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    Cell Signaling Technology Inc phospho egfr y1068
    Phospho Egfr Y1068, supplied by Cell Signaling Technology Inc, 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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    anti phospho egfr y1068  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho egfr y1068
    Correlation of EGFR status vs TAT-Cx43 266–283 response in patient-derived GSCs. A set of GBM patient-derived GSCs and healthy human NSCs were treated with 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± S.E.M. of at least 3 independent experiments, ANOVA: * P value < .05, *** P value < .001). (B) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR <t>Y1068</t> and p-EGFRvIII Y1068) after 24 h treatment. β-actin was used as a loading control. (C) Heatmap summarizing TAT-Cx43 266–283 response and EGFR alterations of human patient-derived GSCs and hNSCs determined by WB, RNAseq, and FISH. For total color score, every square was assigned a numeric value according to its color. Dark red = 1 point, light red = 0.75 points, yellow = 0.5 points, and green = 0 points. (D) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status in patient-derived GSCs and healthy human GSCs. χ 2 test: ** P value < .01.
    Anti Phospho Egfr Y1068, supplied by Cell Signaling Technology Inc, 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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    1) Product Images from "EGFR amplification and EGFRvIII predict and participate in TAT-Cx43 266–283 antitumor response in preclinical glioblastoma models"

    Article Title: EGFR amplification and EGFRvIII predict and participate in TAT-Cx43 266–283 antitumor response in preclinical glioblastoma models

    Journal: Neuro-Oncology

    doi: 10.1093/neuonc/noae060

    Correlation of EGFR status vs TAT-Cx43 266–283 response in patient-derived GSCs. A set of GBM patient-derived GSCs and healthy human NSCs were treated with 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± S.E.M. of at least 3 independent experiments, ANOVA: * P value < .05, *** P value < .001). (B) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR Y1068 and p-EGFRvIII Y1068) after 24 h treatment. β-actin was used as a loading control. (C) Heatmap summarizing TAT-Cx43 266–283 response and EGFR alterations of human patient-derived GSCs and hNSCs determined by WB, RNAseq, and FISH. For total color score, every square was assigned a numeric value according to its color. Dark red = 1 point, light red = 0.75 points, yellow = 0.5 points, and green = 0 points. (D) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status in patient-derived GSCs and healthy human GSCs. χ 2 test: ** P value < .01.
    Figure Legend Snippet: Correlation of EGFR status vs TAT-Cx43 266–283 response in patient-derived GSCs. A set of GBM patient-derived GSCs and healthy human NSCs were treated with 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± S.E.M. of at least 3 independent experiments, ANOVA: * P value < .05, *** P value < .001). (B) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR Y1068 and p-EGFRvIII Y1068) after 24 h treatment. β-actin was used as a loading control. (C) Heatmap summarizing TAT-Cx43 266–283 response and EGFR alterations of human patient-derived GSCs and hNSCs determined by WB, RNAseq, and FISH. For total color score, every square was assigned a numeric value according to its color. Dark red = 1 point, light red = 0.75 points, yellow = 0.5 points, and green = 0 points. (D) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status in patient-derived GSCs and healthy human GSCs. χ 2 test: ** P value < .01.

    Techniques Used: Derivative Assay, Viability Assay, Control, Activity Assay

    The effect of TAT-Cx43 266–283 depends on EGFR alterations. A set of murine SVZ NSCs with EGFR alterations (SVZ-EGFRwt and SVZ-EGFRvIII) and a set of murine SVZ NSCs with EGFRvIII mutation (NSC-EGFRvIII), with Nf1/PTEN deletion (NP) or with a combination of Nf1/PTEN deletion and EGFRvIII mutation (NPE, and their immune evasive version, NPE-IE) and their non-modified counterparts (SVZ-NSCs) were treated with 50 µM TAT, 50 µM TAT-Cx43 274–291 (2 cell-penetrating peptides used as additional controls), 50 µM TAT-Cx43 266–283 , 100 µM temozolomide, 1 µM erlotinib, 0.05% DMSO (v/v) (vehicle for erlotinib) and the combination of 1 µM erlotinib plus 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay of SVZ NSCs with EGFR alterations and healthy NSCs after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± SEM of at least 3 independent experiments, ANOVA: * P < .05, *** P < .001 vs control; ## P < .01, ### P < .001 vs TAT; @@ P < .01 vs TAT-Cx43 274-291 ; +++ P < .001 vs temozolomide). (B) Phase-contrast images of murine NSCs with and without EGFR alterations treated as described previously. Scale bar: 100 µm. (C) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR Y1068 and p-EGFRvIII Y1068) after 24 h treatment. GAPDH was used as a loading control. (D) Alamar blue viability assay of SVZ NSCs with EGFR and additional GBM-driver alterations after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± SEM of at least 3 independent experiments, ANOVA: *** P value < .001). (E) Phase-contrast images of murine SVZ NSCs with GBM-driver alterations treated as described in (A). Scale bar: 100 µm. (F) WB analysis of EGFR, EGFRvIII, and Src levels and activity (p-EGFR Y1068, p-EGFRvIII Y1068, and p-Src Y416) after 24 h treatment. β-actin was used as a loading control. (G) Correlation graph depicting the relationship between GSC EGFR status and Src inhibition after treatment with TAT-Cx43 266–283 in murine and patient-derived GSCs. (H) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status of all the murine NSCs and GSCs. χ 2 test was used for statistical analysis.
    Figure Legend Snippet: The effect of TAT-Cx43 266–283 depends on EGFR alterations. A set of murine SVZ NSCs with EGFR alterations (SVZ-EGFRwt and SVZ-EGFRvIII) and a set of murine SVZ NSCs with EGFRvIII mutation (NSC-EGFRvIII), with Nf1/PTEN deletion (NP) or with a combination of Nf1/PTEN deletion and EGFRvIII mutation (NPE, and their immune evasive version, NPE-IE) and their non-modified counterparts (SVZ-NSCs) were treated with 50 µM TAT, 50 µM TAT-Cx43 274–291 (2 cell-penetrating peptides used as additional controls), 50 µM TAT-Cx43 266–283 , 100 µM temozolomide, 1 µM erlotinib, 0.05% DMSO (v/v) (vehicle for erlotinib) and the combination of 1 µM erlotinib plus 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay of SVZ NSCs with EGFR alterations and healthy NSCs after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± SEM of at least 3 independent experiments, ANOVA: * P < .05, *** P < .001 vs control; ## P < .01, ### P < .001 vs TAT; @@ P < .01 vs TAT-Cx43 274-291 ; +++ P < .001 vs temozolomide). (B) Phase-contrast images of murine NSCs with and without EGFR alterations treated as described previously. Scale bar: 100 µm. (C) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR Y1068 and p-EGFRvIII Y1068) after 24 h treatment. GAPDH was used as a loading control. (D) Alamar blue viability assay of SVZ NSCs with EGFR and additional GBM-driver alterations after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± SEM of at least 3 independent experiments, ANOVA: *** P value < .001). (E) Phase-contrast images of murine SVZ NSCs with GBM-driver alterations treated as described in (A). Scale bar: 100 µm. (F) WB analysis of EGFR, EGFRvIII, and Src levels and activity (p-EGFR Y1068, p-EGFRvIII Y1068, and p-Src Y416) after 24 h treatment. β-actin was used as a loading control. (G) Correlation graph depicting the relationship between GSC EGFR status and Src inhibition after treatment with TAT-Cx43 266–283 in murine and patient-derived GSCs. (H) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status of all the murine NSCs and GSCs. χ 2 test was used for statistical analysis.

    Techniques Used: Mutagenesis, Modification, Viability Assay, Control, Activity Assay, Inhibition, Derivative Assay

    anti phospho egfr tyr1068 rabbit mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho egfr tyr1068 rabbit mab
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    rabbit anti phospho egfr y1045  (Cell Signaling Technology Inc)


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    phospho egfr  (Cell Signaling Technology Inc)


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    rabbit antihuman monoclonal antibodies against phospho egfr  (Cell Signaling Technology Inc)


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    rabbit anti phospho egfr tyr1068  (Cell Signaling Technology Inc)


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    phospho egfr tyr1068  (Cell Signaling Technology Inc)


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    4267 phospho egfr  (Cell Signaling Technology Inc)


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    anti phospho egfr tyr1068  (Cell Signaling Technology Inc)


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    Correlation of EGFR status vs TAT-Cx43 266–283 response in patient-derived GSCs. A set of GBM patient-derived GSCs and healthy human NSCs were treated with 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± S.E.M. of at least 3 independent experiments, ANOVA: * P value < .05, *** P value < .001). (B) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR <t>Y1068</t> and p-EGFRvIII Y1068) after 24 h treatment. β-actin was used as a loading control. (C) Heatmap summarizing TAT-Cx43 266–283 response and EGFR alterations of human patient-derived GSCs and hNSCs determined by WB, RNAseq, and FISH. For total color score, every square was assigned a numeric value according to its color. Dark red = 1 point, light red = 0.75 points, yellow = 0.5 points, and green = 0 points. (D) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status in patient-derived GSCs and healthy human GSCs. χ 2 test: ** P value < .01.
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    Correlation of EGFR status vs TAT-Cx43 266–283 response in patient-derived GSCs. A set of GBM patient-derived GSCs and healthy human NSCs were treated with 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± S.E.M. of at least 3 independent experiments, ANOVA: * P value < .05, *** P value < .001). (B) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR <t>Y1068</t> and p-EGFRvIII Y1068) after 24 h treatment. β-actin was used as a loading control. (C) Heatmap summarizing TAT-Cx43 266–283 response and EGFR alterations of human patient-derived GSCs and hNSCs determined by WB, RNAseq, and FISH. For total color score, every square was assigned a numeric value according to its color. Dark red = 1 point, light red = 0.75 points, yellow = 0.5 points, and green = 0 points. (D) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status in patient-derived GSCs and healthy human GSCs. χ 2 test: ** P value < .01.
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    Correlation of EGFR status vs TAT-Cx43 266–283 response in patient-derived GSCs. A set of GBM patient-derived GSCs and healthy human NSCs were treated with 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± S.E.M. of at least 3 independent experiments, ANOVA: * P value < .05, *** P value < .001). (B) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR <t>Y1068</t> and p-EGFRvIII Y1068) after 24 h treatment. β-actin was used as a loading control. (C) Heatmap summarizing TAT-Cx43 266–283 response and EGFR alterations of human patient-derived GSCs and hNSCs determined by WB, RNAseq, and FISH. For total color score, every square was assigned a numeric value according to its color. Dark red = 1 point, light red = 0.75 points, yellow = 0.5 points, and green = 0 points. (D) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status in patient-derived GSCs and healthy human GSCs. χ 2 test: ** P value < .01.
    Phospho Egfr Tyr1068, supplied by Cell Signaling Technology Inc, 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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    Cell Signaling Technology Inc 4267 phospho egfr
    Correlation of EGFR status vs TAT-Cx43 266–283 response in patient-derived GSCs. A set of GBM patient-derived GSCs and healthy human NSCs were treated with 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± S.E.M. of at least 3 independent experiments, ANOVA: * P value < .05, *** P value < .001). (B) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR <t>Y1068</t> and p-EGFRvIII Y1068) after 24 h treatment. β-actin was used as a loading control. (C) Heatmap summarizing TAT-Cx43 266–283 response and EGFR alterations of human patient-derived GSCs and hNSCs determined by WB, RNAseq, and FISH. For total color score, every square was assigned a numeric value according to its color. Dark red = 1 point, light red = 0.75 points, yellow = 0.5 points, and green = 0 points. (D) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status in patient-derived GSCs and healthy human GSCs. χ 2 test: ** P value < .01.
    4267 Phospho Egfr, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/4267 phospho egfr/product/Cell Signaling Technology Inc
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    Cell Signaling Technology Inc anti phospho egfr tyr1068
    Correlation of EGFR status vs TAT-Cx43 266–283 response in patient-derived GSCs. A set of GBM patient-derived GSCs and healthy human NSCs were treated with 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± S.E.M. of at least 3 independent experiments, ANOVA: * P value < .05, *** P value < .001). (B) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR <t>Y1068</t> and p-EGFRvIII Y1068) after 24 h treatment. β-actin was used as a loading control. (C) Heatmap summarizing TAT-Cx43 266–283 response and EGFR alterations of human patient-derived GSCs and hNSCs determined by WB, RNAseq, and FISH. For total color score, every square was assigned a numeric value according to its color. Dark red = 1 point, light red = 0.75 points, yellow = 0.5 points, and green = 0 points. (D) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status in patient-derived GSCs and healthy human GSCs. χ 2 test: ** P value < .01.
    Anti Phospho Egfr Tyr1068, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti phospho egfr tyr1068/product/Cell Signaling Technology Inc
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    Image Search Results


    Correlation of EGFR status vs TAT-Cx43 266–283 response in patient-derived GSCs. A set of GBM patient-derived GSCs and healthy human NSCs were treated with 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± S.E.M. of at least 3 independent experiments, ANOVA: * P value < .05, *** P value < .001). (B) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR Y1068 and p-EGFRvIII Y1068) after 24 h treatment. β-actin was used as a loading control. (C) Heatmap summarizing TAT-Cx43 266–283 response and EGFR alterations of human patient-derived GSCs and hNSCs determined by WB, RNAseq, and FISH. For total color score, every square was assigned a numeric value according to its color. Dark red = 1 point, light red = 0.75 points, yellow = 0.5 points, and green = 0 points. (D) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status in patient-derived GSCs and healthy human GSCs. χ 2 test: ** P value < .01.

    Journal: Neuro-Oncology

    Article Title: EGFR amplification and EGFRvIII predict and participate in TAT-Cx43 266–283 antitumor response in preclinical glioblastoma models

    doi: 10.1093/neuonc/noae060

    Figure Lengend Snippet: Correlation of EGFR status vs TAT-Cx43 266–283 response in patient-derived GSCs. A set of GBM patient-derived GSCs and healthy human NSCs were treated with 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± S.E.M. of at least 3 independent experiments, ANOVA: * P value < .05, *** P value < .001). (B) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR Y1068 and p-EGFRvIII Y1068) after 24 h treatment. β-actin was used as a loading control. (C) Heatmap summarizing TAT-Cx43 266–283 response and EGFR alterations of human patient-derived GSCs and hNSCs determined by WB, RNAseq, and FISH. For total color score, every square was assigned a numeric value according to its color. Dark red = 1 point, light red = 0.75 points, yellow = 0.5 points, and green = 0 points. (D) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status in patient-derived GSCs and healthy human GSCs. χ 2 test: ** P value < .01.

    Article Snippet: Primary antibodies used for WB were: anti-phospho-EGFR Y1068 (1:1000, Cell Signaling, ref: 3777) and anti-EGFR (1:1000, Cell Signaling, ref: 4267), anti-VEGF (1:200, Santa Cruz Biotechnology, ref: sc-7269), anti-phospho-Src Y416 (1:250, Cell Signaling, ref: 2101), anti-Src (1:500, Cell Signaling, ref: 2110), anti-GAPDH (1:5000, Invitrogen, ref: AM4300), and anti-β-actin (1:1000, Sigma, ref: A5441).

    Techniques: Derivative Assay, Viability Assay, Control, Activity Assay

    The effect of TAT-Cx43 266–283 depends on EGFR alterations. A set of murine SVZ NSCs with EGFR alterations (SVZ-EGFRwt and SVZ-EGFRvIII) and a set of murine SVZ NSCs with EGFRvIII mutation (NSC-EGFRvIII), with Nf1/PTEN deletion (NP) or with a combination of Nf1/PTEN deletion and EGFRvIII mutation (NPE, and their immune evasive version, NPE-IE) and their non-modified counterparts (SVZ-NSCs) were treated with 50 µM TAT, 50 µM TAT-Cx43 274–291 (2 cell-penetrating peptides used as additional controls), 50 µM TAT-Cx43 266–283 , 100 µM temozolomide, 1 µM erlotinib, 0.05% DMSO (v/v) (vehicle for erlotinib) and the combination of 1 µM erlotinib plus 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay of SVZ NSCs with EGFR alterations and healthy NSCs after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± SEM of at least 3 independent experiments, ANOVA: * P < .05, *** P < .001 vs control; ## P < .01, ### P < .001 vs TAT; @@ P < .01 vs TAT-Cx43 274-291 ; +++ P < .001 vs temozolomide). (B) Phase-contrast images of murine NSCs with and without EGFR alterations treated as described previously. Scale bar: 100 µm. (C) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR Y1068 and p-EGFRvIII Y1068) after 24 h treatment. GAPDH was used as a loading control. (D) Alamar blue viability assay of SVZ NSCs with EGFR and additional GBM-driver alterations after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± SEM of at least 3 independent experiments, ANOVA: *** P value < .001). (E) Phase-contrast images of murine SVZ NSCs with GBM-driver alterations treated as described in (A). Scale bar: 100 µm. (F) WB analysis of EGFR, EGFRvIII, and Src levels and activity (p-EGFR Y1068, p-EGFRvIII Y1068, and p-Src Y416) after 24 h treatment. β-actin was used as a loading control. (G) Correlation graph depicting the relationship between GSC EGFR status and Src inhibition after treatment with TAT-Cx43 266–283 in murine and patient-derived GSCs. (H) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status of all the murine NSCs and GSCs. χ 2 test was used for statistical analysis.

    Journal: Neuro-Oncology

    Article Title: EGFR amplification and EGFRvIII predict and participate in TAT-Cx43 266–283 antitumor response in preclinical glioblastoma models

    doi: 10.1093/neuonc/noae060

    Figure Lengend Snippet: The effect of TAT-Cx43 266–283 depends on EGFR alterations. A set of murine SVZ NSCs with EGFR alterations (SVZ-EGFRwt and SVZ-EGFRvIII) and a set of murine SVZ NSCs with EGFRvIII mutation (NSC-EGFRvIII), with Nf1/PTEN deletion (NP) or with a combination of Nf1/PTEN deletion and EGFRvIII mutation (NPE, and their immune evasive version, NPE-IE) and their non-modified counterparts (SVZ-NSCs) were treated with 50 µM TAT, 50 µM TAT-Cx43 274–291 (2 cell-penetrating peptides used as additional controls), 50 µM TAT-Cx43 266–283 , 100 µM temozolomide, 1 µM erlotinib, 0.05% DMSO (v/v) (vehicle for erlotinib) and the combination of 1 µM erlotinib plus 50 µM TAT-Cx43 266–283 . (A) Alamar blue viability assay of SVZ NSCs with EGFR alterations and healthy NSCs after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± SEM of at least 3 independent experiments, ANOVA: * P < .05, *** P < .001 vs control; ## P < .01, ### P < .001 vs TAT; @@ P < .01 vs TAT-Cx43 274-291 ; +++ P < .001 vs temozolomide). (B) Phase-contrast images of murine NSCs with and without EGFR alterations treated as described previously. Scale bar: 100 µm. (C) WB analysis of EGFR and EGFRvIII levels and activity (p-EGFR Y1068 and p-EGFRvIII Y1068) after 24 h treatment. GAPDH was used as a loading control. (D) Alamar blue viability assay of SVZ NSCs with EGFR and additional GBM-driver alterations after 6 days of treatment administered at days 0 and 3. Results are expressed as the percentage of the control (mean ± SEM of at least 3 independent experiments, ANOVA: *** P value < .001). (E) Phase-contrast images of murine SVZ NSCs with GBM-driver alterations treated as described in (A). Scale bar: 100 µm. (F) WB analysis of EGFR, EGFRvIII, and Src levels and activity (p-EGFR Y1068, p-EGFRvIII Y1068, and p-Src Y416) after 24 h treatment. β-actin was used as a loading control. (G) Correlation graph depicting the relationship between GSC EGFR status and Src inhibition after treatment with TAT-Cx43 266–283 in murine and patient-derived GSCs. (H) Contingency table graph showing the magnitude of TAT-Cx43 266–283 response and EGFR status of all the murine NSCs and GSCs. χ 2 test was used for statistical analysis.

    Article Snippet: Primary antibodies used for WB were: anti-phospho-EGFR Y1068 (1:1000, Cell Signaling, ref: 3777) and anti-EGFR (1:1000, Cell Signaling, ref: 4267), anti-VEGF (1:200, Santa Cruz Biotechnology, ref: sc-7269), anti-phospho-Src Y416 (1:250, Cell Signaling, ref: 2101), anti-Src (1:500, Cell Signaling, ref: 2110), anti-GAPDH (1:5000, Invitrogen, ref: AM4300), and anti-β-actin (1:1000, Sigma, ref: A5441).

    Techniques: Mutagenesis, Modification, Viability Assay, Control, Activity Assay, Inhibition, Derivative Assay