nci h1355  (ATCC)


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    ATCC nci h1355
    ( a ) Representative fluorescence images for data in Fig. . Scale bar: 200 μm. ( b-c ) FAS inhibitors repress SARS-CoV-2 viral replication. HEK293T-hACE2 cells treated with Orlistat (1 µM) or TVB-2640 (100 nM) and infected with SARS-CoV-2 at h 0. ( b ) Viral RNA by qPCR at indicated time points. ( c ) Infectious viral titers in supernatant by plaque assay. ( d ) Representative fluorescence images of SARS-CoV-2-mNG infected multiple cell lines. Indicated cells were pre-treated with FAS inhibitors at the following concentration: <t>NCI-H1355</t> and NCI-1437 (Orlistat 20 μM, TVB-2640 2 µM and TVB-3664 1 µM); Caco-2 (Orlistat 80 μM, TVB-2640 2 µM and TVB-3664 1 µM); MEF-hACE2 (Orlistat 5 μM, TVB-2640 1 µM and TVB-3664 0.5 µM), from 16 h before infection and then infected with SARS-CoV-2-mNG at an MOI = 0.1(NCI-H1355, NCI-1437), MOI = 0.05 (Caco-2), MOI = 0.01 (MEF-hACE2). Fluorescence images were acquired at 48 hpi. Hoechst 33342 was used for nuclear staining. Scale bar: 200 μm. ( e , f ) Assessment of anti-SARS-CoV-2 ability of FAS inhibitors in multiple cell lines. Indicated cells were pre-treated with FAS inhibitors and infected with SARS-CoV-2 as described in Extended Data Fig. 2d. 24 h after infection, cells were collected for quantification of intracellular viral RNA by qPCR ( e ), supernatants were collected for quantification of viral titer by plaque assay ( f ). Data in b-c and e-f are representative of three independent experiments and are plotted as the mean ± SD (n = 3 (c, f), n = 4 ( b , e ) per group). The experiment in a and d have been independently repeated three times with similar result. ND: not detected. Statistical analyses were performed with two-way ANOVA followed by Dunnett’s post-test ( b , c ) and one-way ANOVA followed by Dunnett’s post-test ( e , f ). *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001, ns, not significant (p > 0.05), comparing to DMSO-treated cells ( e , f ) or DMSO-treated cells at each time point ( b , c ).
    Nci H1355, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Pharmacological inhibition of fatty acid synthesis blocks SARS-CoV-2 replication"

    Article Title: Pharmacological inhibition of fatty acid synthesis blocks SARS-CoV-2 replication

    Journal: Nature Metabolism

    doi: 10.1038/s42255-021-00479-4

    ( a ) Representative fluorescence images for data in Fig. . Scale bar: 200 μm. ( b-c ) FAS inhibitors repress SARS-CoV-2 viral replication. HEK293T-hACE2 cells treated with Orlistat (1 µM) or TVB-2640 (100 nM) and infected with SARS-CoV-2 at h 0. ( b ) Viral RNA by qPCR at indicated time points. ( c ) Infectious viral titers in supernatant by plaque assay. ( d ) Representative fluorescence images of SARS-CoV-2-mNG infected multiple cell lines. Indicated cells were pre-treated with FAS inhibitors at the following concentration: NCI-H1355 and NCI-1437 (Orlistat 20 μM, TVB-2640 2 µM and TVB-3664 1 µM); Caco-2 (Orlistat 80 μM, TVB-2640 2 µM and TVB-3664 1 µM); MEF-hACE2 (Orlistat 5 μM, TVB-2640 1 µM and TVB-3664 0.5 µM), from 16 h before infection and then infected with SARS-CoV-2-mNG at an MOI = 0.1(NCI-H1355, NCI-1437), MOI = 0.05 (Caco-2), MOI = 0.01 (MEF-hACE2). Fluorescence images were acquired at 48 hpi. Hoechst 33342 was used for nuclear staining. Scale bar: 200 μm. ( e , f ) Assessment of anti-SARS-CoV-2 ability of FAS inhibitors in multiple cell lines. Indicated cells were pre-treated with FAS inhibitors and infected with SARS-CoV-2 as described in Extended Data Fig. 2d. 24 h after infection, cells were collected for quantification of intracellular viral RNA by qPCR ( e ), supernatants were collected for quantification of viral titer by plaque assay ( f ). Data in b-c and e-f are representative of three independent experiments and are plotted as the mean ± SD (n = 3 (c, f), n = 4 ( b , e ) per group). The experiment in a and d have been independently repeated three times with similar result. ND: not detected. Statistical analyses were performed with two-way ANOVA followed by Dunnett’s post-test ( b , c ) and one-way ANOVA followed by Dunnett’s post-test ( e , f ). *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001, ns, not significant (p > 0.05), comparing to DMSO-treated cells ( e , f ) or DMSO-treated cells at each time point ( b , c ).
    Figure Legend Snippet: ( a ) Representative fluorescence images for data in Fig. . Scale bar: 200 μm. ( b-c ) FAS inhibitors repress SARS-CoV-2 viral replication. HEK293T-hACE2 cells treated with Orlistat (1 µM) or TVB-2640 (100 nM) and infected with SARS-CoV-2 at h 0. ( b ) Viral RNA by qPCR at indicated time points. ( c ) Infectious viral titers in supernatant by plaque assay. ( d ) Representative fluorescence images of SARS-CoV-2-mNG infected multiple cell lines. Indicated cells were pre-treated with FAS inhibitors at the following concentration: NCI-H1355 and NCI-1437 (Orlistat 20 μM, TVB-2640 2 µM and TVB-3664 1 µM); Caco-2 (Orlistat 80 μM, TVB-2640 2 µM and TVB-3664 1 µM); MEF-hACE2 (Orlistat 5 μM, TVB-2640 1 µM and TVB-3664 0.5 µM), from 16 h before infection and then infected with SARS-CoV-2-mNG at an MOI = 0.1(NCI-H1355, NCI-1437), MOI = 0.05 (Caco-2), MOI = 0.01 (MEF-hACE2). Fluorescence images were acquired at 48 hpi. Hoechst 33342 was used for nuclear staining. Scale bar: 200 μm. ( e , f ) Assessment of anti-SARS-CoV-2 ability of FAS inhibitors in multiple cell lines. Indicated cells were pre-treated with FAS inhibitors and infected with SARS-CoV-2 as described in Extended Data Fig. 2d. 24 h after infection, cells were collected for quantification of intracellular viral RNA by qPCR ( e ), supernatants were collected for quantification of viral titer by plaque assay ( f ). Data in b-c and e-f are representative of three independent experiments and are plotted as the mean ± SD (n = 3 (c, f), n = 4 ( b , e ) per group). The experiment in a and d have been independently repeated three times with similar result. ND: not detected. Statistical analyses were performed with two-way ANOVA followed by Dunnett’s post-test ( b , c ) and one-way ANOVA followed by Dunnett’s post-test ( e , f ). *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001, ns, not significant (p > 0.05), comparing to DMSO-treated cells ( e , f ) or DMSO-treated cells at each time point ( b , c ).

    Techniques Used: Fluorescence, Infection, Plaque Assay, Concentration Assay, Staining

    ( a ) Representative fluorescence images of palmitoylated protein assay. HEK293T-hACE2 and NCI-H1355 cells were treated with FAS inhibitors (HEK293T-hACE2 cells: Orlistat 1 µM, TVB-2640 100 nM, and TVB-3664 20 nM; NCI-H1355 cells: Orlistat 20 μM, TVB-2640 2 µM, and TVB-3664 1 µM) for 24 h and the EZClick™ palmitic acid label was added to the medium for another 24 h. Cells were then processed and analyzed by microscopy following the manufacturer’s instruction. Scale bar: 40 μm. ( b ) HEK293T-hACE2 and NCI-H1355 cells were treated with FAS inhibitors (HEK293T-hACE2 cells: Orlistat 1 µM, TVB-2640 100 nM, and TVB-3664 20 nM; NCI-H1355 cells: Orlistat 20 μM, TVB-2640 2 µM, and TVB-3664 1 µM) for 24 h, then analyzed with FFA assay following the manufacturer’s instruction. ( c ) Palmitic acid reverses the effects of fatty acid synthase knockout on viral replication. FASN knockout HEK293T-hACE2 cells were pre-treated with bovine serum albumin- conjugated palmitic acid (PA-BSA) at indicated final concentrations 2 hours before infection. The cells were infected with the SARS-CoV-2 virus at an MOI of 0.01. Viral RNA was analyzed at 24 hpi by qPCR. Wild-type (WT) HEK293T-hACE2 were used as a negative control. ( d ) Palmitic acid reverses the effects of FAS inhibitors on viral replication. HEK293T-hACE2 cells were pre-treated FAS inhibitors (Orlistat 1 µM, TVB-2640 100 nM, and TVB-3664 20 nM) for 14 h. PA-BSA was then added at the indicated final concentrations and the cells were treated for another 2 h. The cells were infected with SARS-CoV-2 virus at an MOI of 0.01. Viral RNA was analyzed at 24 hpi by qPCR. DMSO treated cells were used as a negative control. Data in b - d are representative of three independent experiments and are plotted as the mean ± SD (n = 3 ( b ), n = 4 ( c , d ) per group). The experiment in a has been independently repeated three times with similar result. One-way ANOVA followed by Dunnett’s post-test was used for statistical analysis ( b-d ). *p < 0.05, **p < 0.01, ****p < 0.0001, and ns, not significant (p > 0.05), comparing to BSA-treated FASN-KO HEK293T-hACE2 cells ( c ), or DMSO- ( b ) / BSA- ( d ) treated HEK293T-hACE2 cells.
    Figure Legend Snippet: ( a ) Representative fluorescence images of palmitoylated protein assay. HEK293T-hACE2 and NCI-H1355 cells were treated with FAS inhibitors (HEK293T-hACE2 cells: Orlistat 1 µM, TVB-2640 100 nM, and TVB-3664 20 nM; NCI-H1355 cells: Orlistat 20 μM, TVB-2640 2 µM, and TVB-3664 1 µM) for 24 h and the EZClick™ palmitic acid label was added to the medium for another 24 h. Cells were then processed and analyzed by microscopy following the manufacturer’s instruction. Scale bar: 40 μm. ( b ) HEK293T-hACE2 and NCI-H1355 cells were treated with FAS inhibitors (HEK293T-hACE2 cells: Orlistat 1 µM, TVB-2640 100 nM, and TVB-3664 20 nM; NCI-H1355 cells: Orlistat 20 μM, TVB-2640 2 µM, and TVB-3664 1 µM) for 24 h, then analyzed with FFA assay following the manufacturer’s instruction. ( c ) Palmitic acid reverses the effects of fatty acid synthase knockout on viral replication. FASN knockout HEK293T-hACE2 cells were pre-treated with bovine serum albumin- conjugated palmitic acid (PA-BSA) at indicated final concentrations 2 hours before infection. The cells were infected with the SARS-CoV-2 virus at an MOI of 0.01. Viral RNA was analyzed at 24 hpi by qPCR. Wild-type (WT) HEK293T-hACE2 were used as a negative control. ( d ) Palmitic acid reverses the effects of FAS inhibitors on viral replication. HEK293T-hACE2 cells were pre-treated FAS inhibitors (Orlistat 1 µM, TVB-2640 100 nM, and TVB-3664 20 nM) for 14 h. PA-BSA was then added at the indicated final concentrations and the cells were treated for another 2 h. The cells were infected with SARS-CoV-2 virus at an MOI of 0.01. Viral RNA was analyzed at 24 hpi by qPCR. DMSO treated cells were used as a negative control. Data in b - d are representative of three independent experiments and are plotted as the mean ± SD (n = 3 ( b ), n = 4 ( c , d ) per group). The experiment in a has been independently repeated three times with similar result. One-way ANOVA followed by Dunnett’s post-test was used for statistical analysis ( b-d ). *p < 0.05, **p < 0.01, ****p < 0.0001, and ns, not significant (p > 0.05), comparing to BSA-treated FASN-KO HEK293T-hACE2 cells ( c ), or DMSO- ( b ) / BSA- ( d ) treated HEK293T-hACE2 cells.

    Techniques Used: Fluorescence, Microscopy, Knock-Out, Infection, Negative Control

    ( a ) NCI-H1355 cells were pre-treated with FAS inhibitors, Orlistat (20 μM), TVB-2640 (2 µM), or TVB-3664 (1 µM) for 16 h and infected with SARS-CoV-2 variants with an MOI of 0.1. The cells were analyzed by qPCR for viral RNA at 48 hpi. ( b ) MEF-hACE2 cells were pre-treated with FAS inhibitors, Orlistat (5 μM), TVB-2640 (1 µM), or TVB-3664 (0.5 µM) for 16 h and infected with SARS-CoV-2 variants with an MOI of 0.05. The cells were analyzed by qPCR for viral RNA at 48 hpi. Data in a-b are representative of three independent experiments and are plotted as the mean ± SD (n = 3 ( a , b ) per group). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s post-test. ****p < 0.0001.
    Figure Legend Snippet: ( a ) NCI-H1355 cells were pre-treated with FAS inhibitors, Orlistat (20 μM), TVB-2640 (2 µM), or TVB-3664 (1 µM) for 16 h and infected with SARS-CoV-2 variants with an MOI of 0.1. The cells were analyzed by qPCR for viral RNA at 48 hpi. ( b ) MEF-hACE2 cells were pre-treated with FAS inhibitors, Orlistat (5 μM), TVB-2640 (1 µM), or TVB-3664 (0.5 µM) for 16 h and infected with SARS-CoV-2 variants with an MOI of 0.05. The cells were analyzed by qPCR for viral RNA at 48 hpi. Data in a-b are representative of three independent experiments and are plotted as the mean ± SD (n = 3 ( a , b ) per group). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s post-test. ****p < 0.0001.

    Techniques Used: Infection

    crl 5865  (ATCC)


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    ATCC crl 5865
    Crl 5865, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    nci h1355 atcc crl 5865 human  (ATCC)


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    ATCC nci h1355 atcc crl 5865 human
    Nci H1355 Atcc Crl 5865 Human, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    nci h1355  (ATCC)


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    ATCC nci h1355
    ( a ) Representative fluorescence images for data in Fig. . Scale bar: 200 μm. ( b-c ) FAS inhibitors repress SARS-CoV-2 viral replication. HEK293T-hACE2 cells treated with Orlistat (1 µM) or TVB-2640 (100 nM) and infected with SARS-CoV-2 at h 0. ( b ) Viral RNA by qPCR at indicated time points. ( c ) Infectious viral titers in supernatant by plaque assay. ( d ) Representative fluorescence images of SARS-CoV-2-mNG infected multiple cell lines. Indicated cells were pre-treated with FAS inhibitors at the following concentration: <t>NCI-H1355</t> and NCI-1437 (Orlistat 20 μM, TVB-2640 2 µM and TVB-3664 1 µM); Caco-2 (Orlistat 80 μM, TVB-2640 2 µM and TVB-3664 1 µM); MEF-hACE2 (Orlistat 5 μM, TVB-2640 1 µM and TVB-3664 0.5 µM), from 16 h before infection and then infected with SARS-CoV-2-mNG at an MOI = 0.1(NCI-H1355, NCI-1437), MOI = 0.05 (Caco-2), MOI = 0.01 (MEF-hACE2). Fluorescence images were acquired at 48 hpi. Hoechst 33342 was used for nuclear staining. Scale bar: 200 μm. ( e , f ) Assessment of anti-SARS-CoV-2 ability of FAS inhibitors in multiple cell lines. Indicated cells were pre-treated with FAS inhibitors and infected with SARS-CoV-2 as described in Extended Data Fig. 2d. 24 h after infection, cells were collected for quantification of intracellular viral RNA by qPCR ( e ), supernatants were collected for quantification of viral titer by plaque assay ( f ). Data in b-c and e-f are representative of three independent experiments and are plotted as the mean ± SD (n = 3 (c, f), n = 4 ( b , e ) per group). The experiment in a and d have been independently repeated three times with similar result. ND: not detected. Statistical analyses were performed with two-way ANOVA followed by Dunnett’s post-test ( b , c ) and one-way ANOVA followed by Dunnett’s post-test ( e , f ). *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001, ns, not significant (p > 0.05), comparing to DMSO-treated cells ( e , f ) or DMSO-treated cells at each time point ( b , c ).
    Nci H1355, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/nci h1355/product/ATCC
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    nci h1355 - by Bioz Stars, 2024-05
    99/100 stars

    Images

    1) Product Images from "Pharmacological inhibition of fatty acid synthesis blocks SARS-CoV-2 replication"

    Article Title: Pharmacological inhibition of fatty acid synthesis blocks SARS-CoV-2 replication

    Journal: Nature Metabolism

    doi: 10.1038/s42255-021-00479-4

    ( a ) Representative fluorescence images for data in Fig. . Scale bar: 200 μm. ( b-c ) FAS inhibitors repress SARS-CoV-2 viral replication. HEK293T-hACE2 cells treated with Orlistat (1 µM) or TVB-2640 (100 nM) and infected with SARS-CoV-2 at h 0. ( b ) Viral RNA by qPCR at indicated time points. ( c ) Infectious viral titers in supernatant by plaque assay. ( d ) Representative fluorescence images of SARS-CoV-2-mNG infected multiple cell lines. Indicated cells were pre-treated with FAS inhibitors at the following concentration: NCI-H1355 and NCI-1437 (Orlistat 20 μM, TVB-2640 2 µM and TVB-3664 1 µM); Caco-2 (Orlistat 80 μM, TVB-2640 2 µM and TVB-3664 1 µM); MEF-hACE2 (Orlistat 5 μM, TVB-2640 1 µM and TVB-3664 0.5 µM), from 16 h before infection and then infected with SARS-CoV-2-mNG at an MOI = 0.1(NCI-H1355, NCI-1437), MOI = 0.05 (Caco-2), MOI = 0.01 (MEF-hACE2). Fluorescence images were acquired at 48 hpi. Hoechst 33342 was used for nuclear staining. Scale bar: 200 μm. ( e , f ) Assessment of anti-SARS-CoV-2 ability of FAS inhibitors in multiple cell lines. Indicated cells were pre-treated with FAS inhibitors and infected with SARS-CoV-2 as described in Extended Data Fig. 2d. 24 h after infection, cells were collected for quantification of intracellular viral RNA by qPCR ( e ), supernatants were collected for quantification of viral titer by plaque assay ( f ). Data in b-c and e-f are representative of three independent experiments and are plotted as the mean ± SD (n = 3 (c, f), n = 4 ( b , e ) per group). The experiment in a and d have been independently repeated three times with similar result. ND: not detected. Statistical analyses were performed with two-way ANOVA followed by Dunnett’s post-test ( b , c ) and one-way ANOVA followed by Dunnett’s post-test ( e , f ). *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001, ns, not significant (p > 0.05), comparing to DMSO-treated cells ( e , f ) or DMSO-treated cells at each time point ( b , c ).
    Figure Legend Snippet: ( a ) Representative fluorescence images for data in Fig. . Scale bar: 200 μm. ( b-c ) FAS inhibitors repress SARS-CoV-2 viral replication. HEK293T-hACE2 cells treated with Orlistat (1 µM) or TVB-2640 (100 nM) and infected with SARS-CoV-2 at h 0. ( b ) Viral RNA by qPCR at indicated time points. ( c ) Infectious viral titers in supernatant by plaque assay. ( d ) Representative fluorescence images of SARS-CoV-2-mNG infected multiple cell lines. Indicated cells were pre-treated with FAS inhibitors at the following concentration: NCI-H1355 and NCI-1437 (Orlistat 20 μM, TVB-2640 2 µM and TVB-3664 1 µM); Caco-2 (Orlistat 80 μM, TVB-2640 2 µM and TVB-3664 1 µM); MEF-hACE2 (Orlistat 5 μM, TVB-2640 1 µM and TVB-3664 0.5 µM), from 16 h before infection and then infected with SARS-CoV-2-mNG at an MOI = 0.1(NCI-H1355, NCI-1437), MOI = 0.05 (Caco-2), MOI = 0.01 (MEF-hACE2). Fluorescence images were acquired at 48 hpi. Hoechst 33342 was used for nuclear staining. Scale bar: 200 μm. ( e , f ) Assessment of anti-SARS-CoV-2 ability of FAS inhibitors in multiple cell lines. Indicated cells were pre-treated with FAS inhibitors and infected with SARS-CoV-2 as described in Extended Data Fig. 2d. 24 h after infection, cells were collected for quantification of intracellular viral RNA by qPCR ( e ), supernatants were collected for quantification of viral titer by plaque assay ( f ). Data in b-c and e-f are representative of three independent experiments and are plotted as the mean ± SD (n = 3 (c, f), n = 4 ( b , e ) per group). The experiment in a and d have been independently repeated three times with similar result. ND: not detected. Statistical analyses were performed with two-way ANOVA followed by Dunnett’s post-test ( b , c ) and one-way ANOVA followed by Dunnett’s post-test ( e , f ). *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001, ns, not significant (p > 0.05), comparing to DMSO-treated cells ( e , f ) or DMSO-treated cells at each time point ( b , c ).

    Techniques Used: Fluorescence, Infection, Plaque Assay, Concentration Assay, Staining

    ( a ) Representative fluorescence images of palmitoylated protein assay. HEK293T-hACE2 and NCI-H1355 cells were treated with FAS inhibitors (HEK293T-hACE2 cells: Orlistat 1 µM, TVB-2640 100 nM, and TVB-3664 20 nM; NCI-H1355 cells: Orlistat 20 μM, TVB-2640 2 µM, and TVB-3664 1 µM) for 24 h and the EZClick™ palmitic acid label was added to the medium for another 24 h. Cells were then processed and analyzed by microscopy following the manufacturer’s instruction. Scale bar: 40 μm. ( b ) HEK293T-hACE2 and NCI-H1355 cells were treated with FAS inhibitors (HEK293T-hACE2 cells: Orlistat 1 µM, TVB-2640 100 nM, and TVB-3664 20 nM; NCI-H1355 cells: Orlistat 20 μM, TVB-2640 2 µM, and TVB-3664 1 µM) for 24 h, then analyzed with FFA assay following the manufacturer’s instruction. ( c ) Palmitic acid reverses the effects of fatty acid synthase knockout on viral replication. FASN knockout HEK293T-hACE2 cells were pre-treated with bovine serum albumin- conjugated palmitic acid (PA-BSA) at indicated final concentrations 2 hours before infection. The cells were infected with the SARS-CoV-2 virus at an MOI of 0.01. Viral RNA was analyzed at 24 hpi by qPCR. Wild-type (WT) HEK293T-hACE2 were used as a negative control. ( d ) Palmitic acid reverses the effects of FAS inhibitors on viral replication. HEK293T-hACE2 cells were pre-treated FAS inhibitors (Orlistat 1 µM, TVB-2640 100 nM, and TVB-3664 20 nM) for 14 h. PA-BSA was then added at the indicated final concentrations and the cells were treated for another 2 h. The cells were infected with SARS-CoV-2 virus at an MOI of 0.01. Viral RNA was analyzed at 24 hpi by qPCR. DMSO treated cells were used as a negative control. Data in b - d are representative of three independent experiments and are plotted as the mean ± SD (n = 3 ( b ), n = 4 ( c , d ) per group). The experiment in a has been independently repeated three times with similar result. One-way ANOVA followed by Dunnett’s post-test was used for statistical analysis ( b-d ). *p < 0.05, **p < 0.01, ****p < 0.0001, and ns, not significant (p > 0.05), comparing to BSA-treated FASN-KO HEK293T-hACE2 cells ( c ), or DMSO- ( b ) / BSA- ( d ) treated HEK293T-hACE2 cells.
    Figure Legend Snippet: ( a ) Representative fluorescence images of palmitoylated protein assay. HEK293T-hACE2 and NCI-H1355 cells were treated with FAS inhibitors (HEK293T-hACE2 cells: Orlistat 1 µM, TVB-2640 100 nM, and TVB-3664 20 nM; NCI-H1355 cells: Orlistat 20 μM, TVB-2640 2 µM, and TVB-3664 1 µM) for 24 h and the EZClick™ palmitic acid label was added to the medium for another 24 h. Cells were then processed and analyzed by microscopy following the manufacturer’s instruction. Scale bar: 40 μm. ( b ) HEK293T-hACE2 and NCI-H1355 cells were treated with FAS inhibitors (HEK293T-hACE2 cells: Orlistat 1 µM, TVB-2640 100 nM, and TVB-3664 20 nM; NCI-H1355 cells: Orlistat 20 μM, TVB-2640 2 µM, and TVB-3664 1 µM) for 24 h, then analyzed with FFA assay following the manufacturer’s instruction. ( c ) Palmitic acid reverses the effects of fatty acid synthase knockout on viral replication. FASN knockout HEK293T-hACE2 cells were pre-treated with bovine serum albumin- conjugated palmitic acid (PA-BSA) at indicated final concentrations 2 hours before infection. The cells were infected with the SARS-CoV-2 virus at an MOI of 0.01. Viral RNA was analyzed at 24 hpi by qPCR. Wild-type (WT) HEK293T-hACE2 were used as a negative control. ( d ) Palmitic acid reverses the effects of FAS inhibitors on viral replication. HEK293T-hACE2 cells were pre-treated FAS inhibitors (Orlistat 1 µM, TVB-2640 100 nM, and TVB-3664 20 nM) for 14 h. PA-BSA was then added at the indicated final concentrations and the cells were treated for another 2 h. The cells were infected with SARS-CoV-2 virus at an MOI of 0.01. Viral RNA was analyzed at 24 hpi by qPCR. DMSO treated cells were used as a negative control. Data in b - d are representative of three independent experiments and are plotted as the mean ± SD (n = 3 ( b ), n = 4 ( c , d ) per group). The experiment in a has been independently repeated three times with similar result. One-way ANOVA followed by Dunnett’s post-test was used for statistical analysis ( b-d ). *p < 0.05, **p < 0.01, ****p < 0.0001, and ns, not significant (p > 0.05), comparing to BSA-treated FASN-KO HEK293T-hACE2 cells ( c ), or DMSO- ( b ) / BSA- ( d ) treated HEK293T-hACE2 cells.

    Techniques Used: Fluorescence, Microscopy, Knock-Out, Infection, Negative Control

    ( a ) NCI-H1355 cells were pre-treated with FAS inhibitors, Orlistat (20 μM), TVB-2640 (2 µM), or TVB-3664 (1 µM) for 16 h and infected with SARS-CoV-2 variants with an MOI of 0.1. The cells were analyzed by qPCR for viral RNA at 48 hpi. ( b ) MEF-hACE2 cells were pre-treated with FAS inhibitors, Orlistat (5 μM), TVB-2640 (1 µM), or TVB-3664 (0.5 µM) for 16 h and infected with SARS-CoV-2 variants with an MOI of 0.05. The cells were analyzed by qPCR for viral RNA at 48 hpi. Data in a-b are representative of three independent experiments and are plotted as the mean ± SD (n = 3 ( a , b ) per group). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s post-test. ****p < 0.0001.
    Figure Legend Snippet: ( a ) NCI-H1355 cells were pre-treated with FAS inhibitors, Orlistat (20 μM), TVB-2640 (2 µM), or TVB-3664 (1 µM) for 16 h and infected with SARS-CoV-2 variants with an MOI of 0.1. The cells were analyzed by qPCR for viral RNA at 48 hpi. ( b ) MEF-hACE2 cells were pre-treated with FAS inhibitors, Orlistat (5 μM), TVB-2640 (1 µM), or TVB-3664 (0.5 µM) for 16 h and infected with SARS-CoV-2 variants with an MOI of 0.05. The cells were analyzed by qPCR for viral RNA at 48 hpi. Data in a-b are representative of three independent experiments and are plotted as the mean ± SD (n = 3 ( a , b ) per group). Statistical analyses were performed using one-way ANOVA followed by Dunnett’s post-test. ****p < 0.0001.

    Techniques Used: Infection

    mycolicibacterium phlei 5865 t  (ATCC)


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    ATCC mycolicibacterium phlei 5865 t
    Mycolicibacterium Phlei 5865 T, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ev a71  (ATCC)


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    ATCC ev a71
    Effect of novel PI4KIIIβ and capsid inhibitors on the replication of <t>EV-A71</t> in vitro. RD cells infected with EV-A71 was treated with each of the compounds at 5 different concentrations and 0 µM refers to control infected cells treated with 0.1% DMSO. Virus titres achieved at 12 h.p.i. was determined by viral plaque assays and represented as bars on each of the charts. Cell viability of drug-treated non-infected cells was assessed by alamarBLUE Cell Viability Reagent and expressed as a percentage compared to control DMSO-treated cells. Novel PI4KIIIβ inhibitors were: N314, N339, N354, N373, N377, R006, R036, R041, S002, S003, S007, S011 and S014. N373 was selected for further studies based on superior cell viability profile and inhibition of EV-A71 replication. G197 was found to be more effective in inhibiting EV-A71 replication than control capsid inhibitor BTA-798. Bars represent Log 10 virus titres (PFU/ml) and points represent cell viability across the different compound concentrations. Dashed lines indicate negative control virus titre (top line) and a 2 Log 10 unit reduction in virus titre (lower line). Statistical analysis for differences in virus titre due to drug treatment was performed with one-way ANOVA with Dunnett’s post-test: *( p < 0.05), **( p < 0.01), ***( p < 0.005).
    Ev A71, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Novel capsid binder and PI4KIIIbeta inhibitors for EV-A71 replication inhibition"

    Article Title: Novel capsid binder and PI4KIIIbeta inhibitors for EV-A71 replication inhibition

    Journal: Scientific Reports

    doi: 10.1038/s41598-021-89271-8

    Effect of novel PI4KIIIβ and capsid inhibitors on the replication of EV-A71 in vitro. RD cells infected with EV-A71 was treated with each of the compounds at 5 different concentrations and 0 µM refers to control infected cells treated with 0.1% DMSO. Virus titres achieved at 12 h.p.i. was determined by viral plaque assays and represented as bars on each of the charts. Cell viability of drug-treated non-infected cells was assessed by alamarBLUE Cell Viability Reagent and expressed as a percentage compared to control DMSO-treated cells. Novel PI4KIIIβ inhibitors were: N314, N339, N354, N373, N377, R006, R036, R041, S002, S003, S007, S011 and S014. N373 was selected for further studies based on superior cell viability profile and inhibition of EV-A71 replication. G197 was found to be more effective in inhibiting EV-A71 replication than control capsid inhibitor BTA-798. Bars represent Log 10 virus titres (PFU/ml) and points represent cell viability across the different compound concentrations. Dashed lines indicate negative control virus titre (top line) and a 2 Log 10 unit reduction in virus titre (lower line). Statistical analysis for differences in virus titre due to drug treatment was performed with one-way ANOVA with Dunnett’s post-test: *( p < 0.05), **( p < 0.01), ***( p < 0.005).
    Figure Legend Snippet: Effect of novel PI4KIIIβ and capsid inhibitors on the replication of EV-A71 in vitro. RD cells infected with EV-A71 was treated with each of the compounds at 5 different concentrations and 0 µM refers to control infected cells treated with 0.1% DMSO. Virus titres achieved at 12 h.p.i. was determined by viral plaque assays and represented as bars on each of the charts. Cell viability of drug-treated non-infected cells was assessed by alamarBLUE Cell Viability Reagent and expressed as a percentage compared to control DMSO-treated cells. Novel PI4KIIIβ inhibitors were: N314, N339, N354, N373, N377, R006, R036, R041, S002, S003, S007, S011 and S014. N373 was selected for further studies based on superior cell viability profile and inhibition of EV-A71 replication. G197 was found to be more effective in inhibiting EV-A71 replication than control capsid inhibitor BTA-798. Bars represent Log 10 virus titres (PFU/ml) and points represent cell viability across the different compound concentrations. Dashed lines indicate negative control virus titre (top line) and a 2 Log 10 unit reduction in virus titre (lower line). Statistical analysis for differences in virus titre due to drug treatment was performed with one-way ANOVA with Dunnett’s post-test: *( p < 0.05), **( p < 0.01), ***( p < 0.005).

    Techniques Used: In Vitro, Infection, Inhibition, Negative Control

    Treatment with G197 and N373 resulted decreased viral protein translation and treatment with G197 before virus entry resulted in greater inhibition efficacy consistent with the behaviour of capsid binding inhibitors. ( A ) Post-treatment of infected cells with G197 and ( B ) N373 resulted in a decrease in VP2 and precursor VP0 expression. Full length blots available were included as Supplementary Information 1. ( C ) Time-of-addition assay with G197 and N373 at 1 µM and negative control 0.1% DMSO. Treatment of cells with G197 before 0 h result in an abolishment of virus replication and addition of after virus has entered the cells were only able to reduce virus titres by a maximum of 1 Log 10 unit and no inhibition was observed from 2 h.p.i. N373 treatment gradually lost efficacy with delayed treatment up to 2 h.p.i. to no inhibition at 8 h.p.i. ( D ) Treatment of cells with G197 and N373 during the 1 h virus inoculation reduced virus titres significantly and G197 was more effective than N373. Statistical analysis for differences in virus titre due to drug treatment was performed with one-way ANOVA with Dunnett’s post-test: ***( p < 0.005). ( E ) Thermal stability of EV-A71 was assessed by incubating virus suspensions at temperatures from 37 to 60 °C in the presence of 0.1% DMSO or 1 µM G197. The presence of G197 improved the thermal stability of virus particles at elevated temperatures.
    Figure Legend Snippet: Treatment with G197 and N373 resulted decreased viral protein translation and treatment with G197 before virus entry resulted in greater inhibition efficacy consistent with the behaviour of capsid binding inhibitors. ( A ) Post-treatment of infected cells with G197 and ( B ) N373 resulted in a decrease in VP2 and precursor VP0 expression. Full length blots available were included as Supplementary Information 1. ( C ) Time-of-addition assay with G197 and N373 at 1 µM and negative control 0.1% DMSO. Treatment of cells with G197 before 0 h result in an abolishment of virus replication and addition of after virus has entered the cells were only able to reduce virus titres by a maximum of 1 Log 10 unit and no inhibition was observed from 2 h.p.i. N373 treatment gradually lost efficacy with delayed treatment up to 2 h.p.i. to no inhibition at 8 h.p.i. ( D ) Treatment of cells with G197 and N373 during the 1 h virus inoculation reduced virus titres significantly and G197 was more effective than N373. Statistical analysis for differences in virus titre due to drug treatment was performed with one-way ANOVA with Dunnett’s post-test: ***( p < 0.005). ( E ) Thermal stability of EV-A71 was assessed by incubating virus suspensions at temperatures from 37 to 60 °C in the presence of 0.1% DMSO or 1 µM G197. The presence of G197 improved the thermal stability of virus particles at elevated temperatures.

    Techniques Used: Inhibition, Binding Assay, Infection, Expressing, Negative Control

    Treatment with both N373 and G197 exhibited greater inhibition of EV-A71 replication compared to single compounds when cells were treated after virus inoculation and not before. RD cells treated with N373 and G197 at the indicated combinations and concentrations were infected with EV-A71 after compound removal. Combination treatment (N373 + G197) at both concentrations resulted in virus titres lower than either of the single compound treatments at both MOI = 1 ( A ) and MOI = 0.1 ( B ). ( C ) RD cells were pre-treated for 2 h with N373 and G197 at the indicated combinations and concentrations prior to infection at MOI = 1 and ( D ) MOI = 0.1. Combination treatment did not result in a significantly lower virus titre compared to treatment with G197 only and N373 slightly reduced virus titres at a lower MOI. Statistical analysis for differences in virus titre due to drug treatment was performed with one-way ANOVA with Dunnett’s post-test: *( p < 0.05), **( p < 0.01), ***( p < 0.005). Student’s t-test was performed to compare single compound treatments (G197 or N373) to combination treatment at the same concentration.
    Figure Legend Snippet: Treatment with both N373 and G197 exhibited greater inhibition of EV-A71 replication compared to single compounds when cells were treated after virus inoculation and not before. RD cells treated with N373 and G197 at the indicated combinations and concentrations were infected with EV-A71 after compound removal. Combination treatment (N373 + G197) at both concentrations resulted in virus titres lower than either of the single compound treatments at both MOI = 1 ( A ) and MOI = 0.1 ( B ). ( C ) RD cells were pre-treated for 2 h with N373 and G197 at the indicated combinations and concentrations prior to infection at MOI = 1 and ( D ) MOI = 0.1. Combination treatment did not result in a significantly lower virus titre compared to treatment with G197 only and N373 slightly reduced virus titres at a lower MOI. Statistical analysis for differences in virus titre due to drug treatment was performed with one-way ANOVA with Dunnett’s post-test: *( p < 0.05), **( p < 0.01), ***( p < 0.005). Student’s t-test was performed to compare single compound treatments (G197 or N373) to combination treatment at the same concentration.

    Techniques Used: Inhibition, Infection, Concentration Assay

    Treatment with both N373 and G197 improved survival and reduced muscle tissue pathology in EV-A71 infected mice. ( A ) Treatment regimen composed of a single dose 2 h prior to infection and 6 daily doses after infection. Animals were observed and sacrificed at 14 days post-infection for survival group and at 5 days post-infection for tissue harvesting group. ( B ) Survival of EV-A71 infected Balb/c neonates showed the greatest improvement when treated with both N373 and G197 followed by N373 only and a slight improvement with only G197 compared to control group (DMSO). ( C ) Haemotoxylin and eosin staining on harvested limb tissue of infected mice at 5 days post-infection showed breakdown of muscle tissue ranging from extensive in control group to negligible in combination treatment group (N373 + G197).
    Figure Legend Snippet: Treatment with both N373 and G197 improved survival and reduced muscle tissue pathology in EV-A71 infected mice. ( A ) Treatment regimen composed of a single dose 2 h prior to infection and 6 daily doses after infection. Animals were observed and sacrificed at 14 days post-infection for survival group and at 5 days post-infection for tissue harvesting group. ( B ) Survival of EV-A71 infected Balb/c neonates showed the greatest improvement when treated with both N373 and G197 followed by N373 only and a slight improvement with only G197 compared to control group (DMSO). ( C ) Haemotoxylin and eosin staining on harvested limb tissue of infected mice at 5 days post-infection showed breakdown of muscle tissue ranging from extensive in control group to negligible in combination treatment group (N373 + G197).

    Techniques Used: Infection, Staining

    crl5865  (ATCC)


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    ATCC crl5865

    Crl5865, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "PAF remodels the DREAM complex to bypass cell quiescence and promote lung tumorigenesis"

    Article Title: PAF remodels the DREAM complex to bypass cell quiescence and promote lung tumorigenesis

    Journal: Molecular Cell

    doi: 10.1016/j.molcel.2021.02.001


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    Techniques Used: Recombinant, shRNA, Software

    h1355  (ATCC)


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    ATCC h1355
    PAF depletion induces quiescence and growth arrest of lung cancer cells (A–E) Cell growth inhibition by PAF depletion. (A) Cell proliferation was assessed using crystal violet staining of control and Paf knockdown (KD) mouse lung cancer cells (KP); two shRNAs targeting Paf (shPaf #1 and #2) were used. (B) Cumulative population doublings of control and Paf-KD KP cells. (C) Cumulative population doublings of two different KP mouse lung cancer cell lines with Paf KD (KP836 and KP952 were established from two different Ad-Cre-induced KP mice). (D) Cumulative population doublings for Paf rescue experiment in Paf-KD KP cells. Cells were stably transduced with PAF. (E) Cell proliferation analysis of human LUAD cell lines with PAF KD; cumulative population doublings of five LUAD cell lines (A549, H23, H358, H1792, and <t>H1355)</t> that were stably transduced with lentiviruses encoding shPAF #1 or #2. Two-way ANOVA with Tukey post hoc test. (F–J) G0/G1 arrest by PAF KD in mouse and human LUAD cells. (F) Cell-cycle distribution of control (shCtrl) and PAF-KD (shPaf) mouse lung cancer cells was assessed using propidium iodide (PI) staining followed by fluorescence-activated cell sorting (FACS) analysis (n = 30,000 cells). (G) Cell-cycle distribution of control (shCtrl) and PAF-depleted (shPAF) human lung cancer cells (A549 and H1792); PI staining with FACS analysis, n = 30,000 cells. (H) Analysis of cell-cycle distribution in synchronized control and Paf-depleted KP cells by thymidine double block and PI staining-FACS analyses. (I) Visualization of G0/G1 cells by nuclear localization of DHB-Venus in control and Paf-KD A549 and H1792 lung cancer cells stably transfected with shCtrl or shPAF with DHB-Venus; scale bars, 50 μm. (J) Quantification of nuclear localization of DHB-Venus in control and PAF KD A549 and H1792 cells; n > 500 cells in at least ten different fields were counted. (K and L) Increase of cell quiescence (G0) by PAF KD. (K) Density scatterplots of control versus PAF-KD H1792 cells. G0 cells were assessed by pyronin Y and 7-aminoactinomycin D (7-AAD) double staining followed by FACS analysis; cells with low RNA content (low pyronin Y) in G0/G1 phase were considered G0 cells ( <xref ref-type=Schmid et al., 2000 ). (L) Quantification of cell-cycle phases in H1792 cells (control and PAF KD). Representative images are shown. Error bars indicate SEM. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. " width="250" height="auto" />
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    1) Product Images from "PAF remodels the DREAM complex to bypass cell quiescence and promote lung tumorigenesis"

    Article Title: PAF remodels the DREAM complex to bypass cell quiescence and promote lung tumorigenesis

    Journal: Molecular Cell

    doi: 10.1016/j.molcel.2021.02.001

    PAF depletion induces quiescence and growth arrest of lung cancer cells (A–E) Cell growth inhibition by PAF depletion. (A) Cell proliferation was assessed using crystal violet staining of control and Paf knockdown (KD) mouse lung cancer cells (KP); two shRNAs targeting Paf (shPaf #1 and #2) were used. (B) Cumulative population doublings of control and Paf-KD KP cells. (C) Cumulative population doublings of two different KP mouse lung cancer cell lines with Paf KD (KP836 and KP952 were established from two different Ad-Cre-induced KP mice). (D) Cumulative population doublings for Paf rescue experiment in Paf-KD KP cells. Cells were stably transduced with PAF. (E) Cell proliferation analysis of human LUAD cell lines with PAF KD; cumulative population doublings of five LUAD cell lines (A549, H23, H358, H1792, and H1355) that were stably transduced with lentiviruses encoding shPAF #1 or #2. Two-way ANOVA with Tukey post hoc test. (F–J) G0/G1 arrest by PAF KD in mouse and human LUAD cells. (F) Cell-cycle distribution of control (shCtrl) and PAF-KD (shPaf) mouse lung cancer cells was assessed using propidium iodide (PI) staining followed by fluorescence-activated cell sorting (FACS) analysis (n = 30,000 cells). (G) Cell-cycle distribution of control (shCtrl) and PAF-depleted (shPAF) human lung cancer cells (A549 and H1792); PI staining with FACS analysis, n = 30,000 cells. (H) Analysis of cell-cycle distribution in synchronized control and Paf-depleted KP cells by thymidine double block and PI staining-FACS analyses. (I) Visualization of G0/G1 cells by nuclear localization of DHB-Venus in control and Paf-KD A549 and H1792 lung cancer cells stably transfected with shCtrl or shPAF with DHB-Venus; scale bars, 50 μm. (J) Quantification of nuclear localization of DHB-Venus in control and PAF KD A549 and H1792 cells; n > 500 cells in at least ten different fields were counted. (K and L) Increase of cell quiescence (G0) by PAF KD. (K) Density scatterplots of control versus PAF-KD H1792 cells. G0 cells were assessed by pyronin Y and 7-aminoactinomycin D (7-AAD) double staining followed by FACS analysis; cells with low RNA content (low pyronin Y) in G0/G1 phase were considered G0 cells ( <xref ref-type=Schmid et al., 2000 ). (L) Quantification of cell-cycle phases in H1792 cells (control and PAF KD). Representative images are shown. Error bars indicate SEM. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. " title="... LUAD cell lines (A549, H23, H358, H1792, and H1355) that were stably transduced with lentiviruses encoding shPAF ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: PAF depletion induces quiescence and growth arrest of lung cancer cells (A–E) Cell growth inhibition by PAF depletion. (A) Cell proliferation was assessed using crystal violet staining of control and Paf knockdown (KD) mouse lung cancer cells (KP); two shRNAs targeting Paf (shPaf #1 and #2) were used. (B) Cumulative population doublings of control and Paf-KD KP cells. (C) Cumulative population doublings of two different KP mouse lung cancer cell lines with Paf KD (KP836 and KP952 were established from two different Ad-Cre-induced KP mice). (D) Cumulative population doublings for Paf rescue experiment in Paf-KD KP cells. Cells were stably transduced with PAF. (E) Cell proliferation analysis of human LUAD cell lines with PAF KD; cumulative population doublings of five LUAD cell lines (A549, H23, H358, H1792, and H1355) that were stably transduced with lentiviruses encoding shPAF #1 or #2. Two-way ANOVA with Tukey post hoc test. (F–J) G0/G1 arrest by PAF KD in mouse and human LUAD cells. (F) Cell-cycle distribution of control (shCtrl) and PAF-KD (shPaf) mouse lung cancer cells was assessed using propidium iodide (PI) staining followed by fluorescence-activated cell sorting (FACS) analysis (n = 30,000 cells). (G) Cell-cycle distribution of control (shCtrl) and PAF-depleted (shPAF) human lung cancer cells (A549 and H1792); PI staining with FACS analysis, n = 30,000 cells. (H) Analysis of cell-cycle distribution in synchronized control and Paf-depleted KP cells by thymidine double block and PI staining-FACS analyses. (I) Visualization of G0/G1 cells by nuclear localization of DHB-Venus in control and Paf-KD A549 and H1792 lung cancer cells stably transfected with shCtrl or shPAF with DHB-Venus; scale bars, 50 μm. (J) Quantification of nuclear localization of DHB-Venus in control and PAF KD A549 and H1792 cells; n > 500 cells in at least ten different fields were counted. (K and L) Increase of cell quiescence (G0) by PAF KD. (K) Density scatterplots of control versus PAF-KD H1792 cells. G0 cells were assessed by pyronin Y and 7-aminoactinomycin D (7-AAD) double staining followed by FACS analysis; cells with low RNA content (low pyronin Y) in G0/G1 phase were considered G0 cells ( Schmid et al., 2000 ). (L) Quantification of cell-cycle phases in H1792 cells (control and PAF KD). Representative images are shown. Error bars indicate SEM. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

    Techniques Used: Inhibition, Staining, Stable Transfection, Transduction, Fluorescence, FACS, Blocking Assay, Transfection, Double Staining


    Figure Legend Snippet:

    Techniques Used: Recombinant, shRNA, Software

    crl 5865  (ATCC)


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    ATCC crl 5865
    Crl 5865, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    h1355  (ATCC)


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    ATCC h1355
    KEY RESOURCES TABLE
    H1355, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Activation of oxidative stress response in cancer generates a druggable dependency on exogenous non-essential amino acids"

    Article Title: Activation of oxidative stress response in cancer generates a druggable dependency on exogenous non-essential amino acids

    Journal: Cell metabolism

    doi: 10.1016/j.cmet.2019.11.012

    KEY RESOURCES TABLE
    Figure Legend Snippet: KEY RESOURCES TABLE

    Techniques Used: Recombinant

    nci h1355  (ATCC)


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    ATCC nci h1355
    Nci H1355, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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