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c src kinase inhibitor pp2  (Selleck Chemicals)


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    Structured Review

    Selleck Chemicals c src kinase inhibitor pp2
    C Src Kinase Inhibitor Pp2, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 95/100, based on 160 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/src+kinase+inhibitor/PP2/pmc10962971__pnas__2312290121__sapp-21-27-31
    Average 95 stars, based on 160 article reviews
    c src kinase inhibitor pp2 - by Bioz Stars, 2026-10
    95/100 stars

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    Related Articles

    Incubation:

    Article Title: CAR macrophages with built-In CD47 blocker combat tumor antigen heterogeneity and activate T cells via cross-presentation
    Article Snippet: .. For experiments with pharmacological inhibitors, macrophages were incubated with the following pharmacological inhibitors: Src kinase inhibitor, dasatinib; V-ATPase inhibitor, concanamycin D; actin polymerization inhibitor, cytochalasin D; protease inhibitor, leupeptin, and pepstatin A. Inhibitors were sourced from Selleckchem or Caymanchem and adjust to final concentration of 2 uM. ..

    Article Title: CAR macrophages with built-In CD47 blocker combat tumor antigen heterogeneity and activate T cells via cross-presentation.
    Article Snippet: For experiments with pharmacological inhibitors, macrophages were incubated with the following pharmacological inhibitors: Src kinase inhibitor, dasatinib; V-ATPase inhibitor, concanamycin D; actin polymerization inhibitor, cytochalasinD; protease inhibitor, leupeptin, and pepstatin A. Inhibitors were sourced from Selleckchem or Caymanchem and adjust to final concentration of 2 uM. .. For experiments with pharmacological inhibitors, macrophages were incubated with the following pharmacological inhibitors: Src kinase inhibitor, dasatinib; V-ATPase inhibitor, concanamycin D; actin polymerization inhibitor, cytochalasinD; protease inhibitor, leupeptin, and pepstatin A. Inhibitors were sourced from Selleckchem or Caymanchem and adjust to final concentration of 2 uM. ..

    Protease Inhibitor:

    Article Title: CAR macrophages with built-In CD47 blocker combat tumor antigen heterogeneity and activate T cells via cross-presentation
    Article Snippet: .. For experiments with pharmacological inhibitors, macrophages were incubated with the following pharmacological inhibitors: Src kinase inhibitor, dasatinib; V-ATPase inhibitor, concanamycin D; actin polymerization inhibitor, cytochalasin D; protease inhibitor, leupeptin, and pepstatin A. Inhibitors were sourced from Selleckchem or Caymanchem and adjust to final concentration of 2 uM. ..

    Article Title: CAR macrophages with built-In CD47 blocker combat tumor antigen heterogeneity and activate T cells via cross-presentation.
    Article Snippet: For experiments with pharmacological inhibitors, macrophages were incubated with the following pharmacological inhibitors: Src kinase inhibitor, dasatinib; V-ATPase inhibitor, concanamycin D; actin polymerization inhibitor, cytochalasinD; protease inhibitor, leupeptin, and pepstatin A. Inhibitors were sourced from Selleckchem or Caymanchem and adjust to final concentration of 2 uM. .. For experiments with pharmacological inhibitors, macrophages were incubated with the following pharmacological inhibitors: Src kinase inhibitor, dasatinib; V-ATPase inhibitor, concanamycin D; actin polymerization inhibitor, cytochalasinD; protease inhibitor, leupeptin, and pepstatin A. Inhibitors were sourced from Selleckchem or Caymanchem and adjust to final concentration of 2 uM. ..

    Concentration Assay:

    Article Title: CAR macrophages with built-In CD47 blocker combat tumor antigen heterogeneity and activate T cells via cross-presentation
    Article Snippet: .. For experiments with pharmacological inhibitors, macrophages were incubated with the following pharmacological inhibitors: Src kinase inhibitor, dasatinib; V-ATPase inhibitor, concanamycin D; actin polymerization inhibitor, cytochalasin D; protease inhibitor, leupeptin, and pepstatin A. Inhibitors were sourced from Selleckchem or Caymanchem and adjust to final concentration of 2 uM. ..

    Article Title: CAR macrophages with built-In CD47 blocker combat tumor antigen heterogeneity and activate T cells via cross-presentation.
    Article Snippet: For experiments with pharmacological inhibitors, macrophages were incubated with the following pharmacological inhibitors: Src kinase inhibitor, dasatinib; V-ATPase inhibitor, concanamycin D; actin polymerization inhibitor, cytochalasinD; protease inhibitor, leupeptin, and pepstatin A. Inhibitors were sourced from Selleckchem or Caymanchem and adjust to final concentration of 2 uM. .. For experiments with pharmacological inhibitors, macrophages were incubated with the following pharmacological inhibitors: Src kinase inhibitor, dasatinib; V-ATPase inhibitor, concanamycin D; actin polymerization inhibitor, cytochalasinD; protease inhibitor, leupeptin, and pepstatin A. Inhibitors were sourced from Selleckchem or Caymanchem and adjust to final concentration of 2 uM. ..



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    ( A ) Western blots for HOXA5 in WT and Thy-1 KO iHLFs cultured on 5kPa PDMS hydrogel or TCP following stimulation with 20μM SRC specific inhibitor KB SRC 4 or 10μM <t>pan-SFK</t> inhibitor <t>PP2</t> for 6h. Quantification of HOXA5 normalized to loading control was plotted as a ratio of normalized signal relative to DMSO vehicle control. Mean ± S.D. plotted; N = 3 (Thy-1 KO -5kPa and WT-1GPa) or N = 4 (WT-5kPa and Thy-1 KO -1GPa) independent experiments; WT-5kPa and WT-1GPa = 1-way ANOVA with post-hoc uncorrected Fisher’s LSD test, Thy-1 KO -5kPa and Thy-1 KO -1GPa = non-parametric Kruskal-Wallis test with post-hoc uncorrected Dunn’s test. Tests chosen based on data distribution and variance. ( B ) Western blots for HOXA5 in WT and Thy-1 KO iHLFs cultured on 5kPa PDMS hydrogel or TCP substrates coated with αV-promoting (Fn 4G ) or α5-promoting (Fn 9*10 ) peptide fragments of the 9–10FnIII integrin binding site. Quantification of HOXA5 normalized to loading control was plotted as a ratio of normalized signal relative to full length human Fn (Fn Full ) control. Mean ± S.D. plotted; N = 3 (WT-5kPa, WT-1GPa, and Thy-1 KO -5kPa) or N = 4 (Thy-1 KO -1GPa) independent experiments; WT-5kPa = 1-way ANOVA with post-hoc uncorrected Fisher’s LSD test, Thy-1 KO -5kPa = Brown-Forsythe and Welch ANOVA with post-hoc unpaired t-tests with Welch’s correction, WT-1GPa and Thy-1 KO -1GPa = non-parametric Kruskal-Wallis test with post-hoc uncorrected Dunn’s test. Tests chosen based on data distribution and variance. For all statistical tests: ns = p > 0.05; p < 0.05 (*); p < 0.01 (**); p < .001 (***); p < .0001 (****).
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    ( A ) Western blots for HOXA5 in WT and Thy-1 KO iHLFs cultured on 5kPa PDMS hydrogel or TCP following stimulation with 20μM SRC specific inhibitor KB SRC 4 or 10μM <t>pan-SFK</t> inhibitor <t>PP2</t> for 6h. Quantification of HOXA5 normalized to loading control was plotted as a ratio of normalized signal relative to DMSO vehicle control. Mean ± S.D. plotted; N = 3 (Thy-1 KO -5kPa and WT-1GPa) or N = 4 (WT-5kPa and Thy-1 KO -1GPa) independent experiments; WT-5kPa and WT-1GPa = 1-way ANOVA with post-hoc uncorrected Fisher’s LSD test, Thy-1 KO -5kPa and Thy-1 KO -1GPa = non-parametric Kruskal-Wallis test with post-hoc uncorrected Dunn’s test. Tests chosen based on data distribution and variance. ( B ) Western blots for HOXA5 in WT and Thy-1 KO iHLFs cultured on 5kPa PDMS hydrogel or TCP substrates coated with αV-promoting (Fn 4G ) or α5-promoting (Fn 9*10 ) peptide fragments of the 9–10FnIII integrin binding site. Quantification of HOXA5 normalized to loading control was plotted as a ratio of normalized signal relative to full length human Fn (Fn Full ) control. Mean ± S.D. plotted; N = 3 (WT-5kPa, WT-1GPa, and Thy-1 KO -5kPa) or N = 4 (Thy-1 KO -1GPa) independent experiments; WT-5kPa = 1-way ANOVA with post-hoc uncorrected Fisher’s LSD test, Thy-1 KO -5kPa = Brown-Forsythe and Welch ANOVA with post-hoc unpaired t-tests with Welch’s correction, WT-1GPa and Thy-1 KO -1GPa = non-parametric Kruskal-Wallis test with post-hoc uncorrected Dunn’s test. Tests chosen based on data distribution and variance. For all statistical tests: ns = p > 0.05; p < 0.05 (*); p < 0.01 (**); p < .001 (***); p < .0001 (****).
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    Src inhibition inhibits PBF phosphorylation and restores RAIU. (A) MCF-7 (i) and MDA-MB-231 (ii) cells were treated with varying doses of <t>PP1</t> (0–2 μM) for 24 h before PBF-pY174 and total PBF expression levels were determined by Western blot. (B) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. (C) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 cells treated with ATRA and dexamethasone. (D) PBF-pY174 and total PBF expression levels following dasatinib dose response (0–2 μM) treatment for 24 h in MCF-7 (i) and MDA-MB-231 (ii) cells. (E) Effect of 1 nM dasatinib or 10 nM saracatinib treatment on PBF-repressed RAIU in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. n = 3 for all experiments. Error bars = SEM. * = P < 0.05, ** = P < 0.01, *** = P < 0.001.
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    Src inhibition inhibits PBF phosphorylation and restores RAIU. (A) MCF-7 (i) and MDA-MB-231 (ii) cells were treated with varying doses of <t>PP1</t> (0–2 μM) for 24 h before PBF-pY174 and total PBF expression levels were determined by Western blot. (B) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. (C) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 cells treated with ATRA and dexamethasone. (D) PBF-pY174 and total PBF expression levels following dasatinib dose response (0–2 μM) treatment for 24 h in MCF-7 (i) and MDA-MB-231 (ii) cells. (E) Effect of 1 nM dasatinib or 10 nM saracatinib treatment on PBF-repressed RAIU in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. n = 3 for all experiments. Error bars = SEM. * = P < 0.05, ** = P < 0.01, *** = P < 0.001.
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    Src inhibition inhibits PBF phosphorylation and restores RAIU. (A) MCF-7 (i) and MDA-MB-231 (ii) cells were treated with varying doses of <t>PP1</t> (0–2 μM) for 24 h before PBF-pY174 and total PBF expression levels were determined by Western blot. (B) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. (C) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 cells treated with ATRA and dexamethasone. (D) PBF-pY174 and total PBF expression levels following dasatinib dose response (0–2 μM) treatment for 24 h in MCF-7 (i) and MDA-MB-231 (ii) cells. (E) Effect of 1 nM dasatinib or 10 nM saracatinib treatment on PBF-repressed RAIU in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. n = 3 for all experiments. Error bars = SEM. * = P < 0.05, ** = P < 0.01, *** = P < 0.001.
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    Src inhibition inhibits PBF phosphorylation and restores RAIU. (A) MCF-7 (i) and MDA-MB-231 (ii) cells were treated with varying doses of <t>PP1</t> (0–2 μM) for 24 h before PBF-pY174 and total PBF expression levels were determined by Western blot. (B) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. (C) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 cells treated with ATRA and dexamethasone. (D) PBF-pY174 and total PBF expression levels following dasatinib dose response (0–2 μM) treatment for 24 h in MCF-7 (i) and MDA-MB-231 (ii) cells. (E) Effect of 1 nM dasatinib or 10 nM saracatinib treatment on PBF-repressed RAIU in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. n = 3 for all experiments. Error bars = SEM. * = P < 0.05, ** = P < 0.01, *** = P < 0.001.
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    Src inhibition inhibits PBF phosphorylation and restores RAIU. (A) MCF-7 (i) and MDA-MB-231 (ii) cells were treated with varying doses of <t>PP1</t> (0–2 μM) for 24 h before PBF-pY174 and total PBF expression levels were determined by Western blot. (B) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. (C) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 cells treated with ATRA and dexamethasone. (D) PBF-pY174 and total PBF expression levels following dasatinib dose response (0–2 μM) treatment for 24 h in MCF-7 (i) and MDA-MB-231 (ii) cells. (E) Effect of 1 nM dasatinib or 10 nM saracatinib treatment on PBF-repressed RAIU in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. n = 3 for all experiments. Error bars = SEM. * = P < 0.05, ** = P < 0.01, *** = P < 0.001.
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    Image Search Results


    ( A ) Western blots for HOXA5 in WT and Thy-1 KO iHLFs cultured on 5kPa PDMS hydrogel or TCP following stimulation with 20μM SRC specific inhibitor KB SRC 4 or 10μM pan-SFK inhibitor PP2 for 6h. Quantification of HOXA5 normalized to loading control was plotted as a ratio of normalized signal relative to DMSO vehicle control. Mean ± S.D. plotted; N = 3 (Thy-1 KO -5kPa and WT-1GPa) or N = 4 (WT-5kPa and Thy-1 KO -1GPa) independent experiments; WT-5kPa and WT-1GPa = 1-way ANOVA with post-hoc uncorrected Fisher’s LSD test, Thy-1 KO -5kPa and Thy-1 KO -1GPa = non-parametric Kruskal-Wallis test with post-hoc uncorrected Dunn’s test. Tests chosen based on data distribution and variance. ( B ) Western blots for HOXA5 in WT and Thy-1 KO iHLFs cultured on 5kPa PDMS hydrogel or TCP substrates coated with αV-promoting (Fn 4G ) or α5-promoting (Fn 9*10 ) peptide fragments of the 9–10FnIII integrin binding site. Quantification of HOXA5 normalized to loading control was plotted as a ratio of normalized signal relative to full length human Fn (Fn Full ) control. Mean ± S.D. plotted; N = 3 (WT-5kPa, WT-1GPa, and Thy-1 KO -5kPa) or N = 4 (Thy-1 KO -1GPa) independent experiments; WT-5kPa = 1-way ANOVA with post-hoc uncorrected Fisher’s LSD test, Thy-1 KO -5kPa = Brown-Forsythe and Welch ANOVA with post-hoc unpaired t-tests with Welch’s correction, WT-1GPa and Thy-1 KO -1GPa = non-parametric Kruskal-Wallis test with post-hoc uncorrected Dunn’s test. Tests chosen based on data distribution and variance. For all statistical tests: ns = p > 0.05; p < 0.05 (*); p < 0.01 (**); p < .001 (***); p < .0001 (****).

    Journal: PLOS Genetics

    Article Title: Fibroblast mechanoperception instructs pulmonary developmental and pattern specification gene expression programs

    doi: 10.1371/journal.pgen.1011924

    Figure Lengend Snippet: ( A ) Western blots for HOXA5 in WT and Thy-1 KO iHLFs cultured on 5kPa PDMS hydrogel or TCP following stimulation with 20μM SRC specific inhibitor KB SRC 4 or 10μM pan-SFK inhibitor PP2 for 6h. Quantification of HOXA5 normalized to loading control was plotted as a ratio of normalized signal relative to DMSO vehicle control. Mean ± S.D. plotted; N = 3 (Thy-1 KO -5kPa and WT-1GPa) or N = 4 (WT-5kPa and Thy-1 KO -1GPa) independent experiments; WT-5kPa and WT-1GPa = 1-way ANOVA with post-hoc uncorrected Fisher’s LSD test, Thy-1 KO -5kPa and Thy-1 KO -1GPa = non-parametric Kruskal-Wallis test with post-hoc uncorrected Dunn’s test. Tests chosen based on data distribution and variance. ( B ) Western blots for HOXA5 in WT and Thy-1 KO iHLFs cultured on 5kPa PDMS hydrogel or TCP substrates coated with αV-promoting (Fn 4G ) or α5-promoting (Fn 9*10 ) peptide fragments of the 9–10FnIII integrin binding site. Quantification of HOXA5 normalized to loading control was plotted as a ratio of normalized signal relative to full length human Fn (Fn Full ) control. Mean ± S.D. plotted; N = 3 (WT-5kPa, WT-1GPa, and Thy-1 KO -5kPa) or N = 4 (Thy-1 KO -1GPa) independent experiments; WT-5kPa = 1-way ANOVA with post-hoc uncorrected Fisher’s LSD test, Thy-1 KO -5kPa = Brown-Forsythe and Welch ANOVA with post-hoc unpaired t-tests with Welch’s correction, WT-1GPa and Thy-1 KO -1GPa = non-parametric Kruskal-Wallis test with post-hoc uncorrected Dunn’s test. Tests chosen based on data distribution and variance. For all statistical tests: ns = p > 0.05; p < 0.05 (*); p < 0.01 (**); p < .001 (***); p < .0001 (****).

    Article Snippet: After allowing for adhesion, cells were stimulated with 1% FBS DMEM containing 20μM SRC inhibitor KB SRC 4 (Tocris) or 10μM pan-Src Family Kinase (SFK) inhibitor PP2 (Tocris) for periods of 3h or 6h.

    Techniques: Western Blot, Cell Culture, Control, Binding Assay

    Src inhibition inhibits PBF phosphorylation and restores RAIU. (A) MCF-7 (i) and MDA-MB-231 (ii) cells were treated with varying doses of PP1 (0–2 μM) for 24 h before PBF-pY174 and total PBF expression levels were determined by Western blot. (B) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. (C) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 cells treated with ATRA and dexamethasone. (D) PBF-pY174 and total PBF expression levels following dasatinib dose response (0–2 μM) treatment for 24 h in MCF-7 (i) and MDA-MB-231 (ii) cells. (E) Effect of 1 nM dasatinib or 10 nM saracatinib treatment on PBF-repressed RAIU in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. n = 3 for all experiments. Error bars = SEM. * = P < 0.05, ** = P < 0.01, *** = P < 0.001.

    Journal: Endocrine-Related Cancer

    Article Title: Targeting Src tyrosine kinase to enhance radioiodide uptake in breast cancer

    doi: 10.1530/ERC-24-0312

    Figure Lengend Snippet: Src inhibition inhibits PBF phosphorylation and restores RAIU. (A) MCF-7 (i) and MDA-MB-231 (ii) cells were treated with varying doses of PP1 (0–2 μM) for 24 h before PBF-pY174 and total PBF expression levels were determined by Western blot. (B) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. (C) Effect of 2 μM PP1 treatment on PBF-mediated RAIU repression in MCF-7 cells treated with ATRA and dexamethasone. (D) PBF-pY174 and total PBF expression levels following dasatinib dose response (0–2 μM) treatment for 24 h in MCF-7 (i) and MDA-MB-231 (ii) cells. (E) Effect of 1 nM dasatinib or 10 nM saracatinib treatment on PBF-repressed RAIU in MCF-7 (i) and MDA-MB-231 (ii) cells transiently co-transfected with NIS-MYC. n = 3 for all experiments. Error bars = SEM. * = P < 0.05, ** = P < 0.01, *** = P < 0.001.

    Article Snippet: Src family kinase inhibitors PP1 (Tocris, UK), dasatinib and saracatinib (Selleck Chemicals, USA) and NMT inhibitor (DDD85646; Drug Discovery Unit, University of Dundee) were dissolved in DMSO to a 10 mM stock concentration.

    Techniques: Inhibition, Phospho-proteomics, Expressing, Western Blot, Transfection