 (sCD4) was from Genentech Inc., South San Francisco, CA.

Techniques: Binding Assay, Incubation

Journal: BMC Infectious Diseases

Article Title: Anti-HIV-1 activity of cellulose acetate phthalate: Synergy with soluble CD4 and induction of "dead-end" gp41 six-helix bundles

doi: 10.1186/1471-2334-2-6

Figure Lengend Snippet: Synergism between CAP and sCD4 in inhibiting infection by HIV-1 IIIB.

Article Snippet: Recombinant soluble CD4 (sCD4) was from Genentech Inc., South San Francisco, CA.

Techniques: Infection

Journal: BMC Infectious Diseases

Article Title: Anti-HIV-1 activity of cellulose acetate phthalate: Synergy with soluble CD4 and induction of "dead-end" gp41 six-helix bundles

doi: 10.1186/1471-2334-2-6

Figure Lengend Snippet: Synergism between CAP and sCD4 in inhibiting infection by HIV-1 BaL.

Article Snippet: Recombinant soluble CD4 (sCD4) was from Genentech Inc., South San Francisco, CA.

Techniques: Infection

Journal: BMC Infectious Diseases

Article Title: Anti-HIV-1 activity of cellulose acetate phthalate: Synergy with soluble CD4 and induction of "dead-end" gp41 six-helix bundles

doi: 10.1186/1471-2334-2-6

Figure Lengend Snippet: Induction of gp41 six-helix bundles by HIV-1 treatment with sCD4, CAP, CCR5 S-peptide and heat. HIV-1 IIIB and HIV-1 BaL, respectively, were treated with CAP and sCD4 as described in the legend for Fig. or exposed to 60°C for 10 min. HIV-1 BaL was also treated with the S-peptide and a control non-sulfated peptide from CCR5 as described in the legend for Fig. . The treated virus preparations and untreated control virus were treated with lysis buffer (see Methods) for 30 min at 20°C. CAP in lysis buffer (0.078 to 10 mg/ml) was also tested; the results for a 5 mg/ml concentration are shown (identical results were obtained for all other concentrations). The lysates were tested by a sandwich ELISA for the gp41 six-helix bundle (see Methods). All experiments were done at least in triplicate.

Article Snippet: Recombinant soluble CD4 (sCD4) was from Genentech Inc., South San Francisco, CA.

Techniques: Lysis, Concentration Assay, Sandwich ELISA

Journal: BMC Infectious Diseases

Article Title: Anti-HIV-1 activity of cellulose acetate phthalate: Synergy with soluble CD4 and induction of "dead-end" gp41 six-helix bundles

doi: 10.1186/1471-2334-2-6

Figure Lengend Snippet: Electrostatic potential maps of gp120 and the gp120-CD4 complex. Electrostatic potentials are shown for the solvent accessible surfaces. (A) The electrostatic potential map on gp120. Blue indicates electropositive areas whereas red represents electronegative areas. (B) After CD4 binds to gp120, the electropositive surface area (blue) increases markedly while the most negatively charged (red) area on gp120 (arrow) becomes blocked by sCD4.

Article Snippet: Recombinant soluble CD4 (sCD4) was from Genentech Inc., South San Francisco, CA.

Techniques:

Fig. 4 Binding enhancement of mAbs and their fragments to Env in the presence of sCD4. Binding activity to 293T cells expressing Env of JR-FL was examined using flow cytometry. Histogram of fluorescence intensity shows the binding of negative control (gray), mAb alone (blue) and in the presence of sCD4 (red). Enhancement of binding by CD4 engagement against trimeric Env expressed on the cellular surface was observed for anti- CD4i IgG as well as their fragments

Journal: Retrovirology

Article Title: Unique binding modes for the broad neutralizing activity of single-chain variable fragments (scFv) targeting CD4-induced epitopes.

doi: 10.1186/s12977-017-0369-y

Figure Lengend Snippet: Fig. 4 Binding enhancement of mAbs and their fragments to Env in the presence of sCD4. Binding activity to 293T cells expressing Env of JR-FL was examined using flow cytometry. Histogram of fluorescence intensity shows the binding of negative control (gray), mAb alone (blue) and in the presence of sCD4 (red). Enhancement of binding by CD4 engagement against trimeric Env expressed on the cellular surface was observed for anti- CD4i IgG as well as their fragments

Article Snippet: Recombinant human soluble CD4 (sCD4) was purchased commercially (R&D Systems Inc., Minneapolis, MN, USA).

Techniques: Binding Assay, Activity Assay, Expressing, Flow Cytometry, Fluorescence, Negative Control

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