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src 32g6 rabbit mab  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc src 32g6 rabbit mab
    Src 32g6 Rabbit Mab, 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/product/rabbit+monoclonal+anti+src/bio_rxiv__64898__2026__04__02__716058-64-15-78
    Average 86 stars, based on 1 article reviews
    src 32g6 rabbit mab - by Bioz Stars, 2026-10
    86/100 stars

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    Related Articles

    other:

    Article Title: RAPSYN-mediated neddylation of BCR-ABL alternatively determines the fate of Philadelphia chromosome-positive leukemia
    Article Snippet: Antibody , Rabbit monoclonal anti-SRC (clone 36D10) , Cell Signaling Technology , Cat# 2109; RRID: AB_2106059 , 1:1000.

    Article Title: Alarmin S100A8 imparts chemoresistance of esophageal cancer by reprogramming cancer-associated fibroblasts
    Article Snippet: Rabbit Monoclonal anti-Src , Cell Signaling Technology , Cat# 2123; RRID: AB_2106047.

    Western Blot:

    Article Title: Netrin-1 Is an Important Mediator in Microglia Migration.
    Article Snippet: For immunostaining, the following primary antibodies were used: mouse monoclonal anti-Netrin-1 (MAB1109-100, 1:500) and goat polyclonal anti-TAG1 (AF4439; 1:200) from R&D Systems (Minneapolis, MIN, USA); rabbit polyclonal anti-Iba1 (019-19741, 1:500) from FUJIFILM Wako (Wako, Osaka, Japan). .. For Western blotting, the following primary antibodies were used: rabbit polyclonal anti-FAK (sc-557, 1:200) and mouse monoclonal anti-GSK3α/β (sc-7291, 1:400) from Santa Cruz Biotechnology (Santa Cruz, CA, USA); rabbit polyclonal anti-pSrc (Tyr416) (#2101, 1:1000), rabbit monoclonal anti-Src (#2123, 1:1000), rabbit polyclonal pGSK3β (Ser9) (#9336, 1:1000), rabbit monoclonal anti-pAKT (Ser473) (#4060, 1:1000), rabbit polyclonal anti-AKT (#9272, 1:1000), rabbit polyclonal antipERK1/2 (#9101, 1:1000), and mouse monoclonal anti-ERK1/2 (#4696, 1:1000) from Cell Signaling Technology (Danvers, MA, USA); rabbit polyclonal anti-pFAK (Tyr861) (F9176, 1:1000), rabbit polyclonal anti-pFAK (Tyr397) (ABT135, 1:1000), and mouse monoclonal anti-β-Actin (A5441; 1:3000) from Sigma Aldrich (St. Louis, MO, USA); mouse monoclonal anti-GAPDH (HC301, 1:5000) from Transgene (Beijing, China); Alexa Fluor and HRPconjugated secondary antibody against mouse, goat, or rabbit were purchased from Sigma Aldrich. .. Alexa Fluor 488-phalloidin (#A12379) was obtained from Thermo Fisher Scientific (Waltham, MA, USA).



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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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    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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    Image Search Results


    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