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human ls513 cells  (ATCC)


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    Structured Review

    ATCC human ls513 cells
    A. CDK2 and EPHA2 kinase-pathway subnetworks in the humanized CRC KiPNA including ASL and CRAT, synthetic lethal partners in CRCs expressing KRASG12D. B. CDK2 Kinase-pathway subnetwork in the humanized PDAC KiPNA including JUN, MET, SMAD3, and SRSF1, synthetic lethal partners in PDACs expressing KRASG12D. Wilcoxon Mann-Whitney p-values (p < 0.05) and fold changes (FC) are shown for gene essentiality probabilities in colon cell lines (KRASG12D vs. and other KRAS alleles). C. Quantitative real-time PCR (qRT-PCR) analysis of knock-down efficiency with siRNA against indicated genes in colon (n = 4) and pancreas (n = 4) cell lines. Data presented as a mean fold-change relative to scrambled control ± SEM (n = 3 technical replicates in each of 2 biological replicates). D. Caspase 3/7 activity 96 hours after siRNA-mediated gene knock-down in KRASG12D and KRASWT or KRASG13D colon cell lines. Bar plot shows mean of caspase 3/7 activity (normalized to scrambled control) in colon cell lines with KRASG12D mutations <t>(LS513,</t> LS180) or other KRAS allele [HT115 (WT), DLD1 (G13D)]. Bars represent the average of means from cell lines in each group ± SEM (n = 3 technical replicates in each of 2 biological replicates). Data were compared by Welch’s t-test [p > 0.05 (n.s.); p ≤ 0.05 (*); p ≤ 0.01 (**); p ≤ 0.001 (***); p ≤ 0.0001 (****)]. E. Caspase 3/7 activity 96 hours after siRNA-mediated gene knock-down in KRASG12D and KRASG12R pancreas cell lines. Bar plot shows mean of caspase 3/7 activity (normalized to scrambled control) in pancreas cell lines with G12D mutations (SUIT2, KP4) or with G12R mutations (PSN1, TCCPAN2). Bars represent the average of means from cell lines in each group ± SEM (n = 3 technical replicates in each of 2 biological replicates). Data were compared by Welch’s t-test [p > 0.05 (ns); p ≤ 0.05 (*); p ≤ 0.01 (**); p ≤ 0.001 (***); p ≤ 0.0001 (****)]. (See also Figure S4).
    Human Ls513 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 153 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/access+array+multiplex+pcr/LS513/pmc06816257-29-0-4
    Average 95 stars, based on 153 article reviews
    human ls513 cells - by Bioz Stars, 2026-10
    95/100 stars

    Images

    1) Product Images from "Proteogenomic Network Analysis of Context-Specific KRAS Signaling In Mouse-to-Human Cross-Species Translation"

    Article Title: Proteogenomic Network Analysis of Context-Specific KRAS Signaling In Mouse-to-Human Cross-Species Translation

    Journal: Cell systems

    doi: 10.1016/j.cels.2019.07.006

    A. CDK2 and EPHA2 kinase-pathway subnetworks in the humanized CRC KiPNA including ASL and CRAT, synthetic lethal partners in CRCs expressing KRASG12D. B. CDK2 Kinase-pathway subnetwork in the humanized PDAC KiPNA including JUN, MET, SMAD3, and SRSF1, synthetic lethal partners in PDACs expressing KRASG12D. Wilcoxon Mann-Whitney p-values (p < 0.05) and fold changes (FC) are shown for gene essentiality probabilities in colon cell lines (KRASG12D vs. and other KRAS alleles). C. Quantitative real-time PCR (qRT-PCR) analysis of knock-down efficiency with siRNA against indicated genes in colon (n = 4) and pancreas (n = 4) cell lines. Data presented as a mean fold-change relative to scrambled control ± SEM (n = 3 technical replicates in each of 2 biological replicates). D. Caspase 3/7 activity 96 hours after siRNA-mediated gene knock-down in KRASG12D and KRASWT or KRASG13D colon cell lines. Bar plot shows mean of caspase 3/7 activity (normalized to scrambled control) in colon cell lines with KRASG12D mutations (LS513, LS180) or other KRAS allele [HT115 (WT), DLD1 (G13D)]. Bars represent the average of means from cell lines in each group ± SEM (n = 3 technical replicates in each of 2 biological replicates). Data were compared by Welch’s t-test [p > 0.05 (n.s.); p ≤ 0.05 (*); p ≤ 0.01 (**); p ≤ 0.001 (***); p ≤ 0.0001 (****)]. E. Caspase 3/7 activity 96 hours after siRNA-mediated gene knock-down in KRASG12D and KRASG12R pancreas cell lines. Bar plot shows mean of caspase 3/7 activity (normalized to scrambled control) in pancreas cell lines with G12D mutations (SUIT2, KP4) or with G12R mutations (PSN1, TCCPAN2). Bars represent the average of means from cell lines in each group ± SEM (n = 3 technical replicates in each of 2 biological replicates). Data were compared by Welch’s t-test [p > 0.05 (ns); p ≤ 0.05 (*); p ≤ 0.01 (**); p ≤ 0.001 (***); p ≤ 0.0001 (****)]. (See also Figure S4).
    Figure Legend Snippet: A. CDK2 and EPHA2 kinase-pathway subnetworks in the humanized CRC KiPNA including ASL and CRAT, synthetic lethal partners in CRCs expressing KRASG12D. B. CDK2 Kinase-pathway subnetwork in the humanized PDAC KiPNA including JUN, MET, SMAD3, and SRSF1, synthetic lethal partners in PDACs expressing KRASG12D. Wilcoxon Mann-Whitney p-values (p < 0.05) and fold changes (FC) are shown for gene essentiality probabilities in colon cell lines (KRASG12D vs. and other KRAS alleles). C. Quantitative real-time PCR (qRT-PCR) analysis of knock-down efficiency with siRNA against indicated genes in colon (n = 4) and pancreas (n = 4) cell lines. Data presented as a mean fold-change relative to scrambled control ± SEM (n = 3 technical replicates in each of 2 biological replicates). D. Caspase 3/7 activity 96 hours after siRNA-mediated gene knock-down in KRASG12D and KRASWT or KRASG13D colon cell lines. Bar plot shows mean of caspase 3/7 activity (normalized to scrambled control) in colon cell lines with KRASG12D mutations (LS513, LS180) or other KRAS allele [HT115 (WT), DLD1 (G13D)]. Bars represent the average of means from cell lines in each group ± SEM (n = 3 technical replicates in each of 2 biological replicates). Data were compared by Welch’s t-test [p > 0.05 (n.s.); p ≤ 0.05 (*); p ≤ 0.01 (**); p ≤ 0.001 (***); p ≤ 0.0001 (****)]. E. Caspase 3/7 activity 96 hours after siRNA-mediated gene knock-down in KRASG12D and KRASG12R pancreas cell lines. Bar plot shows mean of caspase 3/7 activity (normalized to scrambled control) in pancreas cell lines with G12D mutations (SUIT2, KP4) or with G12R mutations (PSN1, TCCPAN2). Bars represent the average of means from cell lines in each group ± SEM (n = 3 technical replicates in each of 2 biological replicates). Data were compared by Welch’s t-test [p > 0.05 (ns); p ≤ 0.05 (*); p ≤ 0.01 (**); p ≤ 0.001 (***); p ≤ 0.0001 (****)]. (See also Figure S4).

    Techniques Used: Expressing, MANN-WHITNEY, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Knockdown, Control, Activity Assay

    KEY RESOURCES TABLE
    Figure Legend Snippet: KEY RESOURCES TABLE

    Techniques Used: Protein Array, Mutagenesis, Recombinant, BIA-KA, Extraction, Multiplex Assay, Reverse Transcription, Transfection, Phospho-proteomics, Software

    Related Articles

    Resazurin Assay:

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    Article Snippet: HCT116, Ls513, HT29, and LoVo were purchased from the American Type Culture Collection (ATCC).

    Western Blot:

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    Incubation:

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    Derivative Assay:

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    Liquid Chromatography with Mass Spectroscopy:

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    Flow Cytometry:

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    Quantitative Proteomics:

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    Expressing:

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    Mutagenesis:

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    Comparison:

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    Article Snippet: HCT116, Ls513, HT29, and LoVo were purchased from the American Type Culture Collection (ATCC).

    Gene Expression:

    Article Title: Pt(IV) chemotherapeutic prodrug and controlled release thereof for treatment of tumors
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    Quantitative RT-PCR:

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    Article Snippet: HCT116, Ls513, HT29, and LoVo were purchased from the American Type Culture Collection (ATCC).

    Immunofluorescence:

    Article Title: Pt(IV) chemotherapeutic prodrug and controlled release thereof for treatment of tumors
    Article Snippet: HCT116, Ls513, HT29, and LoVo were purchased from the American Type Culture Collection (ATCC).

    Biomarker Discovery:

    Article Title: Pt(IV) chemotherapeutic prodrug and controlled release thereof for treatment of tumors
    Article Snippet: HCT116, Ls513, HT29, and LoVo were purchased from the American Type Culture Collection (ATCC).

    Transfection:

    Article Title: Pt(IV) chemotherapeutic prodrug and controlled release thereof for treatment of tumors
    Article Snippet: HCT116, Ls513, HT29, and LoVo were purchased from the American Type Culture Collection (ATCC).

    Control:

    Article Title: Pt(IV) chemotherapeutic prodrug and controlled release thereof for treatment of tumors
    Article Snippet: HCT116, Ls513, HT29, and LoVo were purchased from the American Type Culture Collection (ATCC).

    Recombinant:

    Article Title: Pt(IV) chemotherapeutic prodrug and controlled release thereof for treatment of tumors
    Article Snippet: HCT116, Ls513, HT29, and LoVo were purchased from the American Type Culture Collection (ATCC).

    Phospho-proteomics:

    Article Title: Pt(IV) chemotherapeutic prodrug and controlled release thereof for treatment of tumors
    Article Snippet: HCT116, Ls513, HT29, and LoVo were purchased from the American Type Culture Collection (ATCC).

    Positive Control:

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    Isolation:

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    Membrane:

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    Cell Culture:

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    Stable Transfection:

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    Wound Healing Assay:

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    Transwell Assay:

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    Invasion Assay:

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    Colony Assay:

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    Article Snippet: HCT116, Ls513, HT29, and LoVo were purchased from the American Type Culture Collection (ATCC).

    CCK-8 Assay:

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    Over Expression:

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    Knockdown:

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    Staining:

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    Injection:

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    Dissection:

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    Immunohistochemistry:

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    Enzyme-linked Immunosorbent Assay:

    Article Title: Pt(IV) chemotherapeutic prodrug and controlled release thereof for treatment of tumors
    Article Snippet: HCT116, Ls513, HT29, and LoVo were purchased from the American Type Culture Collection (ATCC).

    Concentration Assay:

    Article Title: Pt(IV) chemotherapeutic prodrug and controlled release thereof for treatment of tumors
    Article Snippet: HCT116, Ls513, HT29, and LoVo were purchased from the American Type Culture Collection (ATCC).

    Immunohistochemical staining:

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    RNA Sequencing:

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    Agarose Gel Electrophoresis:

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    Protein-Protein interactions:

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