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    Worthington Biochemical reagents recombinant hiv 1 reverse transcriptase
    Alignment of sequences flanking RNA 5′ end-directed cleavage sites recognized by <t>HIV-1</t> RNase H ). In the center column, the sequence surrounding each cleavage site is given, with the location of the cleavage site represented as a gap. The right column gives the position of each cleavage site counting from the 5′ end of the RNA.
    Reagents Recombinant Hiv 1 Reverse Transcriptase, supplied by Worthington Biochemical, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/reagents recombinant hiv 1 reverse transcriptase/product/Worthington Biochemical
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    reagents recombinant hiv 1 reverse transcriptase - by Bioz Stars, 2022-10
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    80
    R&D Systems ccr5 inhibitor maraviroc
    Mechanisms of reduced infectivity in MDDCs and MDMs. (A) RNAseq data showing IFN-subtype gene induction in pDCs at 18 hours post HIV exposure versus mock. (B-C) The median FI of maturation markers, CD80 (n = 9) and CD86 (n = 10) in MDDCs that were either mock, HIV infected MDDCs in the presence and absence of pDCs, and in HIV infected MDDCs treated with exogenous rIFNα8 and/or rTNFα, HIV infected MDDCs treated with antibodies to blocking IFN and/or TNF signaling in pDC cocultures (n = 4 for CD80, n = 5 for CD86). Data is shown as normalized to 100% in mock infected. (D) pDC decreased <t>CCR5</t> median FI in HIV-infected MDDCs (n = 5) and MDMs (n = 7). Data is shown as normalized to 100% in mock infected. (E) Changes in p24 expression at 5 dpi in MDDCs (n = 5) (top panel) and MDMs (n = 5) (bottom panel) upon addition of exogenous rIFNα8 and/or rTNFα, or upon blocking IFN and/or TNF signaling in pDC cocultures. Data was normalized to 100% in HIV infected cells in the absence of pDCs. For all data, *p
    Ccr5 Inhibitor Maraviroc, supplied by R&D Systems, used in various techniques. Bioz Stars score: 80/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ccr5 inhibitor maraviroc/product/R&D Systems
    Average 80 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ccr5 inhibitor maraviroc - by Bioz Stars, 2022-10
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    Image Search Results


    Alignment of sequences flanking RNA 5′ end-directed cleavage sites recognized by HIV-1 RNase H ). In the center column, the sequence surrounding each cleavage site is given, with the location of the cleavage site represented as a gap. The right column gives the position of each cleavage site counting from the 5′ end of the RNA.

    Journal: The Journal of biological chemistry

    Article Title: Sequence, Distance, and Accessibility are Determinants of 5? End-Directed Cleavages by Retroviral RNases H *

    doi: 10.1074/jbc.M510504200

    Figure Lengend Snippet: Alignment of sequences flanking RNA 5′ end-directed cleavage sites recognized by HIV-1 RNase H ). In the center column, the sequence surrounding each cleavage site is given, with the location of the cleavage site represented as a gap. The right column gives the position of each cleavage site counting from the 5′ end of the RNA.

    Article Snippet: Enzymes and reagents —Recombinant HIV-1 reverse transcriptase was obtained from Worthington Biochemicals.

    Techniques: Sequencing

    Comparison of HIV-1 and M-MuLV RNase H 5′ end-directed cleavages in the sequences of RNAs Md1 - Md10 . The sequences of the 29-mer RNAs Md1 through Md10 are aligned by the RNA 5′ ends to compare the positions of 5′ end-directed cleavage sites. In each sequence, the extent of cleavage at a site is indicated as strong (large arrows) or medium (small arrows) for HIV-1 reverse transcriptase (above) or M-MuLV reverse transcriptase (below). As described in the Discussion, the range of the closest and furthest independent 5′ end-directed cleavage sites is indicated by the positions of the bordering nucleotides from the RNA 5′ end, the position of site G in substrates Md1 and Md7 is indicated, and the grey box highlights nucleotide positions +13 and +20 that include the range of distances where the 5′ end-directed cleavages occur.

    Journal: The Journal of biological chemistry

    Article Title: Sequence, Distance, and Accessibility are Determinants of 5? End-Directed Cleavages by Retroviral RNases H *

    doi: 10.1074/jbc.M510504200

    Figure Lengend Snippet: Comparison of HIV-1 and M-MuLV RNase H 5′ end-directed cleavages in the sequences of RNAs Md1 - Md10 . The sequences of the 29-mer RNAs Md1 through Md10 are aligned by the RNA 5′ ends to compare the positions of 5′ end-directed cleavage sites. In each sequence, the extent of cleavage at a site is indicated as strong (large arrows) or medium (small arrows) for HIV-1 reverse transcriptase (above) or M-MuLV reverse transcriptase (below). As described in the Discussion, the range of the closest and furthest independent 5′ end-directed cleavage sites is indicated by the positions of the bordering nucleotides from the RNA 5′ end, the position of site G in substrates Md1 and Md7 is indicated, and the grey box highlights nucleotide positions +13 and +20 that include the range of distances where the 5′ end-directed cleavages occur.

    Article Snippet: Enzymes and reagents —Recombinant HIV-1 reverse transcriptase was obtained from Worthington Biochemicals.

    Techniques: Sequencing

    Extent of cleavage and optimal distances for cleavage at sites F, G, and H in RNAs Md1 through Md10 by HIV-1 and M-MuLV reverse transcriptases . The amount of product generated by cleavage (% of total) at sites F, G, and H in the indicated substrates was determined for HIV-1 (A) or M-MuLV (B) reverse transcriptase. Data from the 1 min time points in three (A) or four (B) independent experiments with 5′ end-labeled RNAs were used to determine the amount of product that resulted from the cleavages at site F (gray bars), site G (black bars), or site H (white bars) (± S.D.). These same data were also used to analyze the optimal distance for cleavage of each site relative to the 5′ RNA ends for HIV-1 (C) or M-MuLV (D) reverse transcriptase. The amount of product generated by cleavage (% of total) for sites F (gray squares), G (black circles), or H (open triangles) is plotted as a function of the cleavage site distance in nucleotides from the 5′ end of each substrate.

    Journal: The Journal of biological chemistry

    Article Title: Sequence, Distance, and Accessibility are Determinants of 5? End-Directed Cleavages by Retroviral RNases H *

    doi: 10.1074/jbc.M510504200

    Figure Lengend Snippet: Extent of cleavage and optimal distances for cleavage at sites F, G, and H in RNAs Md1 through Md10 by HIV-1 and M-MuLV reverse transcriptases . The amount of product generated by cleavage (% of total) at sites F, G, and H in the indicated substrates was determined for HIV-1 (A) or M-MuLV (B) reverse transcriptase. Data from the 1 min time points in three (A) or four (B) independent experiments with 5′ end-labeled RNAs were used to determine the amount of product that resulted from the cleavages at site F (gray bars), site G (black bars), or site H (white bars) (± S.D.). These same data were also used to analyze the optimal distance for cleavage of each site relative to the 5′ RNA ends for HIV-1 (C) or M-MuLV (D) reverse transcriptase. The amount of product generated by cleavage (% of total) for sites F (gray squares), G (black circles), or H (open triangles) is plotted as a function of the cleavage site distance in nucleotides from the 5′ end of each substrate.

    Article Snippet: Enzymes and reagents —Recombinant HIV-1 reverse transcriptase was obtained from Worthington Biochemicals.

    Techniques: Generated, Labeling

    Mechanisms of reduced infectivity in MDDCs and MDMs. (A) RNAseq data showing IFN-subtype gene induction in pDCs at 18 hours post HIV exposure versus mock. (B-C) The median FI of maturation markers, CD80 (n = 9) and CD86 (n = 10) in MDDCs that were either mock, HIV infected MDDCs in the presence and absence of pDCs, and in HIV infected MDDCs treated with exogenous rIFNα8 and/or rTNFα, HIV infected MDDCs treated with antibodies to blocking IFN and/or TNF signaling in pDC cocultures (n = 4 for CD80, n = 5 for CD86). Data is shown as normalized to 100% in mock infected. (D) pDC decreased CCR5 median FI in HIV-infected MDDCs (n = 5) and MDMs (n = 7). Data is shown as normalized to 100% in mock infected. (E) Changes in p24 expression at 5 dpi in MDDCs (n = 5) (top panel) and MDMs (n = 5) (bottom panel) upon addition of exogenous rIFNα8 and/or rTNFα, or upon blocking IFN and/or TNF signaling in pDC cocultures. Data was normalized to 100% in HIV infected cells in the absence of pDCs. For all data, *p

    Journal: PLoS Pathogens

    Article Title: Plasmacytoid dendritic cells have divergent effects on HIV infection of initial target cells and induce a pro-retention phenotype

    doi: 10.1371/journal.ppat.1009522

    Figure Lengend Snippet: Mechanisms of reduced infectivity in MDDCs and MDMs. (A) RNAseq data showing IFN-subtype gene induction in pDCs at 18 hours post HIV exposure versus mock. (B-C) The median FI of maturation markers, CD80 (n = 9) and CD86 (n = 10) in MDDCs that were either mock, HIV infected MDDCs in the presence and absence of pDCs, and in HIV infected MDDCs treated with exogenous rIFNα8 and/or rTNFα, HIV infected MDDCs treated with antibodies to blocking IFN and/or TNF signaling in pDC cocultures (n = 4 for CD80, n = 5 for CD86). Data is shown as normalized to 100% in mock infected. (D) pDC decreased CCR5 median FI in HIV-infected MDDCs (n = 5) and MDMs (n = 7). Data is shown as normalized to 100% in mock infected. (E) Changes in p24 expression at 5 dpi in MDDCs (n = 5) (top panel) and MDMs (n = 5) (bottom panel) upon addition of exogenous rIFNα8 and/or rTNFα, or upon blocking IFN and/or TNF signaling in pDC cocultures. Data was normalized to 100% in HIV infected cells in the absence of pDCs. For all data, *p

    Article Snippet: These reagents included: an inhibitor of the intercellular adhesion molecule and component of the immunologic synapse (anti-ICAM-1, 10μg/mL, R & D systems, clone BBIG-I1); the CCR5 inhibitor maraviroc (10μM, AIDS Reagent Program); the reverse transcription inhibitor Zidovudine (50μM, AIDS Reagent Program); neutralising antibodies to receptors of IFN (IFNAR, 20μg/mL, PBL Assay Science, clone MMHAR-2) and TNF (TNFR1, 10μg/mL, R & D systems, clone 16803) in addition to neutralising antibodies for secreted IFNα8 (20000U/mL, PBL Assay Science), IFNβ (5000U/mL, PBL Assay Science) and TNFα (1μg/mL, R & D systems) to block signalling pathways of INF and TNF; recombinant (r) human TNFα (10ng/mL, R & D systems) and rIFNα8 (PBL Assay Science) was used at 350ng/mL for MDDCs and MDMs and at a graded concentration of 300, 600 and 900ng/mL for TCM, TTM and TEM based on the amount of IFNα detected by ELISA in infected MDDCs ( ) and T cell subsets ( ) upon their co-culture with pDCs.

    Techniques: Infection, Blocking Assay, Expressing

    Addition of pDCs increased intracellular HIV expression but not extracellular virus production in memory CD4 T cells. (A) Workflow for generating memory T cell-pDC cocultures: memory CD4 T cells were sorted into resting TCM, TTM and TEM subsets. Sorted cells were infected with either HIV BaL or HIV TF (MOI of 0.75) overnight. They were cultured for further 2 days before the addition of pDCs. (B) Representative dot plots showing p24 expression at 5 dpi in resting TCM, TTM and TEM that were infected with HIV BaL in the absence (HIV) or presence of pDCs (HIV+pDC). (C) Mean percentage of p24 + cells at 5 dpi with HIV BaL (n = 11). (D) CCR5 expression across T cell subsets in the presence and absence of pDCs (n = 11). (E) Mean percentage of p24 + cells at 5 dpi with the HIV TF in the presence or absence of pDCs (n = 7). (F) Assessment of extracellular viral production by the reverse transcriptase assay using supernatants derived from infected resting CD4 T cell subsets in the absence (HIV) or presence of pDCs (HIV+pDC) (n = 2–5). (G) Same as in F but using p24 ELISA on supernatants derived from infected resting TEM cells (n = 2). For all data, *p

    Journal: PLoS Pathogens

    Article Title: Plasmacytoid dendritic cells have divergent effects on HIV infection of initial target cells and induce a pro-retention phenotype

    doi: 10.1371/journal.ppat.1009522

    Figure Lengend Snippet: Addition of pDCs increased intracellular HIV expression but not extracellular virus production in memory CD4 T cells. (A) Workflow for generating memory T cell-pDC cocultures: memory CD4 T cells were sorted into resting TCM, TTM and TEM subsets. Sorted cells were infected with either HIV BaL or HIV TF (MOI of 0.75) overnight. They were cultured for further 2 days before the addition of pDCs. (B) Representative dot plots showing p24 expression at 5 dpi in resting TCM, TTM and TEM that were infected with HIV BaL in the absence (HIV) or presence of pDCs (HIV+pDC). (C) Mean percentage of p24 + cells at 5 dpi with HIV BaL (n = 11). (D) CCR5 expression across T cell subsets in the presence and absence of pDCs (n = 11). (E) Mean percentage of p24 + cells at 5 dpi with the HIV TF in the presence or absence of pDCs (n = 7). (F) Assessment of extracellular viral production by the reverse transcriptase assay using supernatants derived from infected resting CD4 T cell subsets in the absence (HIV) or presence of pDCs (HIV+pDC) (n = 2–5). (G) Same as in F but using p24 ELISA on supernatants derived from infected resting TEM cells (n = 2). For all data, *p

    Article Snippet: These reagents included: an inhibitor of the intercellular adhesion molecule and component of the immunologic synapse (anti-ICAM-1, 10μg/mL, R & D systems, clone BBIG-I1); the CCR5 inhibitor maraviroc (10μM, AIDS Reagent Program); the reverse transcription inhibitor Zidovudine (50μM, AIDS Reagent Program); neutralising antibodies to receptors of IFN (IFNAR, 20μg/mL, PBL Assay Science, clone MMHAR-2) and TNF (TNFR1, 10μg/mL, R & D systems, clone 16803) in addition to neutralising antibodies for secreted IFNα8 (20000U/mL, PBL Assay Science), IFNβ (5000U/mL, PBL Assay Science) and TNFα (1μg/mL, R & D systems) to block signalling pathways of INF and TNF; recombinant (r) human TNFα (10ng/mL, R & D systems) and rIFNα8 (PBL Assay Science) was used at 350ng/mL for MDDCs and MDMs and at a graded concentration of 300, 600 and 900ng/mL for TCM, TTM and TEM based on the amount of IFNα detected by ELISA in infected MDDCs ( ) and T cell subsets ( ) upon their co-culture with pDCs.

    Techniques: Expressing, Transmission Electron Microscopy, Infection, Cell Culture, Reverse Transcriptase Assay, Derivative Assay, Enzyme-linked Immunosorbent Assay

    Mechanisms of p24 and CD69 induction by pDCs. (A) Normalised p24 expression in resting TEM cells infected with HIV and treated with neutralising antibody to ICAM-1 for 2 hours prior to addition of pDCs (n = 4). (B-C) The effect of virus depleted supernatants (from TEM-pDC cocultures or pDCs) in modulating p24 and CD69 expression in HIV-infected TEM cells (n = 6). (D) Normalised p24 expression and (E) percentage of CD69 expression in resting TEM cells (n = 5) upon modulation of IFN-signaling and/or TNF-signaling via: the addition of exogenous IFNα8 and/or TNFα; blocking the IFNAR1, IFNα and β and/or TNFR1 and TNFα via neutralizing antibodies (a-IFN and a-TNF). (F) Normalised p24 expression in resting TEM cells infected with HIV and treated with maraviroc for 2 hours prior to addition of pDCs (n = 4). (G) Detection of integrated HIV DNA by PCR in infected memory CD4 T cell subsets in the absence (HIV) and presence of pDCs (HIV+pDCs) (n = 4). (H-I) Detection of TEM DNA + cells via DNAScope in the absence (HIV) and presence of pDCs (HIV+pDCs) (n = 4). (J-K) Reversal of viral latency in J-Lat cells measured as increased HIV GFP expression upon co-culture with pDCs or after treatment with supernatants derived from TEM-pDCs. For all data, *p

    Journal: PLoS Pathogens

    Article Title: Plasmacytoid dendritic cells have divergent effects on HIV infection of initial target cells and induce a pro-retention phenotype

    doi: 10.1371/journal.ppat.1009522

    Figure Lengend Snippet: Mechanisms of p24 and CD69 induction by pDCs. (A) Normalised p24 expression in resting TEM cells infected with HIV and treated with neutralising antibody to ICAM-1 for 2 hours prior to addition of pDCs (n = 4). (B-C) The effect of virus depleted supernatants (from TEM-pDC cocultures or pDCs) in modulating p24 and CD69 expression in HIV-infected TEM cells (n = 6). (D) Normalised p24 expression and (E) percentage of CD69 expression in resting TEM cells (n = 5) upon modulation of IFN-signaling and/or TNF-signaling via: the addition of exogenous IFNα8 and/or TNFα; blocking the IFNAR1, IFNα and β and/or TNFR1 and TNFα via neutralizing antibodies (a-IFN and a-TNF). (F) Normalised p24 expression in resting TEM cells infected with HIV and treated with maraviroc for 2 hours prior to addition of pDCs (n = 4). (G) Detection of integrated HIV DNA by PCR in infected memory CD4 T cell subsets in the absence (HIV) and presence of pDCs (HIV+pDCs) (n = 4). (H-I) Detection of TEM DNA + cells via DNAScope in the absence (HIV) and presence of pDCs (HIV+pDCs) (n = 4). (J-K) Reversal of viral latency in J-Lat cells measured as increased HIV GFP expression upon co-culture with pDCs or after treatment with supernatants derived from TEM-pDCs. For all data, *p

    Article Snippet: These reagents included: an inhibitor of the intercellular adhesion molecule and component of the immunologic synapse (anti-ICAM-1, 10μg/mL, R & D systems, clone BBIG-I1); the CCR5 inhibitor maraviroc (10μM, AIDS Reagent Program); the reverse transcription inhibitor Zidovudine (50μM, AIDS Reagent Program); neutralising antibodies to receptors of IFN (IFNAR, 20μg/mL, PBL Assay Science, clone MMHAR-2) and TNF (TNFR1, 10μg/mL, R & D systems, clone 16803) in addition to neutralising antibodies for secreted IFNα8 (20000U/mL, PBL Assay Science), IFNβ (5000U/mL, PBL Assay Science) and TNFα (1μg/mL, R & D systems) to block signalling pathways of INF and TNF; recombinant (r) human TNFα (10ng/mL, R & D systems) and rIFNα8 (PBL Assay Science) was used at 350ng/mL for MDDCs and MDMs and at a graded concentration of 300, 600 and 900ng/mL for TCM, TTM and TEM based on the amount of IFNα detected by ELISA in infected MDDCs ( ) and T cell subsets ( ) upon their co-culture with pDCs.

    Techniques: Expressing, Transmission Electron Microscopy, Infection, Blocking Assay, Polymerase Chain Reaction, Co-Culture Assay, Derivative Assay