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hybridoma cell line pk136  (ATCC)
94
ATCC hybridoma cell line pk136
Hybridoma Cell Line Pk136, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+hbs+antibody/PK136/pm42302794-472-1-15
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hybridoma cell line pk136 - by Bioz Stars, 2026-09
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mouse monoclonal antibodies against cftr  (ATCC)
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ATCC mouse monoclonal antibodies against cftr
Mouse Monoclonal Antibodies Against Cftr, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 1 article reviews
mouse monoclonal antibodies against cftr - by Bioz Stars, 2026-09
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icp4  (ATCC)
93
ATCC icp4
(A) Alignment of the amino acid sequence of HSV-1 <t>ICP4</t> (aa 1060–1073) with the canonical IQ motif and the IQ-like motif. (B) HeLa/puroR or HeLa/Flag-CaM cells were infected with wild-type HSV-1(F) at an MOI of 5. At 9 h post-infection, cell lysates were immunoprecipitated (IP) with an anti-Flag antibody. Input lysates and immunoprecipitates were analyzed by immunoblotting with the indicated antibodies. (C) Schematic diagram of the structure of wild-type ICP4 (ICP4-WT) and the IQ-like motif deletion mutant (ICP4-ΔIQ), which lacks amino acids 1060–1070. (D and E) Purified Flag-tagged ICP4-WT, ICP4-ΔIQ, or EGFP were incubated with calmodulin (CaM) Sepharose beads or Protein A Sepharose (control) beads. Bound proteins were detected by immunoblotting with an anti-Flag antibody (D). (E) Quantification of the relative binding intensity (pull-down/input) from (D). (F and G) HeLa cells were infected with rICP47/vUs11/ICP4ΔIQ (rvICP4ΔIQ) or its repaired virus (rvICP4ΔIQ-repair) at an MOI of 5 and analyzed by time-lapse imaging as in . (F) Dot plots showing IE onset (TagRFP, left) and L onset (Venus, right) times (min post-infection) for individual cells. Cells in which onset was not detected are plotted above the dashed line (onset n.d.) with an imputed value (maximum observed onset + 60 min) and were included in statistical analyses. (G) Time interval between IE and L onset (L onset − IE onset) in cells where both onsets were defined. (H) HeLa cells were infected with ICP4ΔIQ or ICP4ΔIQ-repair virus at an MOI of 5 and fixed at 3.5 h post-infection. ChIP-qPCR was performed using an anti-ICP4 antibody or control IgG to quantify ICP4 occupancy at the 5′ regions of UL54 (IE), UL29 (E), and UL49 (L). (I) WT or CALM1-KO HeLa cells were infected with wild-type HSV-1(F) at an MOI of 5 and analyzed by ChIP-qPCR at 3.5 h post-infection as in (H). Data are representative of three independent experiments (B and D). Each value represents the mean ± SE of three (E, H, and I) biological replicates. In (F and G), each dot represents one cell and bars indicate medians. Adjacent bar graphs indicate the differences in median values relative to rvICP4ΔIQ. The number of analyzed cells was as follows: (F) rvICP4ΔIQ, n = 956; rvICP4ΔIQ-repair, n = 1079; (G) rvICP4ΔIQ, n = 912; rvICP4ΔIQ-repair, n = 1065. Data represent pooled measurements from two independent experiments. Statistical analyses were performed using one-way ANOVA followed by Tukey’s multiple-comparison test (E, H, and I) or Mann–Whitney U-test (F and G). **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant.
Icp4, supplied by ATCC, 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/product/anti+hbs+antibody/58-S/bio_rxiv__64898__2026__06__02__729706-221-22-24
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icp4 - by Bioz Stars, 2026-09
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mab 455  (ATCC)
95
ATCC mab 455
(A) Alignment of the amino acid sequence of HSV-1 <t>ICP4</t> (aa 1060–1073) with the canonical IQ motif and the IQ-like motif. (B) HeLa/puroR or HeLa/Flag-CaM cells were infected with wild-type HSV-1(F) at an MOI of 5. At 9 h post-infection, cell lysates were immunoprecipitated (IP) with an anti-Flag antibody. Input lysates and immunoprecipitates were analyzed by immunoblotting with the indicated antibodies. (C) Schematic diagram of the structure of wild-type ICP4 (ICP4-WT) and the IQ-like motif deletion mutant (ICP4-ΔIQ), which lacks amino acids 1060–1070. (D and E) Purified Flag-tagged ICP4-WT, ICP4-ΔIQ, or EGFP were incubated with calmodulin (CaM) Sepharose beads or Protein A Sepharose (control) beads. Bound proteins were detected by immunoblotting with an anti-Flag antibody (D). (E) Quantification of the relative binding intensity (pull-down/input) from (D). (F and G) HeLa cells were infected with rICP47/vUs11/ICP4ΔIQ (rvICP4ΔIQ) or its repaired virus (rvICP4ΔIQ-repair) at an MOI of 5 and analyzed by time-lapse imaging as in . (F) Dot plots showing IE onset (TagRFP, left) and L onset (Venus, right) times (min post-infection) for individual cells. Cells in which onset was not detected are plotted above the dashed line (onset n.d.) with an imputed value (maximum observed onset + 60 min) and were included in statistical analyses. (G) Time interval between IE and L onset (L onset − IE onset) in cells where both onsets were defined. (H) HeLa cells were infected with ICP4ΔIQ or ICP4ΔIQ-repair virus at an MOI of 5 and fixed at 3.5 h post-infection. ChIP-qPCR was performed using an anti-ICP4 antibody or control IgG to quantify ICP4 occupancy at the 5′ regions of UL54 (IE), UL29 (E), and UL49 (L). (I) WT or CALM1-KO HeLa cells were infected with wild-type HSV-1(F) at an MOI of 5 and analyzed by ChIP-qPCR at 3.5 h post-infection as in (H). Data are representative of three independent experiments (B and D). Each value represents the mean ± SE of three (E, H, and I) biological replicates. In (F and G), each dot represents one cell and bars indicate medians. Adjacent bar graphs indicate the differences in median values relative to rvICP4ΔIQ. The number of analyzed cells was as follows: (F) rvICP4ΔIQ, n = 956; rvICP4ΔIQ-repair, n = 1079; (G) rvICP4ΔIQ, n = 912; rvICP4ΔIQ-repair, n = 1065. Data represent pooled measurements from two independent experiments. Statistical analyses were performed using one-way ANOVA followed by Tukey’s multiple-comparison test (E, H, and I) or Mann–Whitney U-test (F and G). **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant.
Mab 455, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mab 455 - by Bioz Stars, 2026-09
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mab c225  (ATCC)
96
ATCC mab c225
(A) Alignment of the amino acid sequence of HSV-1 <t>ICP4</t> (aa 1060–1073) with the canonical IQ motif and the IQ-like motif. (B) HeLa/puroR or HeLa/Flag-CaM cells were infected with wild-type HSV-1(F) at an MOI of 5. At 9 h post-infection, cell lysates were immunoprecipitated (IP) with an anti-Flag antibody. Input lysates and immunoprecipitates were analyzed by immunoblotting with the indicated antibodies. (C) Schematic diagram of the structure of wild-type ICP4 (ICP4-WT) and the IQ-like motif deletion mutant (ICP4-ΔIQ), which lacks amino acids 1060–1070. (D and E) Purified Flag-tagged ICP4-WT, ICP4-ΔIQ, or EGFP were incubated with calmodulin (CaM) Sepharose beads or Protein A Sepharose (control) beads. Bound proteins were detected by immunoblotting with an anti-Flag antibody (D). (E) Quantification of the relative binding intensity (pull-down/input) from (D). (F and G) HeLa cells were infected with rICP47/vUs11/ICP4ΔIQ (rvICP4ΔIQ) or its repaired virus (rvICP4ΔIQ-repair) at an MOI of 5 and analyzed by time-lapse imaging as in . (F) Dot plots showing IE onset (TagRFP, left) and L onset (Venus, right) times (min post-infection) for individual cells. Cells in which onset was not detected are plotted above the dashed line (onset n.d.) with an imputed value (maximum observed onset + 60 min) and were included in statistical analyses. (G) Time interval between IE and L onset (L onset − IE onset) in cells where both onsets were defined. (H) HeLa cells were infected with ICP4ΔIQ or ICP4ΔIQ-repair virus at an MOI of 5 and fixed at 3.5 h post-infection. ChIP-qPCR was performed using an anti-ICP4 antibody or control IgG to quantify ICP4 occupancy at the 5′ regions of UL54 (IE), UL29 (E), and UL49 (L). (I) WT or CALM1-KO HeLa cells were infected with wild-type HSV-1(F) at an MOI of 5 and analyzed by ChIP-qPCR at 3.5 h post-infection as in (H). Data are representative of three independent experiments (B and D). Each value represents the mean ± SE of three (E, H, and I) biological replicates. In (F and G), each dot represents one cell and bars indicate medians. Adjacent bar graphs indicate the differences in median values relative to rvICP4ΔIQ. The number of analyzed cells was as follows: (F) rvICP4ΔIQ, n = 956; rvICP4ΔIQ-repair, n = 1079; (G) rvICP4ΔIQ, n = 912; rvICP4ΔIQ-repair, n = 1065. Data represent pooled measurements from two independent experiments. Statistical analyses were performed using one-way ANOVA followed by Tukey’s multiple-comparison test (E, H, and I) or Mann–Whitney U-test (F and G). **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant.
Mab C225, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+hbs+antibody/225/us12643885-257-9-11
Average 96 stars, based on 1 article reviews
mab c225 - by Bioz Stars, 2026-09
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mab 225  (ATCC)
96
ATCC mab 225
(A) Alignment of the amino acid sequence of HSV-1 <t>ICP4</t> (aa 1060–1073) with the canonical IQ motif and the IQ-like motif. (B) HeLa/puroR or HeLa/Flag-CaM cells were infected with wild-type HSV-1(F) at an MOI of 5. At 9 h post-infection, cell lysates were immunoprecipitated (IP) with an anti-Flag antibody. Input lysates and immunoprecipitates were analyzed by immunoblotting with the indicated antibodies. (C) Schematic diagram of the structure of wild-type ICP4 (ICP4-WT) and the IQ-like motif deletion mutant (ICP4-ΔIQ), which lacks amino acids 1060–1070. (D and E) Purified Flag-tagged ICP4-WT, ICP4-ΔIQ, or EGFP were incubated with calmodulin (CaM) Sepharose beads or Protein A Sepharose (control) beads. Bound proteins were detected by immunoblotting with an anti-Flag antibody (D). (E) Quantification of the relative binding intensity (pull-down/input) from (D). (F and G) HeLa cells were infected with rICP47/vUs11/ICP4ΔIQ (rvICP4ΔIQ) or its repaired virus (rvICP4ΔIQ-repair) at an MOI of 5 and analyzed by time-lapse imaging as in . (F) Dot plots showing IE onset (TagRFP, left) and L onset (Venus, right) times (min post-infection) for individual cells. Cells in which onset was not detected are plotted above the dashed line (onset n.d.) with an imputed value (maximum observed onset + 60 min) and were included in statistical analyses. (G) Time interval between IE and L onset (L onset − IE onset) in cells where both onsets were defined. (H) HeLa cells were infected with ICP4ΔIQ or ICP4ΔIQ-repair virus at an MOI of 5 and fixed at 3.5 h post-infection. ChIP-qPCR was performed using an anti-ICP4 antibody or control IgG to quantify ICP4 occupancy at the 5′ regions of UL54 (IE), UL29 (E), and UL49 (L). (I) WT or CALM1-KO HeLa cells were infected with wild-type HSV-1(F) at an MOI of 5 and analyzed by ChIP-qPCR at 3.5 h post-infection as in (H). Data are representative of three independent experiments (B and D). Each value represents the mean ± SE of three (E, H, and I) biological replicates. In (F and G), each dot represents one cell and bars indicate medians. Adjacent bar graphs indicate the differences in median values relative to rvICP4ΔIQ. The number of analyzed cells was as follows: (F) rvICP4ΔIQ, n = 956; rvICP4ΔIQ-repair, n = 1079; (G) rvICP4ΔIQ, n = 912; rvICP4ΔIQ-repair, n = 1065. Data represent pooled measurements from two independent experiments. Statistical analyses were performed using one-way ANOVA followed by Tukey’s multiple-comparison test (E, H, and I) or Mann–Whitney U-test (F and G). **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant.
Mab 225, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+hbs+antibody/455/us12643880-515-19-21
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mab 225 - by Bioz Stars, 2026-09
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anti hbs  (Abbott Laboratories)
86
Abbott Laboratories anti hbs
(A) Alignment of the amino acid sequence of HSV-1 <t>ICP4</t> (aa 1060–1073) with the canonical IQ motif and the IQ-like motif. (B) HeLa/puroR or HeLa/Flag-CaM cells were infected with wild-type HSV-1(F) at an MOI of 5. At 9 h post-infection, cell lysates were immunoprecipitated (IP) with an anti-Flag antibody. Input lysates and immunoprecipitates were analyzed by immunoblotting with the indicated antibodies. (C) Schematic diagram of the structure of wild-type ICP4 (ICP4-WT) and the IQ-like motif deletion mutant (ICP4-ΔIQ), which lacks amino acids 1060–1070. (D and E) Purified Flag-tagged ICP4-WT, ICP4-ΔIQ, or EGFP were incubated with calmodulin (CaM) Sepharose beads or Protein A Sepharose (control) beads. Bound proteins were detected by immunoblotting with an anti-Flag antibody (D). (E) Quantification of the relative binding intensity (pull-down/input) from (D). (F and G) HeLa cells were infected with rICP47/vUs11/ICP4ΔIQ (rvICP4ΔIQ) or its repaired virus (rvICP4ΔIQ-repair) at an MOI of 5 and analyzed by time-lapse imaging as in . (F) Dot plots showing IE onset (TagRFP, left) and L onset (Venus, right) times (min post-infection) for individual cells. Cells in which onset was not detected are plotted above the dashed line (onset n.d.) with an imputed value (maximum observed onset + 60 min) and were included in statistical analyses. (G) Time interval between IE and L onset (L onset − IE onset) in cells where both onsets were defined. (H) HeLa cells were infected with ICP4ΔIQ or ICP4ΔIQ-repair virus at an MOI of 5 and fixed at 3.5 h post-infection. ChIP-qPCR was performed using an anti-ICP4 antibody or control IgG to quantify ICP4 occupancy at the 5′ regions of UL54 (IE), UL29 (E), and UL49 (L). (I) WT or CALM1-KO HeLa cells were infected with wild-type HSV-1(F) at an MOI of 5 and analyzed by ChIP-qPCR at 3.5 h post-infection as in (H). Data are representative of three independent experiments (B and D). Each value represents the mean ± SE of three (E, H, and I) biological replicates. In (F and G), each dot represents one cell and bars indicate medians. Adjacent bar graphs indicate the differences in median values relative to rvICP4ΔIQ. The number of analyzed cells was as follows: (F) rvICP4ΔIQ, n = 956; rvICP4ΔIQ-repair, n = 1079; (G) rvICP4ΔIQ, n = 912; rvICP4ΔIQ-repair, n = 1065. Data represent pooled measurements from two independent experiments. Statistical analyses were performed using one-way ANOVA followed by Tukey’s multiple-comparison test (E, H, and I) or Mann–Whitney U-test (F and G). **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant.
Anti Hbs, supplied by Abbott Laboratories, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+hbs+antibody/alinity+i+system/pm42312388-10481-17-20
Average 86 stars, based on 1 article reviews
anti hbs - by Bioz Stars, 2026-09
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mhc  (ATCC)
94
ATCC mhc
(A) Alignment of the amino acid sequence of HSV-1 <t>ICP4</t> (aa 1060–1073) with the canonical IQ motif and the IQ-like motif. (B) HeLa/puroR or HeLa/Flag-CaM cells were infected with wild-type HSV-1(F) at an MOI of 5. At 9 h post-infection, cell lysates were immunoprecipitated (IP) with an anti-Flag antibody. Input lysates and immunoprecipitates were analyzed by immunoblotting with the indicated antibodies. (C) Schematic diagram of the structure of wild-type ICP4 (ICP4-WT) and the IQ-like motif deletion mutant (ICP4-ΔIQ), which lacks amino acids 1060–1070. (D and E) Purified Flag-tagged ICP4-WT, ICP4-ΔIQ, or EGFP were incubated with calmodulin (CaM) Sepharose beads or Protein A Sepharose (control) beads. Bound proteins were detected by immunoblotting with an anti-Flag antibody (D). (E) Quantification of the relative binding intensity (pull-down/input) from (D). (F and G) HeLa cells were infected with rICP47/vUs11/ICP4ΔIQ (rvICP4ΔIQ) or its repaired virus (rvICP4ΔIQ-repair) at an MOI of 5 and analyzed by time-lapse imaging as in . (F) Dot plots showing IE onset (TagRFP, left) and L onset (Venus, right) times (min post-infection) for individual cells. Cells in which onset was not detected are plotted above the dashed line (onset n.d.) with an imputed value (maximum observed onset + 60 min) and were included in statistical analyses. (G) Time interval between IE and L onset (L onset − IE onset) in cells where both onsets were defined. (H) HeLa cells were infected with ICP4ΔIQ or ICP4ΔIQ-repair virus at an MOI of 5 and fixed at 3.5 h post-infection. ChIP-qPCR was performed using an anti-ICP4 antibody or control IgG to quantify ICP4 occupancy at the 5′ regions of UL54 (IE), UL29 (E), and UL49 (L). (I) WT or CALM1-KO HeLa cells were infected with wild-type HSV-1(F) at an MOI of 5 and analyzed by ChIP-qPCR at 3.5 h post-infection as in (H). Data are representative of three independent experiments (B and D). Each value represents the mean ± SE of three (E, H, and I) biological replicates. In (F and G), each dot represents one cell and bars indicate medians. Adjacent bar graphs indicate the differences in median values relative to rvICP4ΔIQ. The number of analyzed cells was as follows: (F) rvICP4ΔIQ, n = 956; rvICP4ΔIQ-repair, n = 1079; (G) rvICP4ΔIQ, n = 912; rvICP4ΔIQ-repair, n = 1065. Data represent pooled measurements from two independent experiments. Statistical analyses were performed using one-way ANOVA followed by Tukey’s multiple-comparison test (E, H, and I) or Mann–Whitney U-test (F and G). **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant.
Mhc, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+hbs+antibody/28-14-8S/bio_rxiv__64898__2026__05__21__726907-88-8-20
Average 94 stars, based on 1 article reviews
mhc - by Bioz Stars, 2026-09
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sf1 1 1 10  (ATCC)
94
ATCC sf1 1 1 10
(A) Alignment of the amino acid sequence of HSV-1 <t>ICP4</t> (aa 1060–1073) with the canonical IQ motif and the IQ-like motif. (B) HeLa/puroR or HeLa/Flag-CaM cells were infected with wild-type HSV-1(F) at an MOI of 5. At 9 h post-infection, cell lysates were immunoprecipitated (IP) with an anti-Flag antibody. Input lysates and immunoprecipitates were analyzed by immunoblotting with the indicated antibodies. (C) Schematic diagram of the structure of wild-type ICP4 (ICP4-WT) and the IQ-like motif deletion mutant (ICP4-ΔIQ), which lacks amino acids 1060–1070. (D and E) Purified Flag-tagged ICP4-WT, ICP4-ΔIQ, or EGFP were incubated with calmodulin (CaM) Sepharose beads or Protein A Sepharose (control) beads. Bound proteins were detected by immunoblotting with an anti-Flag antibody (D). (E) Quantification of the relative binding intensity (pull-down/input) from (D). (F and G) HeLa cells were infected with rICP47/vUs11/ICP4ΔIQ (rvICP4ΔIQ) or its repaired virus (rvICP4ΔIQ-repair) at an MOI of 5 and analyzed by time-lapse imaging as in . (F) Dot plots showing IE onset (TagRFP, left) and L onset (Venus, right) times (min post-infection) for individual cells. Cells in which onset was not detected are plotted above the dashed line (onset n.d.) with an imputed value (maximum observed onset + 60 min) and were included in statistical analyses. (G) Time interval between IE and L onset (L onset − IE onset) in cells where both onsets were defined. (H) HeLa cells were infected with ICP4ΔIQ or ICP4ΔIQ-repair virus at an MOI of 5 and fixed at 3.5 h post-infection. ChIP-qPCR was performed using an anti-ICP4 antibody or control IgG to quantify ICP4 occupancy at the 5′ regions of UL54 (IE), UL29 (E), and UL49 (L). (I) WT or CALM1-KO HeLa cells were infected with wild-type HSV-1(F) at an MOI of 5 and analyzed by ChIP-qPCR at 3.5 h post-infection as in (H). Data are representative of three independent experiments (B and D). Each value represents the mean ± SE of three (E, H, and I) biological replicates. In (F and G), each dot represents one cell and bars indicate medians. Adjacent bar graphs indicate the differences in median values relative to rvICP4ΔIQ. The number of analyzed cells was as follows: (F) rvICP4ΔIQ, n = 956; rvICP4ΔIQ-repair, n = 1079; (G) rvICP4ΔIQ, n = 912; rvICP4ΔIQ-repair, n = 1065. Data represent pooled measurements from two independent experiments. Statistical analyses were performed using one-way ANOVA followed by Tukey’s multiple-comparison test (E, H, and I) or Mann–Whitney U-test (F and G). **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant.
Sf1 1 1 10, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+hbs+antibody/SF1-1%2E1%2E10/bio_rxiv__64898__2026__05__21__726907-88-15-20
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sf1 1 1 10 - by Bioz Stars, 2026-09
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alinity i anti hbs reagent kit  (Abbott Laboratories)
86
Abbott Laboratories alinity i anti hbs reagent kit
(A) Alignment of the amino acid sequence of HSV-1 <t>ICP4</t> (aa 1060–1073) with the canonical IQ motif and the IQ-like motif. (B) HeLa/puroR or HeLa/Flag-CaM cells were infected with wild-type HSV-1(F) at an MOI of 5. At 9 h post-infection, cell lysates were immunoprecipitated (IP) with an anti-Flag antibody. Input lysates and immunoprecipitates were analyzed by immunoblotting with the indicated antibodies. (C) Schematic diagram of the structure of wild-type ICP4 (ICP4-WT) and the IQ-like motif deletion mutant (ICP4-ΔIQ), which lacks amino acids 1060–1070. (D and E) Purified Flag-tagged ICP4-WT, ICP4-ΔIQ, or EGFP were incubated with calmodulin (CaM) Sepharose beads or Protein A Sepharose (control) beads. Bound proteins were detected by immunoblotting with an anti-Flag antibody (D). (E) Quantification of the relative binding intensity (pull-down/input) from (D). (F and G) HeLa cells were infected with rICP47/vUs11/ICP4ΔIQ (rvICP4ΔIQ) or its repaired virus (rvICP4ΔIQ-repair) at an MOI of 5 and analyzed by time-lapse imaging as in . (F) Dot plots showing IE onset (TagRFP, left) and L onset (Venus, right) times (min post-infection) for individual cells. Cells in which onset was not detected are plotted above the dashed line (onset n.d.) with an imputed value (maximum observed onset + 60 min) and were included in statistical analyses. (G) Time interval between IE and L onset (L onset − IE onset) in cells where both onsets were defined. (H) HeLa cells were infected with ICP4ΔIQ or ICP4ΔIQ-repair virus at an MOI of 5 and fixed at 3.5 h post-infection. ChIP-qPCR was performed using an anti-ICP4 antibody or control IgG to quantify ICP4 occupancy at the 5′ regions of UL54 (IE), UL29 (E), and UL49 (L). (I) WT or CALM1-KO HeLa cells were infected with wild-type HSV-1(F) at an MOI of 5 and analyzed by ChIP-qPCR at 3.5 h post-infection as in (H). Data are representative of three independent experiments (B and D). Each value represents the mean ± SE of three (E, H, and I) biological replicates. In (F and G), each dot represents one cell and bars indicate medians. Adjacent bar graphs indicate the differences in median values relative to rvICP4ΔIQ. The number of analyzed cells was as follows: (F) rvICP4ΔIQ, n = 956; rvICP4ΔIQ-repair, n = 1079; (G) rvICP4ΔIQ, n = 912; rvICP4ΔIQ-repair, n = 1065. Data represent pooled measurements from two independent experiments. Statistical analyses were performed using one-way ANOVA followed by Tukey’s multiple-comparison test (E, H, and I) or Mann–Whitney U-test (F and G). **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant.
Alinity I Anti Hbs Reagent Kit, supplied by Abbott Laboratories, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+hbs+antibody/kit+paraffin+pretreatment+reagent/pmc13196985-170-37-42
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alinity i anti hbs reagent kit - by Bioz Stars, 2026-09
86/100 stars
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(A) Alignment of the amino acid sequence of HSV-1 ICP4 (aa 1060–1073) with the canonical IQ motif and the IQ-like motif. (B) HeLa/puroR or HeLa/Flag-CaM cells were infected with wild-type HSV-1(F) at an MOI of 5. At 9 h post-infection, cell lysates were immunoprecipitated (IP) with an anti-Flag antibody. Input lysates and immunoprecipitates were analyzed by immunoblotting with the indicated antibodies. (C) Schematic diagram of the structure of wild-type ICP4 (ICP4-WT) and the IQ-like motif deletion mutant (ICP4-ΔIQ), which lacks amino acids 1060–1070. (D and E) Purified Flag-tagged ICP4-WT, ICP4-ΔIQ, or EGFP were incubated with calmodulin (CaM) Sepharose beads or Protein A Sepharose (control) beads. Bound proteins were detected by immunoblotting with an anti-Flag antibody (D). (E) Quantification of the relative binding intensity (pull-down/input) from (D). (F and G) HeLa cells were infected with rICP47/vUs11/ICP4ΔIQ (rvICP4ΔIQ) or its repaired virus (rvICP4ΔIQ-repair) at an MOI of 5 and analyzed by time-lapse imaging as in . (F) Dot plots showing IE onset (TagRFP, left) and L onset (Venus, right) times (min post-infection) for individual cells. Cells in which onset was not detected are plotted above the dashed line (onset n.d.) with an imputed value (maximum observed onset + 60 min) and were included in statistical analyses. (G) Time interval between IE and L onset (L onset − IE onset) in cells where both onsets were defined. (H) HeLa cells were infected with ICP4ΔIQ or ICP4ΔIQ-repair virus at an MOI of 5 and fixed at 3.5 h post-infection. ChIP-qPCR was performed using an anti-ICP4 antibody or control IgG to quantify ICP4 occupancy at the 5′ regions of UL54 (IE), UL29 (E), and UL49 (L). (I) WT or CALM1-KO HeLa cells were infected with wild-type HSV-1(F) at an MOI of 5 and analyzed by ChIP-qPCR at 3.5 h post-infection as in (H). Data are representative of three independent experiments (B and D). Each value represents the mean ± SE of three (E, H, and I) biological replicates. In (F and G), each dot represents one cell and bars indicate medians. Adjacent bar graphs indicate the differences in median values relative to rvICP4ΔIQ. The number of analyzed cells was as follows: (F) rvICP4ΔIQ, n = 956; rvICP4ΔIQ-repair, n = 1079; (G) rvICP4ΔIQ, n = 912; rvICP4ΔIQ-repair, n = 1065. Data represent pooled measurements from two independent experiments. Statistical analyses were performed using one-way ANOVA followed by Tukey’s multiple-comparison test (E, H, and I) or Mann–Whitney U-test (F and G). **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant.

Journal: bioRxiv

Article Title: Calmodulin controls the tempo of HSV-1 gene-expression cascade to reshape infection heterogeneity

doi: 10.64898/2026.06.02.729706

Figure Lengend Snippet: (A) Alignment of the amino acid sequence of HSV-1 ICP4 (aa 1060–1073) with the canonical IQ motif and the IQ-like motif. (B) HeLa/puroR or HeLa/Flag-CaM cells were infected with wild-type HSV-1(F) at an MOI of 5. At 9 h post-infection, cell lysates were immunoprecipitated (IP) with an anti-Flag antibody. Input lysates and immunoprecipitates were analyzed by immunoblotting with the indicated antibodies. (C) Schematic diagram of the structure of wild-type ICP4 (ICP4-WT) and the IQ-like motif deletion mutant (ICP4-ΔIQ), which lacks amino acids 1060–1070. (D and E) Purified Flag-tagged ICP4-WT, ICP4-ΔIQ, or EGFP were incubated with calmodulin (CaM) Sepharose beads or Protein A Sepharose (control) beads. Bound proteins were detected by immunoblotting with an anti-Flag antibody (D). (E) Quantification of the relative binding intensity (pull-down/input) from (D). (F and G) HeLa cells were infected with rICP47/vUs11/ICP4ΔIQ (rvICP4ΔIQ) or its repaired virus (rvICP4ΔIQ-repair) at an MOI of 5 and analyzed by time-lapse imaging as in . (F) Dot plots showing IE onset (TagRFP, left) and L onset (Venus, right) times (min post-infection) for individual cells. Cells in which onset was not detected are plotted above the dashed line (onset n.d.) with an imputed value (maximum observed onset + 60 min) and were included in statistical analyses. (G) Time interval between IE and L onset (L onset − IE onset) in cells where both onsets were defined. (H) HeLa cells were infected with ICP4ΔIQ or ICP4ΔIQ-repair virus at an MOI of 5 and fixed at 3.5 h post-infection. ChIP-qPCR was performed using an anti-ICP4 antibody or control IgG to quantify ICP4 occupancy at the 5′ regions of UL54 (IE), UL29 (E), and UL49 (L). (I) WT or CALM1-KO HeLa cells were infected with wild-type HSV-1(F) at an MOI of 5 and analyzed by ChIP-qPCR at 3.5 h post-infection as in (H). Data are representative of three independent experiments (B and D). Each value represents the mean ± SE of three (E, H, and I) biological replicates. In (F and G), each dot represents one cell and bars indicate medians. Adjacent bar graphs indicate the differences in median values relative to rvICP4ΔIQ. The number of analyzed cells was as follows: (F) rvICP4ΔIQ, n = 956; rvICP4ΔIQ-repair, n = 1079; (G) rvICP4ΔIQ, n = 912; rvICP4ΔIQ-repair, n = 1065. Data represent pooled measurements from two independent experiments. Statistical analyses were performed using one-way ANOVA followed by Tukey’s multiple-comparison test (E, H, and I) or Mann–Whitney U-test (F and G). **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant.

Article Snippet: Commercial antibodies used in this study included mouse monoclonal antibodies to Flag (M2; Sigma), α-tubulin (DM1A; Sigma), gD (sc-21719; Santa Cruz), and ICP4 (58S; ATCC); a rabbit monoclonal antibody to calmodulin (ab45689; Abcam); and rabbit polyclonal antibodies to green fluorescent protein (GFP) (598; Medical & Biological Laboratories [MBL]) and TagRFP (AB233; Evrogen).

Techniques: Sequencing, Infection, Immunoprecipitation, Western Blot, Mutagenesis, Purification, Incubation, Control, Binding Assay, Virus, Imaging, ChIP-qPCR, Comparison, MANN-WHITNEY