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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 2354 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/phospho+src+tyr416/Phospho-Src+Family+(Tyr416)+Antibody/us12594421-308-66-69
    Average 96 stars, based on 2354 article reviews
    phospho src tyr416 - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    other:


    Electrophoresis:

    Article Title: Compositions and methods for increasing cancer cell sensitivity to alternating electric fields
    Article Snippet: Samples were run on SDS-polyacrylamide gel electrophoresis (Bolt 8% Bis-Tris base gel NW00080BOX, Thermo-Fischer). .. After electrophoresis, proteins were transferred to 0.2 μm polyvinylidene difluoride membrane (Immuno-Blot PVDF #162-0177, Bio-Rad) and probed with the appropriate primary antibody: GAPDH (SC-32233, Santa Cruz), Vinculin (ab140007, Abcam), Cyclin D1 (2922, Cell Signaling), Rb (9309, Cell Signaling), pRb S807/811 (8516, Cell Signaling), pAkt 5473, (4051, Cell signaling), Akt (2920, Cell signaling)), FAK (3283S, Cell signaling), Phospho-FAK (Tyr397) (3283S, Cell signaling, Src (2109S, cell signaling) and Phospho-Src (Tyr416) (2101S, Cell signaling). followed by horseradish peroxidase-conjugated secondary antibody (goat anti rabbit 7074, Cell Signaling and goat anti mouse 7076, Cell Signaling) and a chemiluminescent substrate (WBLUF0100, Signa-Aldrich). ..

    Membrane:

    Article Title: Compositions and methods for increasing cancer cell sensitivity to alternating electric fields
    Article Snippet: Samples were run on SDS-polyacrylamide gel electrophoresis (Bolt 8% Bis-Tris base gel NW00080BOX, Thermo-Fischer). .. After electrophoresis, proteins were transferred to 0.2 μm polyvinylidene difluoride membrane (Immuno-Blot PVDF #162-0177, Bio-Rad) and probed with the appropriate primary antibody: GAPDH (SC-32233, Santa Cruz), Vinculin (ab140007, Abcam), Cyclin D1 (2922, Cell Signaling), Rb (9309, Cell Signaling), pRb S807/811 (8516, Cell Signaling), pAkt 5473, (4051, Cell signaling), Akt (2920, Cell signaling)), FAK (3283S, Cell signaling), Phospho-FAK (Tyr397) (3283S, Cell signaling, Src (2109S, cell signaling) and Phospho-Src (Tyr416) (2101S, Cell signaling). followed by horseradish peroxidase-conjugated secondary antibody (goat anti rabbit 7074, Cell Signaling and goat anti mouse 7076, Cell Signaling) and a chemiluminescent substrate (WBLUF0100, Signa-Aldrich). ..

    Western Blot:

    Article Title: Mechanistic Exploration of Shugan Jianpi Formula for Treating Triple-Negative Breast Cancer Under Chronic Stress: A Network Pharmacology-Guided Experimental Study
    Article Snippet: Protein bands were detected using the ECL reagent and analyzed with a chemiluminescence Western blot detection system (Tanon, China). .. Phospho-Src (Tyr416) (CST; cat. #6943), Src (CST; cat. #2109), Phospho-Stat3 (Tyr705) (CST; cat. #9145), Stat3 (CST; cat. #9139), p44/42 mitogen-activated protein kinase (MAPK) (Erk1/2) (CST; cat. #4695), Phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) (CST; cat. #4370), Plk1 (208G4) (CST; cat. #4513), Skp2 (CST; cat. #2652), VEGFA (Proteintech; cat. #19003-1-AP), Vimentin (Proteintech; cat. #10366-1-AP), E-Cadherin (Proteintech; cat. #20874-1-AP), N-Cadherin (Proteintech; cat. #22018-1-AP), Bax (Proteintech; cat. #50599-2-Ig), Bcl2 (Proteintech; cat. #68103-1-Ig), Caspase-3 (CST; cat. #9662), Caspase-9 (CST; cat. #9502),Vinculin (CST; cat. #66305-1-Ig) were used for Western blot. ..

    Article Title: PEAK1 maintains tight junctions in intestinal epithelial cells and resists colitis by inhibiting autophagy-mediated ZO-1 degradation.
    Article Snippet: Antibodies against the following proteins were purchased from Invitrogen: ZO-1 Alexa FluorTM 555 (IF 1:100, MA3-39100-A555), Claudin-2 (WB 1:1,000, IF 1:100, 32-5600), Goat anti-Mouse IgG (H + L) Alexa Fluor® 488 Secondary Antibody (1:500, A-11029), Goat antiRabbit IgG (H+ L) Alexa Fluor® 488 Secondary Antibody (1:500, A11034), Goat anti-Mouse IgG (H + L) Alexa Fluor® 555 Secondary Antibody (1:500, A-21424), Goat anti-Rabbit IgG (H + L) Alexa Fluor® 555 Secondary Antibody (1:500, A-21429). .. Antibodies against the following proteins were purchased from Cell Signaling Technology: Src (WB 1:1,000, #2108), Phospho-Src (Tyr416) (1:1,000, #2101), Phospho-Src (Tyr527) (WB 1:1,000, #2105), ERK1/2 (WB 1:1,000, #4695), LC-3B (WB 1:1,000, #2775), Phospho-Myosin Light Chain 2 (Ser19) (WB 1:1,000, #3671), Myosin Light Chain 2 (WB 1:1,000, #8505), Conformation Specific Mouse Anti-Rabbit IgG (WB 1:2,000, #5127S). .. Antibodies against the following proteins were purchased from Bioworld: Occludin (WB 1:1,000, AP0765), GFP (WB 1:2,000, MB9233), and E-cadherin (WB 1:1,000, BS1098).

    Incubation:

    Article Title: Omentin-1 attenuates atrial fibrillation via Src/PI3K/Akt signaling-mediated anti-fibrotic effects in cardiac fibroblasts.
    Article Snippet: Background: Atrial fibrillation (AF) is characterized by progressive atrial fibrosis, leading to increased morbidity and mortality.. While the novel adipokine Omentin-1 demonstrates anti-fibrotic potential across organ systems, its role in AF pathogenesis remains unclear.. This study investigates Omentin-1’s therapeutic effects and the underlying mechanisms in angiotensin II (Ang II)-induced atrial fibrosis and AF.

    Article Title: Modulation of blood-tumor barrier transcriptional programs improves intratumoral drug delivery and potentiates chemotherapy in GBM.
    Article Snippet: Blocking was performed in 5% milk with 0.1% Triton X- 100 in 1× PBS (TBST) (Gibco) for 1 hour at room temperature under shaking. .. Primary antibodies used were incubated in the cold under shaking overnight: antipCHK1 (Ser345) (1:100; Cell Signaling Technology), anti- CHK1 (1:1000; Cell Signaling Technology), anti- pH2AX (Ser139) (1:1000; Cell Signaling Technology), anti- WNT7A/B (1:1000; Proteintech), anti–IL- 6 (1:1000; Thermo Fisher Scientific), anti–phospho- GSK3b (Ser9) (1:1000; Cell Signaling Technology), anti- vinculin (1:1000; Proteintech), anti–phospho- TYK2 (Tyr1054 and Tyr1055) (1:1000; Thermo Fisher Scientific), anti- phospho- STAT5A/B (Tyr694) (1:1000; Cell Signaling Technology), anti–phospho- p38α (Thr180 and Tyr182) (1:1000; Thermo Fisher Scientific), anti–phospho- SRC (Tyr416) (1:1000; Cell Signaling Technology), anti–phospho- CREB (Ser133) (1:500; Thermo Fisher Scientific), anti- MFSD2A (1:500; Proteintech), anti- CAV1 (1:1000; Proteintech), anti- CD144 (VE- cadherin) (1:1000; Thermo Fisher Scientific), and anti–β- actin (1:2000; Cell Signaling Technology). .. The appropriate secondary antibody goat anti–mouse– horseradish peroxidase (HRP; Sigma- Aldrich) or goat anti–rabbitHRP (Sigma- Aldrich) was used in 5% milk in 1× TBST with 1:5000 dilution for 1 hour at room temperature.



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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