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sk n sh  (ATCC)


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    Structured Review

    ATCC sk n sh
    (A, B) Correlation between PRKDC gene expression levels and NB tumor progression to stage 4. (C) Heatmap of differential expression of DNA replication and repair pathway (KEGG) genes in PTCs (green) at diagnosis and DTCs (red) at relapse. Color intensity represents expression level. Heatmap of KEGG pathways involved in DNA replication and repair in primary tumor cells (PTCs) at diagnosis (green) and in disseminated tumors cells (DTCs) at relapse (red). (D) PRKDC gene expression in PTCs at diagnosis, DTCs at diagnosis and in DTCs at relapse (Ambros study, n=86) revealed a significant upregulation of PRKDC in DTCs at relapse. (E) Western blot analysis in MYCN-amplified (BE(2)-C, LAN-1, IMR-32 and SK-N-DZ) and MYCN-non-amplified (SK-N-AS, <t>SK-N-SH)</t> NB cell lines (*p<0.05, ***p<0.001, ****p<0.0001).
    Sk N Sh, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1676 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sk n sh/product/ATCC
    Average 96 stars, based on 1676 article reviews
    sk n sh - by Bioz Stars, 2026-05
    96/100 stars

    Images

    1) Product Images from "DNA-PKcs promotes therapy resistance and metastatic recurrence in neuroblastoma"

    Article Title: DNA-PKcs promotes therapy resistance and metastatic recurrence in neuroblastoma

    Journal: Cancer letters

    doi: 10.1016/j.canlet.2026.218383

    (A, B) Correlation between PRKDC gene expression levels and NB tumor progression to stage 4. (C) Heatmap of differential expression of DNA replication and repair pathway (KEGG) genes in PTCs (green) at diagnosis and DTCs (red) at relapse. Color intensity represents expression level. Heatmap of KEGG pathways involved in DNA replication and repair in primary tumor cells (PTCs) at diagnosis (green) and in disseminated tumors cells (DTCs) at relapse (red). (D) PRKDC gene expression in PTCs at diagnosis, DTCs at diagnosis and in DTCs at relapse (Ambros study, n=86) revealed a significant upregulation of PRKDC in DTCs at relapse. (E) Western blot analysis in MYCN-amplified (BE(2)-C, LAN-1, IMR-32 and SK-N-DZ) and MYCN-non-amplified (SK-N-AS, SK-N-SH) NB cell lines (*p<0.05, ***p<0.001, ****p<0.0001).
    Figure Legend Snippet: (A, B) Correlation between PRKDC gene expression levels and NB tumor progression to stage 4. (C) Heatmap of differential expression of DNA replication and repair pathway (KEGG) genes in PTCs (green) at diagnosis and DTCs (red) at relapse. Color intensity represents expression level. Heatmap of KEGG pathways involved in DNA replication and repair in primary tumor cells (PTCs) at diagnosis (green) and in disseminated tumors cells (DTCs) at relapse (red). (D) PRKDC gene expression in PTCs at diagnosis, DTCs at diagnosis and in DTCs at relapse (Ambros study, n=86) revealed a significant upregulation of PRKDC in DTCs at relapse. (E) Western blot analysis in MYCN-amplified (BE(2)-C, LAN-1, IMR-32 and SK-N-DZ) and MYCN-non-amplified (SK-N-AS, SK-N-SH) NB cell lines (*p<0.05, ***p<0.001, ****p<0.0001).

    Techniques Used: Gene Expression, Quantitative Proteomics, Biomarker Discovery, Expressing, Western Blot, Amplification



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    (A, B) Correlation between PRKDC gene expression levels and NB tumor progression to stage 4. (C) Heatmap of differential expression of DNA replication and repair pathway (KEGG) genes in PTCs (green) at diagnosis and DTCs (red) at relapse. Color intensity represents expression level. Heatmap of KEGG pathways involved in DNA replication and repair in primary tumor cells (PTCs) at diagnosis (green) and in disseminated tumors cells (DTCs) at relapse (red). (D) PRKDC gene expression in PTCs at diagnosis, DTCs at diagnosis and in DTCs at relapse (Ambros study, n=86) revealed a significant upregulation of PRKDC in DTCs at relapse. (E) Western blot analysis in MYCN-amplified (BE(2)-C, LAN-1, IMR-32 and SK-N-DZ) and MYCN-non-amplified (SK-N-AS, <t>SK-N-SH)</t> NB cell lines (*p<0.05, ***p<0.001, ****p<0.0001).
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    (A, B) Correlation between PRKDC gene expression levels and NB tumor progression to stage 4. (C) Heatmap of differential expression of DNA replication and repair pathway (KEGG) genes in PTCs (green) at diagnosis and DTCs (red) at relapse. Color intensity represents expression level. Heatmap of KEGG pathways involved in DNA replication and repair in primary tumor cells (PTCs) at diagnosis (green) and in disseminated tumors cells (DTCs) at relapse (red). (D) PRKDC gene expression in PTCs at diagnosis, DTCs at diagnosis and in DTCs at relapse (Ambros study, n=86) revealed a significant upregulation of PRKDC in DTCs at relapse. (E) Western blot analysis in MYCN-amplified (BE(2)-C, LAN-1, IMR-32 and SK-N-DZ) and MYCN-non-amplified (SK-N-AS, <t>SK-N-SH)</t> NB cell lines (*p<0.05, ***p<0.001, ****p<0.0001).
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    (A, B) Correlation between PRKDC gene expression levels and NB tumor progression to stage 4. (C) Heatmap of differential expression of DNA replication and repair pathway (KEGG) genes in PTCs (green) at diagnosis and DTCs (red) at relapse. Color intensity represents expression level. Heatmap of KEGG pathways involved in DNA replication and repair in primary tumor cells (PTCs) at diagnosis (green) and in disseminated tumors cells (DTCs) at relapse (red). (D) PRKDC gene expression in PTCs at diagnosis, DTCs at diagnosis and in DTCs at relapse (Ambros study, n=86) revealed a significant upregulation of PRKDC in DTCs at relapse. (E) Western blot analysis in MYCN-amplified (BE(2)-C, LAN-1, IMR-32 and SK-N-DZ) and MYCN-non-amplified (SK-N-AS, <t>SK-N-SH)</t> NB cell lines (*p<0.05, ***p<0.001, ****p<0.0001).
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    ATCC sk n sh ecacc
    Percentage changes calculated for the surface area per molecule, the surface pressure (π coll ) at the moment of monolayer collapse, and the static compressive modulus (C s − 1 ) obtained for Langmuir model membranes that mimic HL-60 <t>and</t> <t>the</t> <t>SK-N-SH</t> cell lines.Values represent the mean ± SD calculated from 3-5 counts, based on independently recorded isotherms (n = 5). Statistically significant differences between concentrations observed for the SK-N-SH model membranes were indicated by uppercase letters, whereas for the HL-60 membranes, the differences were indicated by lowercase letters.
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    Percentage changes calculated for the surface area per molecule, the surface pressure (π coll ) at the moment of monolayer collapse, and the static compressive modulus (C s − 1 ) obtained for Langmuir model membranes that mimic HL-60 <t>and</t> <t>the</t> <t>SK-N-SH</t> cell lines.Values represent the mean ± SD calculated from 3-5 counts, based on independently recorded isotherms (n = 5). Statistically significant differences between concentrations observed for the SK-N-SH model membranes were indicated by uppercase letters, whereas for the HL-60 membranes, the differences were indicated by lowercase letters.
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    Procell Inc sk n sh cells
    Percentage changes calculated for the surface area per molecule, the surface pressure (π coll ) at the moment of monolayer collapse, and the static compressive modulus (C s − 1 ) obtained for Langmuir model membranes that mimic HL-60 <t>and</t> <t>the</t> <t>SK-N-SH</t> cell lines.Values represent the mean ± SD calculated from 3-5 counts, based on independently recorded isotherms (n = 5). Statistically significant differences between concentrations observed for the SK-N-SH model membranes were indicated by uppercase letters, whereas for the HL-60 membranes, the differences were indicated by lowercase letters.
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    ATCC sh sy5y
    Percentage changes calculated for the surface area per molecule, the surface pressure (π coll ) at the moment of monolayer collapse, and the static compressive modulus (C s − 1 ) obtained for Langmuir model membranes that mimic HL-60 <t>and</t> <t>the</t> <t>SK-N-SH</t> cell lines.Values represent the mean ± SD calculated from 3-5 counts, based on independently recorded isotherms (n = 5). Statistically significant differences between concentrations observed for the SK-N-SH model membranes were indicated by uppercase letters, whereas for the HL-60 membranes, the differences were indicated by lowercase letters.
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    ATCC sk n sh cells
    ( a ) Volcano plots of H3 1-18 Q5ser vs. H3 1-18 unmodified binders from HeLa nuclear extracts identified by Streptavidin capture and LC-MS/MS ( n = 4; –log 10 P value < 0.05; Log 2 fold difference > 1). Inset: immunoblotting validation of QR2, but not QR1, binding to H3Q5ser in HeLa cells. ( b ) Workflow of TMT-based chemical proteomic profiling of H3Q5ser binding proteins. ( c ) Volcano plot of proteins captured by serotonylated probe 1 vs. unmodified probe <t>C</t> <t>from</t> <t>SK-N-SH</t> cell lysates. Statistical analysis was conducted using an unpaired two-tailed Student’s t -test. Cutoffs: significance P < 0.05; TMT ratio Log 2 (probe 1/probe C) > 1.5 ( n = 5). ( d ) Photo-crosslinking pulldown validation of QR2 binding to H3Q5ser in SK-N-SH cell lysates. ( e ) H3 1-18 Q5ser vs. H3 1-18 unmodified peptide pulldowns from human brain nuclear extracts, followed by immunoblotting for QR2 or QR1. ( f ) Recombinant QR2, but not its paralog QR1, could be labeled by probe 1. ( g ) Peptide pulldowns with recombinant QR2, followed by immunoblotting for QR2. ( h-i ) Titration and fitting curves of peptides titrated into QR2. K D values are provided. See for ITC statistics. All immunoblotting experiments repeated 3X. See for uncropped blots.
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    Image Search Results


    (A, B) Correlation between PRKDC gene expression levels and NB tumor progression to stage 4. (C) Heatmap of differential expression of DNA replication and repair pathway (KEGG) genes in PTCs (green) at diagnosis and DTCs (red) at relapse. Color intensity represents expression level. Heatmap of KEGG pathways involved in DNA replication and repair in primary tumor cells (PTCs) at diagnosis (green) and in disseminated tumors cells (DTCs) at relapse (red). (D) PRKDC gene expression in PTCs at diagnosis, DTCs at diagnosis and in DTCs at relapse (Ambros study, n=86) revealed a significant upregulation of PRKDC in DTCs at relapse. (E) Western blot analysis in MYCN-amplified (BE(2)-C, LAN-1, IMR-32 and SK-N-DZ) and MYCN-non-amplified (SK-N-AS, SK-N-SH) NB cell lines (*p<0.05, ***p<0.001, ****p<0.0001).

    Journal: Cancer letters

    Article Title: DNA-PKcs promotes therapy resistance and metastatic recurrence in neuroblastoma

    doi: 10.1016/j.canlet.2026.218383

    Figure Lengend Snippet: (A, B) Correlation between PRKDC gene expression levels and NB tumor progression to stage 4. (C) Heatmap of differential expression of DNA replication and repair pathway (KEGG) genes in PTCs (green) at diagnosis and DTCs (red) at relapse. Color intensity represents expression level. Heatmap of KEGG pathways involved in DNA replication and repair in primary tumor cells (PTCs) at diagnosis (green) and in disseminated tumors cells (DTCs) at relapse (red). (D) PRKDC gene expression in PTCs at diagnosis, DTCs at diagnosis and in DTCs at relapse (Ambros study, n=86) revealed a significant upregulation of PRKDC in DTCs at relapse. (E) Western blot analysis in MYCN-amplified (BE(2)-C, LAN-1, IMR-32 and SK-N-DZ) and MYCN-non-amplified (SK-N-AS, SK-N-SH) NB cell lines (*p<0.05, ***p<0.001, ****p<0.0001).

    Article Snippet: MYCN -amplified human NB cell lines (BE(2)-C (CVCL_V006), IMR-32 (CVCL_0346), LAN-1 (CVCL_1827) and SK-N-DZ (CVCL_1701)) and MYCN -non-amplified cells (SK-N-AS (CVCL_1700), and SK-N-SH (CVCL_0531)) were purchased from ATCC.

    Techniques: Gene Expression, Quantitative Proteomics, Biomarker Discovery, Expressing, Western Blot, Amplification

    Percentage changes calculated for the surface area per molecule, the surface pressure (π coll ) at the moment of monolayer collapse, and the static compressive modulus (C s − 1 ) obtained for Langmuir model membranes that mimic HL-60 and the SK-N-SH cell lines.Values represent the mean ± SD calculated from 3-5 counts, based on independently recorded isotherms (n = 5). Statistically significant differences between concentrations observed for the SK-N-SH model membranes were indicated by uppercase letters, whereas for the HL-60 membranes, the differences were indicated by lowercase letters.

    Journal: PLOS Neglected Tropical Diseases

    Article Title: Comparative studies of the effects of Naja ashei venom-derived proteins on model and native lipid membranes

    doi: 10.1371/journal.pntd.0014122

    Figure Lengend Snippet: Percentage changes calculated for the surface area per molecule, the surface pressure (π coll ) at the moment of monolayer collapse, and the static compressive modulus (C s − 1 ) obtained for Langmuir model membranes that mimic HL-60 and the SK-N-SH cell lines.Values represent the mean ± SD calculated from 3-5 counts, based on independently recorded isotherms (n = 5). Statistically significant differences between concentrations observed for the SK-N-SH model membranes were indicated by uppercase letters, whereas for the HL-60 membranes, the differences were indicated by lowercase letters.

    Article Snippet: The SK-N-SH (ECACC) and HL-60 (ATCC) cell lines were cultured in DMEM and RPMI 1640 media, respectively, each supplemented with 10% FBS and 1% penicillin-streptomycin (CytoGen GmbH).

    Techniques:

    Values represent the average ± SD (n = 5). Different letters indicate significant differences between concentrations (lower case letters for HL-60 cells, uppercase letters for SK-N-SH). The 100% reference value was defined as the enzyme leakage measured in cells that were not exposed to the tested venom proteins.

    Journal: PLOS Neglected Tropical Diseases

    Article Title: Comparative studies of the effects of Naja ashei venom-derived proteins on model and native lipid membranes

    doi: 10.1371/journal.pntd.0014122

    Figure Lengend Snippet: Values represent the average ± SD (n = 5). Different letters indicate significant differences between concentrations (lower case letters for HL-60 cells, uppercase letters for SK-N-SH). The 100% reference value was defined as the enzyme leakage measured in cells that were not exposed to the tested venom proteins.

    Article Snippet: The SK-N-SH (ECACC) and HL-60 (ATCC) cell lines were cultured in DMEM and RPMI 1640 media, respectively, each supplemented with 10% FBS and 1% penicillin-streptomycin (CytoGen GmbH).

    Techniques:

    ( a ) Volcano plots of H3 1-18 Q5ser vs. H3 1-18 unmodified binders from HeLa nuclear extracts identified by Streptavidin capture and LC-MS/MS ( n = 4; –log 10 P value < 0.05; Log 2 fold difference > 1). Inset: immunoblotting validation of QR2, but not QR1, binding to H3Q5ser in HeLa cells. ( b ) Workflow of TMT-based chemical proteomic profiling of H3Q5ser binding proteins. ( c ) Volcano plot of proteins captured by serotonylated probe 1 vs. unmodified probe C from SK-N-SH cell lysates. Statistical analysis was conducted using an unpaired two-tailed Student’s t -test. Cutoffs: significance P < 0.05; TMT ratio Log 2 (probe 1/probe C) > 1.5 ( n = 5). ( d ) Photo-crosslinking pulldown validation of QR2 binding to H3Q5ser in SK-N-SH cell lysates. ( e ) H3 1-18 Q5ser vs. H3 1-18 unmodified peptide pulldowns from human brain nuclear extracts, followed by immunoblotting for QR2 or QR1. ( f ) Recombinant QR2, but not its paralog QR1, could be labeled by probe 1. ( g ) Peptide pulldowns with recombinant QR2, followed by immunoblotting for QR2. ( h-i ) Titration and fitting curves of peptides titrated into QR2. K D values are provided. See for ITC statistics. All immunoblotting experiments repeated 3X. See for uncropped blots.

    Journal: bioRxiv

    Article Title: Quinone reductase 2 reads H3 serotonylation to support neuronal maturation

    doi: 10.64898/2026.03.17.712426

    Figure Lengend Snippet: ( a ) Volcano plots of H3 1-18 Q5ser vs. H3 1-18 unmodified binders from HeLa nuclear extracts identified by Streptavidin capture and LC-MS/MS ( n = 4; –log 10 P value < 0.05; Log 2 fold difference > 1). Inset: immunoblotting validation of QR2, but not QR1, binding to H3Q5ser in HeLa cells. ( b ) Workflow of TMT-based chemical proteomic profiling of H3Q5ser binding proteins. ( c ) Volcano plot of proteins captured by serotonylated probe 1 vs. unmodified probe C from SK-N-SH cell lysates. Statistical analysis was conducted using an unpaired two-tailed Student’s t -test. Cutoffs: significance P < 0.05; TMT ratio Log 2 (probe 1/probe C) > 1.5 ( n = 5). ( d ) Photo-crosslinking pulldown validation of QR2 binding to H3Q5ser in SK-N-SH cell lysates. ( e ) H3 1-18 Q5ser vs. H3 1-18 unmodified peptide pulldowns from human brain nuclear extracts, followed by immunoblotting for QR2 or QR1. ( f ) Recombinant QR2, but not its paralog QR1, could be labeled by probe 1. ( g ) Peptide pulldowns with recombinant QR2, followed by immunoblotting for QR2. ( h-i ) Titration and fitting curves of peptides titrated into QR2. K D values are provided. See for ITC statistics. All immunoblotting experiments repeated 3X. See for uncropped blots.

    Article Snippet: SK-N-SH cells (American Type Culture Collection, HTB-11) were cultured in DMEM supplemented with 10% fetal bovine serum (FBS), 100 U/mL penicillin, and 100 μg/mL streptomycin.

    Techniques: Liquid Chromatography with Mass Spectroscopy, Western Blot, Biomarker Discovery, Binding Assay, Two Tailed Test, Recombinant, Labeling, Titration