phospho akt ser473 d9e xp rabbit mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho akt ser473 d9e xp rabbit mab

    Phospho Akt Ser473 D9e Xp 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
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    Images

    1) Product Images from "Glucose starvation causes ferroptosis-mediated lysosomal dysfunction"

    Article Title: Glucose starvation causes ferroptosis-mediated lysosomal dysfunction

    Journal: iScience

    doi: 10.1016/j.isci.2024.109735


    Figure Legend Snippet:

    Techniques Used: Recombinant, Produced, Activity Assay, Modification, Protease Inhibitor, Blocking Assay, Software, Real-time Polymerase Chain Reaction

    phospho akt ser473 d9e xp rabbit mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho akt ser473 d9e xp rabbit mab
    CCL5 activates AR signaling in PCa cells in order to potentiate Enz resistance (A–D) Apoptosis analysis of 22RV1 and C4-2 cells with indicated treatments. 22RV1 and C4-2 cells were stimulated with CCL5 (20 ng/mL or 40 ng/ml) or vehicle (PBS) for 24 h followed by the administration of Enz (10 μM) or DMSO for 24 h ( n = 3). (E and F) Cell survival analysis of 22RV1 and C4-2 cells with indicated treatments. 22RV1 and C4-2 cells were stimulated with CCL5 (20 ng/mL or 40 ng/ml) or the Control (PBS) for 24 h followed by the administration of Enz (10 μM) or DMSO for 24 h ( n = 3). (G and H) Cell survival analysis of 22RV1 and C4-2 cells with indicated treatments. CM from CAFs expressing siNC or siCCL5 (si-1 or si-2) was collected and added to 22RV1 and C4-2 cells for 24 h. 22RV1 and C4-2 cells were treated with Enz (10 μM) after CM addition for 24 h ( n = 3). (I and J) Apoptosis analysis of 22RV1 and C4-2 cells with indicated treatments. CM from CAFs expressing siNC or siCCL5 (si-1 or si-2) was collected and added to 22RV1 and C4-2 cells for 24 h, and 22RV1 and C4-2 cells were treated with Enz (10 μM) for 24 h. n = 3 biologically independent CAFs samples. (K) Cell survival analysis of 22RV1 and C4-2 cells with indicated treatments. CAF-CM was pretreated with the neutralizing anti-CCL5 antibody or IgG for 1 h and then added to 22RV1 and C4-2 cells. 22RV1 and C4-2 cells were treated with Enz (10 μM) for 24 h. n = 3 biologically independent CAFs samples. (L and M) Apoptosis analysis of 22RV1 and C4-2 cells with indicated treatments. CAF-CM was pretreated with the neutralizing anti-CCL5 antibody or IgG for 1 h and then added to 22RV1 and C4-2 cells for 24 h. 22RV1 and C4-2 cells were treated with Enz (10 μM) for 24 h. n = 3 biologically independent CAFs samples. (N and O) Representative western blot image and quantification of AR, AKT, phosphorylated <t>AKT(Ser473)</t> and GAPDH in 22RV1 and C4-2 cells with indicated treatments for 24 h. Data are reported as the mean ± SEM. ns: no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. One-way ANOVA with Tukey’s test for pairwise comparisons for statistical significance analysis in <xref ref-type=Figure 3 B, 3D–3H, 3J, 3K, 3M, and 3O. " width="250" height="auto" />
    Phospho Akt Ser473 D9e Xp 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/result/phospho akt ser473 d9e xp rabbit mab/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    phospho akt ser473 d9e xp rabbit mab - by Bioz Stars, 2024-06
    86/100 stars

    Images

    1) Product Images from "Cancer-associated fibroblasts promote enzalutamide resistance and PD-L1 expression in prostate cancer through CCL5-CCR5 paracrine axis"

    Article Title: Cancer-associated fibroblasts promote enzalutamide resistance and PD-L1 expression in prostate cancer through CCL5-CCR5 paracrine axis

    Journal: iScience

    doi: 10.1016/j.isci.2024.109674

    CCL5 activates AR signaling in PCa cells in order to potentiate Enz resistance (A–D) Apoptosis analysis of 22RV1 and C4-2 cells with indicated treatments. 22RV1 and C4-2 cells were stimulated with CCL5 (20 ng/mL or 40 ng/ml) or vehicle (PBS) for 24 h followed by the administration of Enz (10 μM) or DMSO for 24 h ( n = 3). (E and F) Cell survival analysis of 22RV1 and C4-2 cells with indicated treatments. 22RV1 and C4-2 cells were stimulated with CCL5 (20 ng/mL or 40 ng/ml) or the Control (PBS) for 24 h followed by the administration of Enz (10 μM) or DMSO for 24 h ( n = 3). (G and H) Cell survival analysis of 22RV1 and C4-2 cells with indicated treatments. CM from CAFs expressing siNC or siCCL5 (si-1 or si-2) was collected and added to 22RV1 and C4-2 cells for 24 h. 22RV1 and C4-2 cells were treated with Enz (10 μM) after CM addition for 24 h ( n = 3). (I and J) Apoptosis analysis of 22RV1 and C4-2 cells with indicated treatments. CM from CAFs expressing siNC or siCCL5 (si-1 or si-2) was collected and added to 22RV1 and C4-2 cells for 24 h, and 22RV1 and C4-2 cells were treated with Enz (10 μM) for 24 h. n = 3 biologically independent CAFs samples. (K) Cell survival analysis of 22RV1 and C4-2 cells with indicated treatments. CAF-CM was pretreated with the neutralizing anti-CCL5 antibody or IgG for 1 h and then added to 22RV1 and C4-2 cells. 22RV1 and C4-2 cells were treated with Enz (10 μM) for 24 h. n = 3 biologically independent CAFs samples. (L and M) Apoptosis analysis of 22RV1 and C4-2 cells with indicated treatments. CAF-CM was pretreated with the neutralizing anti-CCL5 antibody or IgG for 1 h and then added to 22RV1 and C4-2 cells for 24 h. 22RV1 and C4-2 cells were treated with Enz (10 μM) for 24 h. n = 3 biologically independent CAFs samples. (N and O) Representative western blot image and quantification of AR, AKT, phosphorylated AKT(Ser473) and GAPDH in 22RV1 and C4-2 cells with indicated treatments for 24 h. Data are reported as the mean ± SEM. ns: no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. One-way ANOVA with Tukey’s test for pairwise comparisons for statistical significance analysis in <xref ref-type=Figure 3 B, 3D–3H, 3J, 3K, 3M, and 3O. " title="... blot image and quantification of AR, AKT, phosphorylated AKT(Ser473) and GAPDH in 22RV1 and C4-2 cells with ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: CCL5 activates AR signaling in PCa cells in order to potentiate Enz resistance (A–D) Apoptosis analysis of 22RV1 and C4-2 cells with indicated treatments. 22RV1 and C4-2 cells were stimulated with CCL5 (20 ng/mL or 40 ng/ml) or vehicle (PBS) for 24 h followed by the administration of Enz (10 μM) or DMSO for 24 h ( n = 3). (E and F) Cell survival analysis of 22RV1 and C4-2 cells with indicated treatments. 22RV1 and C4-2 cells were stimulated with CCL5 (20 ng/mL or 40 ng/ml) or the Control (PBS) for 24 h followed by the administration of Enz (10 μM) or DMSO for 24 h ( n = 3). (G and H) Cell survival analysis of 22RV1 and C4-2 cells with indicated treatments. CM from CAFs expressing siNC or siCCL5 (si-1 or si-2) was collected and added to 22RV1 and C4-2 cells for 24 h. 22RV1 and C4-2 cells were treated with Enz (10 μM) after CM addition for 24 h ( n = 3). (I and J) Apoptosis analysis of 22RV1 and C4-2 cells with indicated treatments. CM from CAFs expressing siNC or siCCL5 (si-1 or si-2) was collected and added to 22RV1 and C4-2 cells for 24 h, and 22RV1 and C4-2 cells were treated with Enz (10 μM) for 24 h. n = 3 biologically independent CAFs samples. (K) Cell survival analysis of 22RV1 and C4-2 cells with indicated treatments. CAF-CM was pretreated with the neutralizing anti-CCL5 antibody or IgG for 1 h and then added to 22RV1 and C4-2 cells. 22RV1 and C4-2 cells were treated with Enz (10 μM) for 24 h. n = 3 biologically independent CAFs samples. (L and M) Apoptosis analysis of 22RV1 and C4-2 cells with indicated treatments. CAF-CM was pretreated with the neutralizing anti-CCL5 antibody or IgG for 1 h and then added to 22RV1 and C4-2 cells for 24 h. 22RV1 and C4-2 cells were treated with Enz (10 μM) for 24 h. n = 3 biologically independent CAFs samples. (N and O) Representative western blot image and quantification of AR, AKT, phosphorylated AKT(Ser473) and GAPDH in 22RV1 and C4-2 cells with indicated treatments for 24 h. Data are reported as the mean ± SEM. ns: no significance, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. One-way ANOVA with Tukey’s test for pairwise comparisons for statistical significance analysis in Figure 3 B, 3D–3H, 3J, 3K, 3M, and 3O.

    Techniques Used: Expressing, Western Blot

    CCL5-CCR5 paracrine signaling activates AKT/AR signaling in PCa cells in order to potentiate Enz resistance (A and B) Correlation analysis of CCL5 level (A) or CCR5 level (B) and PI3K/AKT/mTOR pathway in TCGA database. (C and D) Representative western blot image and quantification of phosphorylated AKT (Ser473), AKT, and AR in 22RV1 and C4-2 cells with indicated treatments. 22RV1 and C4-2 cells were pretreated with MVC (1 μM) or DMSO for 1 h, followed by CAF-CM stimulation for 24 h. Western blot analyses were performed 24 h after Enz (10 μM) treatment. n = 3 biologically independent CAFs samples. (E and F) Representative western blot image and quantification of phosphorylated AKT (Ser473), AKT, and AR in 22RV1 and C4-2 cells with indicated treatments. 22RV1 and C4-2 cells were pretreated with MVC (1 μM) or DMSO for 1 h, followed by CCL5 (20 ng/mL) stimulation for 24 h. Western blot analyses were performed 24 h after Enz (10 μM) treatment ( n = 3). (G and H) Representative western blot image and quantification of phosphorylated AKT (Ser473), AKT, and AR in 22RV1 and C4-2 cells, which were pretreated with the AKT inhibitor (MK-2206 500 nM) for 1 h, and then treated with CCL5 (20 ng/mL) or PBS for 24 h ( n = 3). Data are reported as the Mean ± SEM. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. One-way ANOVA with Tukey’s test for pairwise comparisons for statistical significance analysis in <xref ref-type=Figures 5 D, 5F, and 5H. " title="... western blot image and quantification of phosphorylated AKT (Ser473), AKT, and AR in 22RV1 and C4-2 cells ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: CCL5-CCR5 paracrine signaling activates AKT/AR signaling in PCa cells in order to potentiate Enz resistance (A and B) Correlation analysis of CCL5 level (A) or CCR5 level (B) and PI3K/AKT/mTOR pathway in TCGA database. (C and D) Representative western blot image and quantification of phosphorylated AKT (Ser473), AKT, and AR in 22RV1 and C4-2 cells with indicated treatments. 22RV1 and C4-2 cells were pretreated with MVC (1 μM) or DMSO for 1 h, followed by CAF-CM stimulation for 24 h. Western blot analyses were performed 24 h after Enz (10 μM) treatment. n = 3 biologically independent CAFs samples. (E and F) Representative western blot image and quantification of phosphorylated AKT (Ser473), AKT, and AR in 22RV1 and C4-2 cells with indicated treatments. 22RV1 and C4-2 cells were pretreated with MVC (1 μM) or DMSO for 1 h, followed by CCL5 (20 ng/mL) stimulation for 24 h. Western blot analyses were performed 24 h after Enz (10 μM) treatment ( n = 3). (G and H) Representative western blot image and quantification of phosphorylated AKT (Ser473), AKT, and AR in 22RV1 and C4-2 cells, which were pretreated with the AKT inhibitor (MK-2206 500 nM) for 1 h, and then treated with CCL5 (20 ng/mL) or PBS for 24 h ( n = 3). Data are reported as the Mean ± SEM. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. One-way ANOVA with Tukey’s test for pairwise comparisons for statistical significance analysis in Figures 5 D, 5F, and 5H.

    Techniques Used: Western Blot

    CCL5-CCR5 paracrine signaling activates AKT signaling in PCa cells to induced PD-L1 expression (A) Pearson correlation analysis of CCL5 level and PD-L1 in the TCGA cohort. (B and C) The RT-qPCR analysis showing that CCL5 increased the mRNA expression of PD-L1 in 22RV1 and C4-2 cells ( n = 3). (D and E) Representative western blot image and quantification showing that CCL5 increased the protein level of PD-L1 in 22RV1 and C4-2 cells ( n = 3). (F) Flow cytometric analysis showing that CCL5 increased the mRNA expression of PD-L1 in 22RV1 and C4-2 cells ( n = 3). (G) Pearson correlation analysis of CCR5 level and PD-L1 in TCGA cohort. (H and I) Representative western blot image and quantification of phosphorylated-AKT (Ser473), AKT and PD-L1 in 22RV1 and C4-2 cells pretreated with CCL5 (20 ng/mL) followed by the treatment of the CCR5 inhibitor MVC (1 μM) or AKT inhibitor MK-2206 (500 nM) ( n = 3). (J) Flow cytometric analysis showing that phosphorylated-AKT (Ser473), AKT, and PD-L1 in 22RV1 and C4-2 cells pretreated with CCL5 (20 ng/mL) followed by the treatment of the CCR5 inhibitor MVC (1 μM) or AKT inhibitor MK-2206 (500 nM) ( n = 3). Data are reported as the Mean ± SEM. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. One-way ANOVA with Tukey’s test for pairwise comparisons for statistical significance analysis in <xref ref-type=Figures 7 B–7D and 7I. " title="... Representative western blot image and quantification of phosphorylated-AKT (Ser473), AKT and PD-L1 in 22RV1 and C4-2 cells ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: CCL5-CCR5 paracrine signaling activates AKT signaling in PCa cells to induced PD-L1 expression (A) Pearson correlation analysis of CCL5 level and PD-L1 in the TCGA cohort. (B and C) The RT-qPCR analysis showing that CCL5 increased the mRNA expression of PD-L1 in 22RV1 and C4-2 cells ( n = 3). (D and E) Representative western blot image and quantification showing that CCL5 increased the protein level of PD-L1 in 22RV1 and C4-2 cells ( n = 3). (F) Flow cytometric analysis showing that CCL5 increased the mRNA expression of PD-L1 in 22RV1 and C4-2 cells ( n = 3). (G) Pearson correlation analysis of CCR5 level and PD-L1 in TCGA cohort. (H and I) Representative western blot image and quantification of phosphorylated-AKT (Ser473), AKT and PD-L1 in 22RV1 and C4-2 cells pretreated with CCL5 (20 ng/mL) followed by the treatment of the CCR5 inhibitor MVC (1 μM) or AKT inhibitor MK-2206 (500 nM) ( n = 3). (J) Flow cytometric analysis showing that phosphorylated-AKT (Ser473), AKT, and PD-L1 in 22RV1 and C4-2 cells pretreated with CCL5 (20 ng/mL) followed by the treatment of the CCR5 inhibitor MVC (1 μM) or AKT inhibitor MK-2206 (500 nM) ( n = 3). Data are reported as the Mean ± SEM. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. One-way ANOVA with Tukey’s test for pairwise comparisons for statistical significance analysis in Figures 7 B–7D and 7I.

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot


    Figure Legend Snippet:

    Techniques Used: Activation Assay, Recombinant, Saline, Marker, CCK-8 Assay, Protease Inhibitor, Purification, Lysis, Bicinchoninic Acid Protein Assay, Enzyme-linked Immunosorbent Assay, Sequencing, Software

    phospho akt ser473 d9e xp rabbit mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho akt ser473 d9e xp rabbit mab
    Phospho Akt Ser473 D9e Xp 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
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    Cell Signaling Technology Inc anti phospho akt ser473 d9e xp rabbit mab
    Anti Phospho Akt Ser473 D9e Xp 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
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    anti phospho akt ser473 d9e xp rabbit mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho akt ser473 d9e xp rabbit mab
    Anti Phospho Akt Ser473 D9e Xp 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
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    phospho akt ser473 d9e xp rabbit mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho akt ser473 d9e xp rabbit mab

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    1) Product Images from "Trichinella spiralis inhibits myoblast differentiation by targeting SQSTM1/p62 with a secreted E3 ubiquitin ligase"

    Article Title: Trichinella spiralis inhibits myoblast differentiation by targeting SQSTM1/p62 with a secreted E3 ubiquitin ligase

    Journal: iScience

    doi: 10.1016/j.isci.2024.109102


    Figure Legend Snippet:

    Techniques Used: Recombinant, Conjugation Assay, Transfection, Plasmid Preparation, Software

    phospho-akt (ser473) (d9e) xp (rabbit mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho-akt (ser473) (d9e) xp (rabbit mab
    Phospho Akt (Ser473) (D9e) Xp (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
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    Phospho Akt (Ser473) (D9e) Xp (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
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    Cell Signaling Technology Inc phospho akt ser473 d9e xp rabbit mab
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    Cell Signaling Technology Inc phospho akt ser473 d9e xp rabbit mab
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    Journal: iScience

    Article Title: Glucose starvation causes ferroptosis-mediated lysosomal dysfunction

    doi: 10.1016/j.isci.2024.109735

    Figure Lengend Snippet:

    Article Snippet: Phospho-Akt (Ser473) (D9E) XP Rabbit mAb , Cell Signaling Technology , #4060.

    Techniques: Recombinant, Produced, Activity Assay, Modification, Protease Inhibitor, Blocking Assay, Software, Real-time Polymerase Chain Reaction