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u 87 mg cell lines  (ATCC)


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    ATCC u 87 mg cell lines
    Hypoxia impacts gene expression and signaling pathways in GBM cells (A) Hypoxia-responsive pathways were identified using Partek Flow software under double filter MI50 and fold change >+1.5 criteria. (B) Expression of candidate genes in PBT030 cells following 48-h hypoxia exposure compared to cells under normoxic conditions. (C) Expression of candidate genes <t>in</t> <t>U-87</t> MG cells after 48 h of hypoxia compared to cells maintained under normoxic conditions. Representative bar graphs are derived from at least two independent experiments, with 28S used as the reference gene for all experiments.
    U 87 Mg Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 10281 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/u 87 mg cell lines/product/ATCC
    Average 99 stars, based on 10281 article reviews
    u 87 mg cell lines - by Bioz Stars, 2026-05
    99/100 stars

    Images

    1) Product Images from "CBX6 and CA9 as predictive indicators and therapeutic targets in GBM"

    Article Title: CBX6 and CA9 as predictive indicators and therapeutic targets in GBM

    Journal: Molecular Therapy Oncology

    doi: 10.1016/j.omton.2026.201159

    Hypoxia impacts gene expression and signaling pathways in GBM cells (A) Hypoxia-responsive pathways were identified using Partek Flow software under double filter MI50 and fold change >+1.5 criteria. (B) Expression of candidate genes in PBT030 cells following 48-h hypoxia exposure compared to cells under normoxic conditions. (C) Expression of candidate genes in U-87 MG cells after 48 h of hypoxia compared to cells maintained under normoxic conditions. Representative bar graphs are derived from at least two independent experiments, with 28S used as the reference gene for all experiments.
    Figure Legend Snippet: Hypoxia impacts gene expression and signaling pathways in GBM cells (A) Hypoxia-responsive pathways were identified using Partek Flow software under double filter MI50 and fold change >+1.5 criteria. (B) Expression of candidate genes in PBT030 cells following 48-h hypoxia exposure compared to cells under normoxic conditions. (C) Expression of candidate genes in U-87 MG cells after 48 h of hypoxia compared to cells maintained under normoxic conditions. Representative bar graphs are derived from at least two independent experiments, with 28S used as the reference gene for all experiments.

    Techniques Used: Gene Expression, Protein-Protein interactions, Software, Expressing, Derivative Assay



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    Hypoxia impacts gene expression and signaling pathways in GBM cells (A) Hypoxia-responsive pathways were identified using Partek Flow software under double filter MI50 and fold change >+1.5 criteria. (B) Expression of candidate genes in PBT030 cells following 48-h hypoxia exposure compared to cells under normoxic conditions. (C) Expression of candidate genes <t>in</t> <t>U-87</t> MG cells after 48 h of hypoxia compared to cells maintained under normoxic conditions. Representative bar graphs are derived from at least two independent experiments, with 28S used as the reference gene for all experiments.
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    u 87mg human glioblastoma cells  (ATCC)
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    Hypoxia impacts gene expression and signaling pathways in GBM cells (A) Hypoxia-responsive pathways were identified using Partek Flow software under double filter MI50 and fold change >+1.5 criteria. (B) Expression of candidate genes in PBT030 cells following 48-h hypoxia exposure compared to cells under normoxic conditions. (C) Expression of candidate genes <t>in</t> <t>U-87</t> MG cells after 48 h of hypoxia compared to cells maintained under normoxic conditions. Representative bar graphs are derived from at least two independent experiments, with 28S used as the reference gene for all experiments.
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    u87 mg atcc version  (ATCC)
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    Hypoxia impacts gene expression and signaling pathways in GBM cells (A) Hypoxia-responsive pathways were identified using Partek Flow software under double filter MI50 and fold change >+1.5 criteria. (B) Expression of candidate genes in PBT030 cells following 48-h hypoxia exposure compared to cells under normoxic conditions. (C) Expression of candidate genes <t>in</t> <t>U-87</t> MG cells after 48 h of hypoxia compared to cells maintained under normoxic conditions. Representative bar graphs are derived from at least two independent experiments, with 28S used as the reference gene for all experiments.
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    u87mg  (ATCC)
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    Cells expressing IGF-1R ( A and E ), SH-SY5Y ( B and F ), <t>U87MG</t> ( C and G ), and rat primary neuronal culture ( D and H ) were stimulated with 10 nM ligands for 20 min. Phosphorylation of Akt (A to D) and Erk1/2 (E to H) was assessed by Western blot. Data were normalized to GAPDH loading control and are shown relative to IGF-1–induced signal. Identical GAPDH loading controls are shown for the figure pairs (A) and (E), (B) and (F), and (D) and (H) because the samples in each pair were run on the same gel. Representative blots are shown and all blots are shown in the Supplementary Materials. Color coding as in . Asterisks indicate significance versus IGF-1 [(A), (B), and (E)] or versus control [(C), (D), (F), (G), and (H)]. (* P < 0.05; ** P < 0.01; *** P < 0.001; # P < 0.0001; ns, not significant according to ANOVA). X indicates that this sample was not included in the study.
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    Cells expressing IGF-1R ( A and E ), SH-SY5Y ( B and F ), <t>U87MG</t> ( C and G ), and rat primary neuronal culture ( D and H ) were stimulated with 10 nM ligands for 20 min. Phosphorylation of Akt (A to D) and Erk1/2 (E to H) was assessed by Western blot. Data were normalized to GAPDH loading control and are shown relative to IGF-1–induced signal. Identical GAPDH loading controls are shown for the figure pairs (A) and (E), (B) and (F), and (D) and (H) because the samples in each pair were run on the same gel. Representative blots are shown and all blots are shown in the Supplementary Materials. Color coding as in . Asterisks indicate significance versus IGF-1 [(A), (B), and (E)] or versus control [(C), (D), (F), (G), and (H)]. (* P < 0.05; ** P < 0.01; *** P < 0.001; # P < 0.0001; ns, not significant according to ANOVA). X indicates that this sample was not included in the study.
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    human u87 mg glioblastoma cells  (ATCC)
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    ATCC human u87 mg glioblastoma cells
    Cells expressing IGF-1R ( A and E ), SH-SY5Y ( B and F ), <t>U87MG</t> ( C and G ), and rat primary neuronal culture ( D and H ) were stimulated with 10 nM ligands for 20 min. Phosphorylation of Akt (A to D) and Erk1/2 (E to H) was assessed by Western blot. Data were normalized to GAPDH loading control and are shown relative to IGF-1–induced signal. Identical GAPDH loading controls are shown for the figure pairs (A) and (E), (B) and (F), and (D) and (H) because the samples in each pair were run on the same gel. Representative blots are shown and all blots are shown in the Supplementary Materials. Color coding as in . Asterisks indicate significance versus IGF-1 [(A), (B), and (E)] or versus control [(C), (D), (F), (G), and (H)]. (* P < 0.05; ** P < 0.01; *** P < 0.001; # P < 0.0001; ns, not significant according to ANOVA). X indicates that this sample was not included in the study.
    Human U87 Mg Glioblastoma Cells, 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/human u87 mg glioblastoma cells/product/ATCC
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    Image Search Results


    Hypoxia impacts gene expression and signaling pathways in GBM cells (A) Hypoxia-responsive pathways were identified using Partek Flow software under double filter MI50 and fold change >+1.5 criteria. (B) Expression of candidate genes in PBT030 cells following 48-h hypoxia exposure compared to cells under normoxic conditions. (C) Expression of candidate genes in U-87 MG cells after 48 h of hypoxia compared to cells maintained under normoxic conditions. Representative bar graphs are derived from at least two independent experiments, with 28S used as the reference gene for all experiments.

    Journal: Molecular Therapy Oncology

    Article Title: CBX6 and CA9 as predictive indicators and therapeutic targets in GBM

    doi: 10.1016/j.omton.2026.201159

    Figure Lengend Snippet: Hypoxia impacts gene expression and signaling pathways in GBM cells (A) Hypoxia-responsive pathways were identified using Partek Flow software under double filter MI50 and fold change >+1.5 criteria. (B) Expression of candidate genes in PBT030 cells following 48-h hypoxia exposure compared to cells under normoxic conditions. (C) Expression of candidate genes in U-87 MG cells after 48 h of hypoxia compared to cells maintained under normoxic conditions. Representative bar graphs are derived from at least two independent experiments, with 28S used as the reference gene for all experiments.

    Article Snippet: U-251 MG and U-87 MG cell lines were purchased from the American Type Culture Collection (ATCC).

    Techniques: Gene Expression, Protein-Protein interactions, Software, Expressing, Derivative Assay

    Cells expressing IGF-1R ( A and E ), SH-SY5Y ( B and F ), U87MG ( C and G ), and rat primary neuronal culture ( D and H ) were stimulated with 10 nM ligands for 20 min. Phosphorylation of Akt (A to D) and Erk1/2 (E to H) was assessed by Western blot. Data were normalized to GAPDH loading control and are shown relative to IGF-1–induced signal. Identical GAPDH loading controls are shown for the figure pairs (A) and (E), (B) and (F), and (D) and (H) because the samples in each pair were run on the same gel. Representative blots are shown and all blots are shown in the Supplementary Materials. Color coding as in . Asterisks indicate significance versus IGF-1 [(A), (B), and (E)] or versus control [(C), (D), (F), (G), and (H)]. (* P < 0.05; ** P < 0.01; *** P < 0.001; # P < 0.0001; ns, not significant according to ANOVA). X indicates that this sample was not included in the study.

    Journal: Science Advances

    Article Title: An engineered insulin analog with dual insulin and IGF-1 receptor agonism and distinct signaling

    doi: 10.1126/sciadv.aeb7558

    Figure Lengend Snippet: Cells expressing IGF-1R ( A and E ), SH-SY5Y ( B and F ), U87MG ( C and G ), and rat primary neuronal culture ( D and H ) were stimulated with 10 nM ligands for 20 min. Phosphorylation of Akt (A to D) and Erk1/2 (E to H) was assessed by Western blot. Data were normalized to GAPDH loading control and are shown relative to IGF-1–induced signal. Identical GAPDH loading controls are shown for the figure pairs (A) and (E), (B) and (F), and (D) and (H) because the samples in each pair were run on the same gel. Representative blots are shown and all blots are shown in the Supplementary Materials. Color coding as in . Asterisks indicate significance versus IGF-1 [(A), (B), and (E)] or versus control [(C), (D), (F), (G), and (H)]. (* P < 0.05; ** P < 0.01; *** P < 0.001; # P < 0.0001; ns, not significant according to ANOVA). X indicates that this sample was not included in the study.

    Article Snippet: The U87MG (ATCC, HTB-14) glioblastoma cell line was grown in minimum essential medium supplemented with 10% FBS, 1% streptomycin-penicillin, and 2 mM l -glutamine.

    Techniques: Expressing, Phospho-proteomics, Western Blot, Control