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phospho src tyr416  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc phospho src tyr416
    Phospho Src Tyr416, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 2298 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    A Western blot analysis of the oral squamous carcinoma cell lines to monitor numerous signaling pathways. The phosphorylated and total protein levels were determined as indicated. B Cell viability (%) of the oral squamous carcinoma cell lines treated with each Src inhibitor for 72 h. Viability was measured using CellTiter-Glo, and values are indicated relative to the 1% dimethyl sulfoxide (DMSO) control. Data represent mean ± standard deviation from three independent experiments (n = 3). C IC50 curves of the oral squamous carcinoma cell lines treated with each Src inhibitor for 36 h. Viability was measured using CellTiter-Glo and normalized to that of the 1% DMSO control. Values represent the mean of n = 3. D, E Western blot analysis of the oral squamous carcinoma cell lines to investigate Src (D) and MAPK (E) activity induced by different Src inhibitors. Oral squamous carcinoma cell lines were treated with an Src inhibitor for 18 h, followed by western blot analysis. D indicates the Src phosphorylation <t>(Tyr416),</t> and E reveals MAPK pathway-related proteins. Supplementary Table S1 lists the concentrations of the Src inhibitors used.
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    A Western blot analysis of the oral squamous carcinoma cell lines to monitor numerous signaling pathways. The phosphorylated and total protein levels were determined as indicated. B Cell viability (%) of the oral squamous carcinoma cell lines treated with each Src inhibitor for 72 h. Viability was measured using CellTiter-Glo, and values are indicated relative to the 1% dimethyl sulfoxide (DMSO) control. Data represent mean ± standard deviation from three independent experiments (n = 3). C IC50 curves of the oral squamous carcinoma cell lines treated with each Src inhibitor for 36 h. Viability was measured using CellTiter-Glo and normalized to that of the 1% DMSO control. Values represent the mean of n = 3. D, E Western blot analysis of the oral squamous carcinoma cell lines to investigate Src (D) and MAPK (E) activity induced by different Src inhibitors. Oral squamous carcinoma cell lines were treated with an Src inhibitor for 18 h, followed by western blot analysis. D indicates the Src phosphorylation <t>(Tyr416),</t> and E reveals MAPK pathway-related proteins. Supplementary Table S1 lists the concentrations of the Src inhibitors used.
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    A Western blot analysis of the oral squamous carcinoma cell lines to monitor numerous signaling pathways. The phosphorylated and total protein levels were determined as indicated. B Cell viability (%) of the oral squamous carcinoma cell lines treated with each Src inhibitor for 72 h. Viability was measured using CellTiter-Glo, and values are indicated relative to the 1% dimethyl sulfoxide (DMSO) control. Data represent mean ± standard deviation from three independent experiments (n = 3). C IC50 curves of the oral squamous carcinoma cell lines treated with each Src inhibitor for 36 h. Viability was measured using CellTiter-Glo and normalized to that of the 1% DMSO control. Values represent the mean of n = 3. D, E Western blot analysis of the oral squamous carcinoma cell lines to investigate Src (D) and MAPK (E) activity induced by different Src inhibitors. Oral squamous carcinoma cell lines were treated with an Src inhibitor for 18 h, followed by western blot analysis. D indicates the Src phosphorylation <t>(Tyr416),</t> and E reveals MAPK pathway-related proteins. Supplementary Table S1 lists the concentrations of the Src inhibitors used.
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    A Western blot analysis of the oral squamous carcinoma cell lines to monitor numerous signaling pathways. The phosphorylated and total protein levels were determined as indicated. B Cell viability (%) of the oral squamous carcinoma cell lines treated with each Src inhibitor for 72 h. Viability was measured using CellTiter-Glo, and values are indicated relative to the 1% dimethyl sulfoxide (DMSO) control. Data represent mean ± standard deviation from three independent experiments (n = 3). C IC50 curves of the oral squamous carcinoma cell lines treated with each Src inhibitor for 36 h. Viability was measured using CellTiter-Glo and normalized to that of the 1% DMSO control. Values represent the mean of n = 3. D, E Western blot analysis of the oral squamous carcinoma cell lines to investigate Src (D) and MAPK (E) activity induced by different Src inhibitors. Oral squamous carcinoma cell lines were treated with an Src inhibitor for 18 h, followed by western blot analysis. D indicates the Src phosphorylation <t>(Tyr416),</t> and E reveals MAPK pathway-related proteins. Supplementary Table S1 lists the concentrations of the Src inhibitors used.
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    A Western blot analysis of the oral squamous carcinoma cell lines to monitor numerous signaling pathways. The phosphorylated and total protein levels were determined as indicated. B Cell viability (%) of the oral squamous carcinoma cell lines treated with each Src inhibitor for 72 h. Viability was measured using CellTiter-Glo, and values are indicated relative to the 1% dimethyl sulfoxide (DMSO) control. Data represent mean ± standard deviation from three independent experiments (n = 3). C IC50 curves of the oral squamous carcinoma cell lines treated with each Src inhibitor for 36 h. Viability was measured using CellTiter-Glo and normalized to that of the 1% DMSO control. Values represent the mean of n = 3. D, E Western blot analysis of the oral squamous carcinoma cell lines to investigate Src (D) and MAPK (E) activity induced by different Src inhibitors. Oral squamous carcinoma cell lines were treated with an Src inhibitor for 18 h, followed by western blot analysis. D indicates the Src phosphorylation <t>(Tyr416),</t> and E reveals MAPK pathway-related proteins. Supplementary Table S1 lists the concentrations of the Src inhibitors used.
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    A Western blot analysis of the oral squamous carcinoma cell lines to monitor numerous signaling pathways. The phosphorylated and total protein levels were determined as indicated. B Cell viability (%) of the oral squamous carcinoma cell lines treated with each Src inhibitor for 72 h. Viability was measured using CellTiter-Glo, and values are indicated relative to the 1% dimethyl sulfoxide (DMSO) control. Data represent mean ± standard deviation from three independent experiments (n = 3). C IC50 curves of the oral squamous carcinoma cell lines treated with each Src inhibitor for 36 h. Viability was measured using CellTiter-Glo and normalized to that of the 1% DMSO control. Values represent the mean of n = 3. D, E Western blot analysis of the oral squamous carcinoma cell lines to investigate Src (D) and MAPK (E) activity induced by different Src inhibitors. Oral squamous carcinoma cell lines were treated with an Src inhibitor for 18 h, followed by western blot analysis. D indicates the Src phosphorylation <t>(Tyr416),</t> and E reveals MAPK pathway-related proteins. Supplementary Table S1 lists the concentrations of the Src inhibitors used.
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    Cell Signaling Technology Inc p src
    A Western blot analysis of the oral squamous carcinoma cell lines to monitor numerous signaling pathways. The phosphorylated and total protein levels were determined as indicated. B Cell viability (%) of the oral squamous carcinoma cell lines treated with each Src inhibitor for 72 h. Viability was measured using CellTiter-Glo, and values are indicated relative to the 1% dimethyl sulfoxide (DMSO) control. Data represent mean ± standard deviation from three independent experiments (n = 3). C IC50 curves of the oral squamous carcinoma cell lines treated with each Src inhibitor for 36 h. Viability was measured using CellTiter-Glo and normalized to that of the 1% DMSO control. Values represent the mean of n = 3. D, E Western blot analysis of the oral squamous carcinoma cell lines to investigate Src (D) and MAPK (E) activity induced by different Src inhibitors. Oral squamous carcinoma cell lines were treated with an Src inhibitor for 18 h, followed by western blot analysis. D indicates the Src phosphorylation <t>(Tyr416),</t> and E reveals MAPK pathway-related proteins. Supplementary Table S1 lists the concentrations of the Src inhibitors used.
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    A Western blot analysis of the oral squamous carcinoma cell lines to monitor numerous signaling pathways. The phosphorylated and total protein levels were determined as indicated. B Cell viability (%) of the oral squamous carcinoma cell lines treated with each Src inhibitor for 72 h. Viability was measured using CellTiter-Glo, and values are indicated relative to the 1% dimethyl sulfoxide (DMSO) control. Data represent mean ± standard deviation from three independent experiments (n = 3). C IC50 curves of the oral squamous carcinoma cell lines treated with each Src inhibitor for 36 h. Viability was measured using CellTiter-Glo and normalized to that of the 1% DMSO control. Values represent the mean of n = 3. D, E Western blot analysis of the oral squamous carcinoma cell lines to investigate Src (D) and MAPK (E) activity induced by different Src inhibitors. Oral squamous carcinoma cell lines were treated with an Src inhibitor for 18 h, followed by western blot analysis. D indicates the Src phosphorylation (Tyr416), and E reveals MAPK pathway-related proteins. Supplementary Table S1 lists the concentrations of the Src inhibitors used.

    Journal: bioRxiv

    Article Title: Heterogeneous Sensitivity to Src Inhibitors in Oral Squamous Cell Carcinoma and Its Implications for Combination Therapy with Cisplatin

    doi: 10.64898/2026.04.02.716058

    Figure Lengend Snippet: A Western blot analysis of the oral squamous carcinoma cell lines to monitor numerous signaling pathways. The phosphorylated and total protein levels were determined as indicated. B Cell viability (%) of the oral squamous carcinoma cell lines treated with each Src inhibitor for 72 h. Viability was measured using CellTiter-Glo, and values are indicated relative to the 1% dimethyl sulfoxide (DMSO) control. Data represent mean ± standard deviation from three independent experiments (n = 3). C IC50 curves of the oral squamous carcinoma cell lines treated with each Src inhibitor for 36 h. Viability was measured using CellTiter-Glo and normalized to that of the 1% DMSO control. Values represent the mean of n = 3. D, E Western blot analysis of the oral squamous carcinoma cell lines to investigate Src (D) and MAPK (E) activity induced by different Src inhibitors. Oral squamous carcinoma cell lines were treated with an Src inhibitor for 18 h, followed by western blot analysis. D indicates the Src phosphorylation (Tyr416), and E reveals MAPK pathway-related proteins. Supplementary Table S1 lists the concentrations of the Src inhibitors used.

    Article Snippet: The following primary antibodies were used: Phospho-Src Family (Tyr416) (D49G4) Rabbit mAb (#6943), Phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) (D13.14.4E) XP Rabbit mAb (#4370), Phospho-p38 MAPK (Thr180/Tyr182) (D3F9) XP Rabbit mAb (#4511), and Phospho-SAPK/JNK (Thr183/Tyr185) (81E11) Rabbit mAb (#4668) (all from Cell Signaling Technology).

    Techniques: Western Blot, Protein-Protein interactions, Control, Standard Deviation, Activity Assay, Phospho-proteomics