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pcig3n (n-tropic mlv gag-pol)  (Addgene inc)


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    Addgene inc pcig3n (n-tropic mlv gag-pol)
    Pcig3n (N Tropic Mlv Gag Pol), supplied by Addgene 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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    a , b Neutralization potency ( a ) and breadth ( b ) of FD22, in comparison with VRC01, against a 145-isolate Env-pseudovirus panel. c , d The neutralization activity ( c ) and percentage ( d ) of FD22 were evaluated against different clades of HIV-1 pseudoviruses from a 145-virus panel, including the two predominant circulating strains in China, CRF01_AE and CRF07_BC. VRC01 served as a control. e Activation of HIV-1 latency in ACH-2 cells. HIV-1 latency reversal in ACH-2 cells was induced by treatment with TNF-α or panobinostat for 48 h. Viral reactivation was assessed by quantifying <t>p24</t> antigen concentrations using a standardized ELISA. f Inhibitory activity of FD22 against latent HIV-1 in ACH-2 cells activated by TNF-α or panobinostat, as measured in TZM-bl cells. ACH-2 cells were treated with TNF-α (10 ng/mL) or panobinostat (1 μM) to induce HIV-1 reactivation. After activation, FD22 was added at various concentrations to assess its inhibitory activity. Reactivated virus production was measured by coculturing supernatants from treated ACH-2 cells with TZM-bl indicator cells.
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    a , b Neutralization potency ( a ) and breadth ( b ) of FD22, in comparison with VRC01, against a 145-isolate Env-pseudovirus panel. c , d The neutralization activity ( c ) and percentage ( d ) of FD22 were evaluated against different clades of HIV-1 pseudoviruses from a 145-virus panel, including the two predominant circulating strains in China, CRF01_AE and CRF07_BC. VRC01 served as a control. e Activation of HIV-1 latency in ACH-2 cells. HIV-1 latency reversal in ACH-2 cells was induced by treatment with TNF-α or panobinostat for 48 h. Viral reactivation was assessed by quantifying <t>p24</t> antigen concentrations using a standardized ELISA. f Inhibitory activity of FD22 against latent HIV-1 in ACH-2 cells activated by TNF-α or panobinostat, as measured in TZM-bl cells. ACH-2 cells were treated with TNF-α (10 ng/mL) or panobinostat (1 μM) to induce HIV-1 reactivation. After activation, FD22 was added at various concentrations to assess its inhibitory activity. Reactivated virus production was measured by coculturing supernatants from treated ACH-2 cells with TZM-bl indicator cells.
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    a , b Neutralization potency ( a ) and breadth ( b ) of FD22, in comparison with VRC01, against a 145-isolate Env-pseudovirus panel. c , d The neutralization activity ( c ) and percentage ( d ) of FD22 were evaluated against different clades of HIV-1 pseudoviruses from a 145-virus panel, including the two predominant circulating strains in China, CRF01_AE and CRF07_BC. VRC01 served as a control. e Activation of HIV-1 latency in ACH-2 cells. HIV-1 latency reversal in ACH-2 cells was induced by treatment with TNF-α or panobinostat for 48 h. Viral reactivation was assessed by quantifying p24 antigen concentrations using a standardized ELISA. f Inhibitory activity of FD22 against latent HIV-1 in ACH-2 cells activated by TNF-α or panobinostat, as measured in TZM-bl cells. ACH-2 cells were treated with TNF-α (10 ng/mL) or panobinostat (1 μM) to induce HIV-1 reactivation. After activation, FD22 was added at various concentrations to assess its inhibitory activity. Reactivated virus production was measured by coculturing supernatants from treated ACH-2 cells with TZM-bl indicator cells.

    Journal: Cell Discovery

    Article Title: A potent and broad CD4 binding site neutralizing antibody with strong ADCC activity from a Chinese HIV-1 elite neutralizer

    doi: 10.1038/s41421-025-00808-x

    Figure Lengend Snippet: a , b Neutralization potency ( a ) and breadth ( b ) of FD22, in comparison with VRC01, against a 145-isolate Env-pseudovirus panel. c , d The neutralization activity ( c ) and percentage ( d ) of FD22 were evaluated against different clades of HIV-1 pseudoviruses from a 145-virus panel, including the two predominant circulating strains in China, CRF01_AE and CRF07_BC. VRC01 served as a control. e Activation of HIV-1 latency in ACH-2 cells. HIV-1 latency reversal in ACH-2 cells was induced by treatment with TNF-α or panobinostat for 48 h. Viral reactivation was assessed by quantifying p24 antigen concentrations using a standardized ELISA. f Inhibitory activity of FD22 against latent HIV-1 in ACH-2 cells activated by TNF-α or panobinostat, as measured in TZM-bl cells. ACH-2 cells were treated with TNF-α (10 ng/mL) or panobinostat (1 μM) to induce HIV-1 reactivation. After activation, FD22 was added at various concentrations to assess its inhibitory activity. Reactivated virus production was measured by coculturing supernatants from treated ACH-2 cells with TZM-bl indicator cells.

    Article Snippet: Rabbit polyclonal anti-Gag-p24 antibodies (Sino Biological Inc.) were used to coat ELISA plates.

    Techniques: Neutralization, Comparison, Activity Assay, Virus, Control, Activation Assay, Enzyme-linked Immunosorbent Assay