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Real-time PCR primers used
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Real-time PCR primers used
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Bacterial isolates evaluated in this study a
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Phosphorylated <t>H2AX</t> accumulates at late times after infection with wild-type adenovirus. (A) HeLa cells were mock infected, exposed to 40 Gy of radiation, or infected at an MOI of 5 with the wild-type virus dl309. Cells were processed for immunofluorescence microscopy for the E2A DNA-binding protein (E2A-DBP) and phosphorylated H2AX (γH2AX) immediately after irradiation or 24 h after infection. Representative images predominantly of the nucleus are presented. Multiple foci were observed in the irradiated cells, but only those in the plane of focus are seen in this image. (B) HeLa cells were infected at an MOI of 5 and harvested at the indicate times postinfection. Material representing equivalent numbers of initially infected cells was separated by SDS-polyacrylamide gel electrophoresis and analyzed by immunoblotting with the indicated antibodies. (C) Viral DNA levels were measured by quantitative real-time PCR from HeLa cells infected at an MOI of 5 with dl309 at the indicated times after infection (open symbols). The relative level of γH2AX (closed symbols) was determined as the ratio of γH2AX signal to total H2AX signal for each time point from a blot similar to the representative blot in panel B. The ratio measured for mock-infected cells was set to 1.
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Influenza viruses used in the study
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Influenza viruses used in the study
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Influenza viruses used in the study
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Image Search Results


Real-time PCR primers used

Journal: American Journal of Physiology - Renal Physiology

Article Title: Gene deletion of the Na + -glucose cotransporter SGLT1 ameliorates kidney recovery in a murine model of acute kidney injury induced by ischemia-reperfusion

doi: 10.1152/ajprenal.00111.2019

Figure Lengend Snippet: Real-time PCR primers used

Article Snippet: See primer details in . table ft1 table-wrap mode="anchored" t5 Table 1. caption a7 Target Gene Assay ID Aqp2 Mm00437575_m1 MCP1/ Ccl2 Mm00441242_m1 Col1a1 Mm00801666_g1 Epo Mm01202755_m1 Fn1 Mm01256744_m1 KIM-1/ Havcr1 Mm00506686_m1 Hk2 Mm00443385_m1 Hprt Mm00446968_m1 Ppargc1a Mm01208835_m1 Ren Mm02342889_g1 SGLT1/ Slc5a1 Mm00451203_m1 SGLT2/ Slc5a2 Mm00453831_m1 NKCC2/ Slc12a1 Mm01275821_m1 Open in a separate window Aqp2 , aquaporin-2; MCP1/ Ccl2 , monocyte chemoattractant protein-1/chemokine (C-C motif) ligand 2; Col1a1 , collagen type I-α 1 ; Epo , erythropoietin; Fn1 , fibronectin 1; KIM-1/ Havcr1 , kidney injury molecule-1/hepatitis A virus cellular receptor 1, Hk2 , hexokinase-2; Hprt , hypoxanthine-guanine phosphoribosyltransferase; Ppargc1a , peroxisome proliferator-activated receptor-γ coactivator-1α; Ren , renin; SGLT, Na + -glucose cotransporter; NKCC2, Na + -K + -2Cl – cotransporter.

Techniques: Real-time Polymerase Chain Reaction, Gene Assay

Bacterial isolates evaluated in this study a

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Spheroplast-Mediated Carbapenem Tolerance in Gram-Negative Pathogens

doi: 10.1128/AAC.00756-19

Figure Lengend Snippet: Bacterial isolates evaluated in this study a

Article Snippet: Our results suggest that measurement of antibiotic susceptibility and, ultimately, treatment outcome could include more-nuanced responses, such as tolerance, in Gram-negative pathogens. table ft1 table-wrap mode="anchored" t5 TABLE 1 caption a7 Isolate Carbapenemase Specimen source MHA MIC value (μg/ml) MHA MIC value interpretation e BHI + agar MIC value (μg/ml) BHI + agar MIC value interpretation f E. cloacae complex ARB0008 b NA NA 1 SUS 1.5 NA E. cloacae complex ATCC 13047 NA NA 0.064 SUS 0.094 NA E. cloacae complex WCM0001 NA Blood 0.023 SUS 0.023 NA E. coli WCM0001 NA Urine 0.016 SUS 0.016 NA E. coli TUV93-0 NA NA 0.023 SUS 0.023 NA K. aerogenes ARB0007 NA NA 0.064 SUS 0.047 NA K. aerogenes WCM0001 NA Respiratory/sinus 0.032 SUS 0.032 NA K. pneumoniae WCM0001 NA Blood 0.047 SUS 0.032 NA K. pneumoniae WCM0002 NA Respiratory/sinus 0.032 SUS 0.064 NA P. aeruginosa PA14 NA NA 0.25 SUS 0.25 NA V. cholerae N16961 NA NA 0.125 SUS 0.125 NA E. cloacae complex 41952 KPC NA >32 RES >32 NA E. coli 52862 KPC NA >32 RES 32 NA K. aerogenes 28944 KPC NA >32 RES >32 NA K. pneumoniae ARB0120 c KPC NA 16 RES 16 NA P. aeruginosa ARB0090 d KPC NA >32 RES >32 NA Open in a separate window a ARB, Centers for Disease Control and Prevention and U.S. Food and Drug Administration Antibiotic Resistance Isolate Bank; ATCC, American Type Culture Collection; BHI + , brain heart infusion agar with supplements; MHA, Mueller-Hinton agar; NA, not applicable; RES, resistant; SUS, susceptible; WCM, Weill Cornell Medicine. b For ARB0008, the meropenem MIC value determined by the ARB is 2 μg/ml (intermediate).

Techniques:

Meropenem-induced spheroplasts can recover to form an exponentially growing population. A time-lapse montage of spheroplasts imaged upon removal of meropenem after 6 h of treatment is shown. The antibiotic was removed by addition of purified NDM-1 carbapenemase, followed by time-lapse microscopy on BHI+ agarose pads (0.8% [wt/vol] agarose). Images were then acquired 5 min apart for another 2 h. Both E. coli isolates were omitted since no spheroplasts were observed after 6 h of meropenem treatment. Scale bars, 5 μm.

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Spheroplast-Mediated Carbapenem Tolerance in Gram-Negative Pathogens

doi: 10.1128/AAC.00756-19

Figure Lengend Snippet: Meropenem-induced spheroplasts can recover to form an exponentially growing population. A time-lapse montage of spheroplasts imaged upon removal of meropenem after 6 h of treatment is shown. The antibiotic was removed by addition of purified NDM-1 carbapenemase, followed by time-lapse microscopy on BHI+ agarose pads (0.8% [wt/vol] agarose). Images were then acquired 5 min apart for another 2 h. Both E. coli isolates were omitted since no spheroplasts were observed after 6 h of meropenem treatment. Scale bars, 5 μm.

Article Snippet: Our results suggest that measurement of antibiotic susceptibility and, ultimately, treatment outcome could include more-nuanced responses, such as tolerance, in Gram-negative pathogens. table ft1 table-wrap mode="anchored" t5 TABLE 1 caption a7 Isolate Carbapenemase Specimen source MHA MIC value (μg/ml) MHA MIC value interpretation e BHI + agar MIC value (μg/ml) BHI + agar MIC value interpretation f E. cloacae complex ARB0008 b NA NA 1 SUS 1.5 NA E. cloacae complex ATCC 13047 NA NA 0.064 SUS 0.094 NA E. cloacae complex WCM0001 NA Blood 0.023 SUS 0.023 NA E. coli WCM0001 NA Urine 0.016 SUS 0.016 NA E. coli TUV93-0 NA NA 0.023 SUS 0.023 NA K. aerogenes ARB0007 NA NA 0.064 SUS 0.047 NA K. aerogenes WCM0001 NA Respiratory/sinus 0.032 SUS 0.032 NA K. pneumoniae WCM0001 NA Blood 0.047 SUS 0.032 NA K. pneumoniae WCM0002 NA Respiratory/sinus 0.032 SUS 0.064 NA P. aeruginosa PA14 NA NA 0.25 SUS 0.25 NA V. cholerae N16961 NA NA 0.125 SUS 0.125 NA E. cloacae complex 41952 KPC NA >32 RES >32 NA E. coli 52862 KPC NA >32 RES 32 NA K. aerogenes 28944 KPC NA >32 RES >32 NA K. pneumoniae ARB0120 c KPC NA 16 RES 16 NA P. aeruginosa ARB0090 d KPC NA >32 RES >32 NA Open in a separate window a ARB, Centers for Disease Control and Prevention and U.S. Food and Drug Administration Antibiotic Resistance Isolate Bank; ATCC, American Type Culture Collection; BHI + , brain heart infusion agar with supplements; MHA, Mueller-Hinton agar; NA, not applicable; RES, resistant; SUS, susceptible; WCM, Weill Cornell Medicine. b For ARB0008, the meropenem MIC value determined by the ARB is 2 μg/ml (intermediate).

Techniques: Purification, Time-lapse Microscopy

Spheroplast formation and recovery in human serum. (A and B) The indicated isolates were grown overnight in serum growth medium (SGM), diluted 1:10 (final volume, 500 μl) into fresh SGM, and incubated in the presence (A) or absence (B) of 10 μg/ml meropenem. Cells were plated (CFU per milliliter) at the indicated time points. (C) After 6 h of incubation, purified NDM-1 carbapenemase was added to remove meropenem, followed by time-lapse microscopy on agarose pads containing 40% (vol/vol) human serum. All values represent means of results from three biological replicates; error bars represent standard errors of the means. The red circle indicates the initial growth steps of a recovering spheroplast within cell debris.

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Spheroplast-Mediated Carbapenem Tolerance in Gram-Negative Pathogens

doi: 10.1128/AAC.00756-19

Figure Lengend Snippet: Spheroplast formation and recovery in human serum. (A and B) The indicated isolates were grown overnight in serum growth medium (SGM), diluted 1:10 (final volume, 500 μl) into fresh SGM, and incubated in the presence (A) or absence (B) of 10 μg/ml meropenem. Cells were plated (CFU per milliliter) at the indicated time points. (C) After 6 h of incubation, purified NDM-1 carbapenemase was added to remove meropenem, followed by time-lapse microscopy on agarose pads containing 40% (vol/vol) human serum. All values represent means of results from three biological replicates; error bars represent standard errors of the means. The red circle indicates the initial growth steps of a recovering spheroplast within cell debris.

Article Snippet: Our results suggest that measurement of antibiotic susceptibility and, ultimately, treatment outcome could include more-nuanced responses, such as tolerance, in Gram-negative pathogens. table ft1 table-wrap mode="anchored" t5 TABLE 1 caption a7 Isolate Carbapenemase Specimen source MHA MIC value (μg/ml) MHA MIC value interpretation e BHI + agar MIC value (μg/ml) BHI + agar MIC value interpretation f E. cloacae complex ARB0008 b NA NA 1 SUS 1.5 NA E. cloacae complex ATCC 13047 NA NA 0.064 SUS 0.094 NA E. cloacae complex WCM0001 NA Blood 0.023 SUS 0.023 NA E. coli WCM0001 NA Urine 0.016 SUS 0.016 NA E. coli TUV93-0 NA NA 0.023 SUS 0.023 NA K. aerogenes ARB0007 NA NA 0.064 SUS 0.047 NA K. aerogenes WCM0001 NA Respiratory/sinus 0.032 SUS 0.032 NA K. pneumoniae WCM0001 NA Blood 0.047 SUS 0.032 NA K. pneumoniae WCM0002 NA Respiratory/sinus 0.032 SUS 0.064 NA P. aeruginosa PA14 NA NA 0.25 SUS 0.25 NA V. cholerae N16961 NA NA 0.125 SUS 0.125 NA E. cloacae complex 41952 KPC NA >32 RES >32 NA E. coli 52862 KPC NA >32 RES 32 NA K. aerogenes 28944 KPC NA >32 RES >32 NA K. pneumoniae ARB0120 c KPC NA 16 RES 16 NA P. aeruginosa ARB0090 d KPC NA >32 RES >32 NA Open in a separate window a ARB, Centers for Disease Control and Prevention and U.S. Food and Drug Administration Antibiotic Resistance Isolate Bank; ATCC, American Type Culture Collection; BHI + , brain heart infusion agar with supplements; MHA, Mueller-Hinton agar; NA, not applicable; RES, resistant; SUS, susceptible; WCM, Weill Cornell Medicine. b For ARB0008, the meropenem MIC value determined by the ARB is 2 μg/ml (intermediate).

Techniques: Incubation, Purification, Time-lapse Microscopy

Phosphorylated H2AX accumulates at late times after infection with wild-type adenovirus. (A) HeLa cells were mock infected, exposed to 40 Gy of radiation, or infected at an MOI of 5 with the wild-type virus dl309. Cells were processed for immunofluorescence microscopy for the E2A DNA-binding protein (E2A-DBP) and phosphorylated H2AX (γH2AX) immediately after irradiation or 24 h after infection. Representative images predominantly of the nucleus are presented. Multiple foci were observed in the irradiated cells, but only those in the plane of focus are seen in this image. (B) HeLa cells were infected at an MOI of 5 and harvested at the indicate times postinfection. Material representing equivalent numbers of initially infected cells was separated by SDS-polyacrylamide gel electrophoresis and analyzed by immunoblotting with the indicated antibodies. (C) Viral DNA levels were measured by quantitative real-time PCR from HeLa cells infected at an MOI of 5 with dl309 at the indicated times after infection (open symbols). The relative level of γH2AX (closed symbols) was determined as the ratio of γH2AX signal to total H2AX signal for each time point from a blot similar to the representative blot in panel B. The ratio measured for mock-infected cells was set to 1.

Journal:

Article Title: Widespread Phosphorylation of Histone H2AX by Species C Adenovirus Infection Requires Viral DNA Replication

doi: 10.1128/JVI.00091-09

Figure Lengend Snippet: Phosphorylated H2AX accumulates at late times after infection with wild-type adenovirus. (A) HeLa cells were mock infected, exposed to 40 Gy of radiation, or infected at an MOI of 5 with the wild-type virus dl309. Cells were processed for immunofluorescence microscopy for the E2A DNA-binding protein (E2A-DBP) and phosphorylated H2AX (γH2AX) immediately after irradiation or 24 h after infection. Representative images predominantly of the nucleus are presented. Multiple foci were observed in the irradiated cells, but only those in the plane of focus are seen in this image. (B) HeLa cells were infected at an MOI of 5 and harvested at the indicate times postinfection. Material representing equivalent numbers of initially infected cells was separated by SDS-polyacrylamide gel electrophoresis and analyzed by immunoblotting with the indicated antibodies. (C) Viral DNA levels were measured by quantitative real-time PCR from HeLa cells infected at an MOI of 5 with dl309 at the indicated times after infection (open symbols). The relative level of γH2AX (closed symbols) was determined as the ratio of γH2AX signal to total H2AX signal for each time point from a blot similar to the representative blot in panel B. The ratio measured for mock-infected cells was set to 1.

Article Snippet: Because this pattern of phosphorylation was observed with three different phospho-specific antibodies raised in mice and rabbits (Bethyl A300-081A; Upstate 05-636, Upstate 16-202A), it seems unlikely that this staining pattern was due to a spurious interaction between the phospho-specific antibody and the infected cell. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window FIG. 1. caption a7 Phosphorylated H2AX accumulates at late times after infection with wild-type adenovirus. (A) HeLa cells were mock infected, exposed to 40 Gy of radiation, or infected at an MOI of 5 with the wild-type virus dl 309.

Techniques: Infection, Immunofluorescence, Microscopy, Binding Assay, Irradiation, Polyacrylamide Gel Electrophoresis, Western Blot, Real-time Polymerase Chain Reaction

PI3K-like kinase inhibitors decrease H2AX phosphorylation in infected cells. HeLa cells were mock infected or infected with the wild-type virus at an MOI of 5. After 3 h, either caffeine or wortmannin was added to the infected cells at the indicated concentration, and the cells were harvested for analysis after 24 h by immunoblotting for γH2AX and total H2AX. The relative levels of H2AX phosphorylation were determined as the ratio of γH2AX to total H2AX where the ratio measured for mock-infected cells was set to 1. (A to D) Representative results of four experiments for caffeine treatment are shown in panels A and B and for wortmannin treatment in panels C and D. (E and F) HeLa cells were mock infected (−) or infected with the E4 deletion virus, dl366* (+), at an MOI of 10. After 3 h, either caffeine or wortmannin was added to the infected cells at the indicated concentration, and cells were harvested for analysis at 24 h by immunoblotting for RPA32. An open arrowhead indicates nonphosphorylated RPA32, and a filled arrowhead indicates the phosphorylated form of RPA32.

Journal:

Article Title: Widespread Phosphorylation of Histone H2AX by Species C Adenovirus Infection Requires Viral DNA Replication

doi: 10.1128/JVI.00091-09

Figure Lengend Snippet: PI3K-like kinase inhibitors decrease H2AX phosphorylation in infected cells. HeLa cells were mock infected or infected with the wild-type virus at an MOI of 5. After 3 h, either caffeine or wortmannin was added to the infected cells at the indicated concentration, and the cells were harvested for analysis after 24 h by immunoblotting for γH2AX and total H2AX. The relative levels of H2AX phosphorylation were determined as the ratio of γH2AX to total H2AX where the ratio measured for mock-infected cells was set to 1. (A to D) Representative results of four experiments for caffeine treatment are shown in panels A and B and for wortmannin treatment in panels C and D. (E and F) HeLa cells were mock infected (−) or infected with the E4 deletion virus, dl366* (+), at an MOI of 10. After 3 h, either caffeine or wortmannin was added to the infected cells at the indicated concentration, and cells were harvested for analysis at 24 h by immunoblotting for RPA32. An open arrowhead indicates nonphosphorylated RPA32, and a filled arrowhead indicates the phosphorylated form of RPA32.

Article Snippet: Because this pattern of phosphorylation was observed with three different phospho-specific antibodies raised in mice and rabbits (Bethyl A300-081A; Upstate 05-636, Upstate 16-202A), it seems unlikely that this staining pattern was due to a spurious interaction between the phospho-specific antibody and the infected cell. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window FIG. 1. caption a7 Phosphorylated H2AX accumulates at late times after infection with wild-type adenovirus. (A) HeLa cells were mock infected, exposed to 40 Gy of radiation, or infected at an MOI of 5 with the wild-type virus dl 309.

Techniques: Infection, Concentration Assay, Western Blot

Widespread H2AX phosphorylation during adenovirus infection requires viral DNA synthesis. (A) HeLa cells were mock infected, infected with the wild-type virus dl309, or infected with the DNA replication-deficient adenovirus H5wt300-ΔpTP (ΔpTP) at an MOI of 5 and processed for immunofluorescence after 24 h for the E2A-DBP protein and γH2AX. (B) HeLa cells that stably express the E2B preterminal protein gene (HeLa-pTP) were infected and processed as in panel A. The restoration of centers of viral DNA replication is seen by the appearance of foci of E2A-DBP staining.

Journal:

Article Title: Widespread Phosphorylation of Histone H2AX by Species C Adenovirus Infection Requires Viral DNA Replication

doi: 10.1128/JVI.00091-09

Figure Lengend Snippet: Widespread H2AX phosphorylation during adenovirus infection requires viral DNA synthesis. (A) HeLa cells were mock infected, infected with the wild-type virus dl309, or infected with the DNA replication-deficient adenovirus H5wt300-ΔpTP (ΔpTP) at an MOI of 5 and processed for immunofluorescence after 24 h for the E2A-DBP protein and γH2AX. (B) HeLa cells that stably express the E2B preterminal protein gene (HeLa-pTP) were infected and processed as in panel A. The restoration of centers of viral DNA replication is seen by the appearance of foci of E2A-DBP staining.

Article Snippet: Because this pattern of phosphorylation was observed with three different phospho-specific antibodies raised in mice and rabbits (Bethyl A300-081A; Upstate 05-636, Upstate 16-202A), it seems unlikely that this staining pattern was due to a spurious interaction between the phospho-specific antibody and the infected cell. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window FIG. 1. caption a7 Phosphorylated H2AX accumulates at late times after infection with wild-type adenovirus. (A) HeLa cells were mock infected, exposed to 40 Gy of radiation, or infected at an MOI of 5 with the wild-type virus dl 309.

Techniques: Infection, DNA Synthesis, Immunofluorescence, Stable Transfection, Staining

Exposure to empty viral capsids fails to elicit γH2AX. (A) HeLa cells were exposed to empty viral capsids corresponding to the number of viral particles required for the indicated MOI of wild-type virus. After 24 h, γH2AX was visualized by immunofluorescence and photographed using the identical exposure settings in Fig. ​Fig.5.5. (B) HeLa cells were mock infected, infected with the wild-type virus dl309, or exposed to empty capsids at the indicated equivalent MOI. After 24 h, cellular lysates were prepared and analyzed by immunoblotting for γH2AX, total H2AX, and β-actin.

Journal:

Article Title: Widespread Phosphorylation of Histone H2AX by Species C Adenovirus Infection Requires Viral DNA Replication

doi: 10.1128/JVI.00091-09

Figure Lengend Snippet: Exposure to empty viral capsids fails to elicit γH2AX. (A) HeLa cells were exposed to empty viral capsids corresponding to the number of viral particles required for the indicated MOI of wild-type virus. After 24 h, γH2AX was visualized by immunofluorescence and photographed using the identical exposure settings in Fig. ​Fig.5.5. (B) HeLa cells were mock infected, infected with the wild-type virus dl309, or exposed to empty capsids at the indicated equivalent MOI. After 24 h, cellular lysates were prepared and analyzed by immunoblotting for γH2AX, total H2AX, and β-actin.

Article Snippet: Because this pattern of phosphorylation was observed with three different phospho-specific antibodies raised in mice and rabbits (Bethyl A300-081A; Upstate 05-636, Upstate 16-202A), it seems unlikely that this staining pattern was due to a spurious interaction between the phospho-specific antibody and the infected cell. fig ft0 fig mode=article f1 fig/graphic|fig/alternatives/graphic mode="anchored" m1 Open in a separate window FIG. 1. caption a7 Phosphorylated H2AX accumulates at late times after infection with wild-type adenovirus. (A) HeLa cells were mock infected, exposed to 40 Gy of radiation, or infected at an MOI of 5 with the wild-type virus dl 309.

Techniques: Immunofluorescence, Infection, Western Blot

Influenza viruses used in the study

Journal:

Article Title: Comparison of the Anti-Influenza Virus Activity of RWJ-270201 with Those of Oseltamivir and Zanamivir

doi: 10.1128/AAC.45.4.1162-1167.2001

Figure Lengend Snippet: Influenza viruses used in the study

Article Snippet: The influenza viruses used in this study, together with their sources, are shown in Table . table ft1 table-wrap mode="anchored" t5 TABLE 1 caption a7 Virus Type Source A/PR/8/34 H1N1 ATCC, USA a A1/FM/1/47 H1N1 ATCC, USA a A/NWS/33 H1N1 ATCC, USA a A/Brazil/11/78 H1N1 Skehel, United Kingdom b A/Taiwan/1/86 H1N1 Hayden, USA c A2/Hong Kong/8/68 H2N2 ATCC, USA a A/Singapore/1/57 H2N2 Memphis, Tenn., USA d A/Tokyo/3/67 H2N2 Canberra, Australia e A/Japan H2N2 ATCC, USA a A/Aichi H3N2 ATCC, USA a A/Belgium/2/81 H3N2 Skehel, United Kingdom b A/Shangdong/09/93 H3N2 Logan, Utah, USA f A/Virginia/88 H3N2 Hayden, USA c A/Turkey/Mass/76A/Beijing/32/92 [R] H6N2 Valhalla, N.Y., USA g B/Hong Kong/5/72 B ATCC, USA a B/Hong Kong/5/72 B Hayden, USA c B/Lee/40 B ATCC, USA a B/Victoria/70 B Canberra, Australia e B/Harbin/07/94 B Logan, Utah, USA f B/Y177 B Pasteur Institute, Brussels, Belgium h B/Y253 B Pasteur Institute, Brussels, Belgium h B/Y263 B Pasteur Institute, Brussels, Belgium h Open in a separate window a American Type Culture Collection, Manassas, Va. b Skehel, World Influenza Centre, Mill Hill, United Kingdom. c Frederic Hayden, University of Virginia, Charlottesville, Va. d Robert Webster, St. Jude Children's Hospital, Memphis, Tenn. e Graeme Laver, Australian National University, Canberra, Australia. f Robert Sidwell, Utah State University, Logan, Utah. g Bert Johannson, New York Medical College, Valhalla, N.Y. h Ferdinand Yane, Pasteur Institute, Brussels, Belgium.

Techniques:

Comparison of IC 50 s and IC 90 s of RWJ-270201, oseltamivir carboxylate, and zanamivir against various influenza neuraminidases

Journal:

Article Title: Comparison of the Anti-Influenza Virus Activity of RWJ-270201 with Those of Oseltamivir and Zanamivir

doi: 10.1128/AAC.45.4.1162-1167.2001

Figure Lengend Snippet: Comparison of IC 50 s and IC 90 s of RWJ-270201, oseltamivir carboxylate, and zanamivir against various influenza neuraminidases

Article Snippet: The influenza viruses used in this study, together with their sources, are shown in Table . table ft1 table-wrap mode="anchored" t5 TABLE 1 caption a7 Virus Type Source A/PR/8/34 H1N1 ATCC, USA a A1/FM/1/47 H1N1 ATCC, USA a A/NWS/33 H1N1 ATCC, USA a A/Brazil/11/78 H1N1 Skehel, United Kingdom b A/Taiwan/1/86 H1N1 Hayden, USA c A2/Hong Kong/8/68 H2N2 ATCC, USA a A/Singapore/1/57 H2N2 Memphis, Tenn., USA d A/Tokyo/3/67 H2N2 Canberra, Australia e A/Japan H2N2 ATCC, USA a A/Aichi H3N2 ATCC, USA a A/Belgium/2/81 H3N2 Skehel, United Kingdom b A/Shangdong/09/93 H3N2 Logan, Utah, USA f A/Virginia/88 H3N2 Hayden, USA c A/Turkey/Mass/76A/Beijing/32/92 [R] H6N2 Valhalla, N.Y., USA g B/Hong Kong/5/72 B ATCC, USA a B/Hong Kong/5/72 B Hayden, USA c B/Lee/40 B ATCC, USA a B/Victoria/70 B Canberra, Australia e B/Harbin/07/94 B Logan, Utah, USA f B/Y177 B Pasteur Institute, Brussels, Belgium h B/Y253 B Pasteur Institute, Brussels, Belgium h B/Y263 B Pasteur Institute, Brussels, Belgium h Open in a separate window a American Type Culture Collection, Manassas, Va. b Skehel, World Influenza Centre, Mill Hill, United Kingdom. c Frederic Hayden, University of Virginia, Charlottesville, Va. d Robert Webster, St. Jude Children's Hospital, Memphis, Tenn. e Graeme Laver, Australian National University, Canberra, Australia. f Robert Sidwell, Utah State University, Logan, Utah. g Bert Johannson, New York Medical College, Valhalla, N.Y. h Ferdinand Yane, Pasteur Institute, Brussels, Belgium.

Techniques: Comparison

Mean IC 90 s according to influenza virus type

Journal:

Article Title: Comparison of the Anti-Influenza Virus Activity of RWJ-270201 with Those of Oseltamivir and Zanamivir

doi: 10.1128/AAC.45.4.1162-1167.2001

Figure Lengend Snippet: Mean IC 90 s according to influenza virus type

Article Snippet: The influenza viruses used in this study, together with their sources, are shown in Table . table ft1 table-wrap mode="anchored" t5 TABLE 1 caption a7 Virus Type Source A/PR/8/34 H1N1 ATCC, USA a A1/FM/1/47 H1N1 ATCC, USA a A/NWS/33 H1N1 ATCC, USA a A/Brazil/11/78 H1N1 Skehel, United Kingdom b A/Taiwan/1/86 H1N1 Hayden, USA c A2/Hong Kong/8/68 H2N2 ATCC, USA a A/Singapore/1/57 H2N2 Memphis, Tenn., USA d A/Tokyo/3/67 H2N2 Canberra, Australia e A/Japan H2N2 ATCC, USA a A/Aichi H3N2 ATCC, USA a A/Belgium/2/81 H3N2 Skehel, United Kingdom b A/Shangdong/09/93 H3N2 Logan, Utah, USA f A/Virginia/88 H3N2 Hayden, USA c A/Turkey/Mass/76A/Beijing/32/92 [R] H6N2 Valhalla, N.Y., USA g B/Hong Kong/5/72 B ATCC, USA a B/Hong Kong/5/72 B Hayden, USA c B/Lee/40 B ATCC, USA a B/Victoria/70 B Canberra, Australia e B/Harbin/07/94 B Logan, Utah, USA f B/Y177 B Pasteur Institute, Brussels, Belgium h B/Y253 B Pasteur Institute, Brussels, Belgium h B/Y263 B Pasteur Institute, Brussels, Belgium h Open in a separate window a American Type Culture Collection, Manassas, Va. b Skehel, World Influenza Centre, Mill Hill, United Kingdom. c Frederic Hayden, University of Virginia, Charlottesville, Va. d Robert Webster, St. Jude Children's Hospital, Memphis, Tenn. e Graeme Laver, Australian National University, Canberra, Australia. f Robert Sidwell, Utah State University, Logan, Utah. g Bert Johannson, New York Medical College, Valhalla, N.Y. h Ferdinand Yane, Pasteur Institute, Brussels, Belgium.

Techniques: Virus

Effect of oral gavage treatment with RWJ-270201 on influenza virus infections in mice (prophylaxis model)

Journal:

Article Title: Comparison of the Anti-Influenza Virus Activity of RWJ-270201 with Those of Oseltamivir and Zanamivir

doi: 10.1128/AAC.45.4.1162-1167.2001

Figure Lengend Snippet: Effect of oral gavage treatment with RWJ-270201 on influenza virus infections in mice (prophylaxis model)

Article Snippet: The influenza viruses used in this study, together with their sources, are shown in Table . table ft1 table-wrap mode="anchored" t5 TABLE 1 caption a7 Virus Type Source A/PR/8/34 H1N1 ATCC, USA a A1/FM/1/47 H1N1 ATCC, USA a A/NWS/33 H1N1 ATCC, USA a A/Brazil/11/78 H1N1 Skehel, United Kingdom b A/Taiwan/1/86 H1N1 Hayden, USA c A2/Hong Kong/8/68 H2N2 ATCC, USA a A/Singapore/1/57 H2N2 Memphis, Tenn., USA d A/Tokyo/3/67 H2N2 Canberra, Australia e A/Japan H2N2 ATCC, USA a A/Aichi H3N2 ATCC, USA a A/Belgium/2/81 H3N2 Skehel, United Kingdom b A/Shangdong/09/93 H3N2 Logan, Utah, USA f A/Virginia/88 H3N2 Hayden, USA c A/Turkey/Mass/76A/Beijing/32/92 [R] H6N2 Valhalla, N.Y., USA g B/Hong Kong/5/72 B ATCC, USA a B/Hong Kong/5/72 B Hayden, USA c B/Lee/40 B ATCC, USA a B/Victoria/70 B Canberra, Australia e B/Harbin/07/94 B Logan, Utah, USA f B/Y177 B Pasteur Institute, Brussels, Belgium h B/Y253 B Pasteur Institute, Brussels, Belgium h B/Y263 B Pasteur Institute, Brussels, Belgium h Open in a separate window a American Type Culture Collection, Manassas, Va. b Skehel, World Influenza Centre, Mill Hill, United Kingdom. c Frederic Hayden, University of Virginia, Charlottesville, Va. d Robert Webster, St. Jude Children's Hospital, Memphis, Tenn. e Graeme Laver, Australian National University, Canberra, Australia. f Robert Sidwell, Utah State University, Logan, Utah. g Bert Johannson, New York Medical College, Valhalla, N.Y. h Ferdinand Yane, Pasteur Institute, Brussels, Belgium.

Techniques: Virus, Saline