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pakt r d systems mab7419 wb mouse  (R&D Systems)


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    Structured Review

    R&D Systems pakt r d systems mab7419 wb mouse
    Pakt R D Systems Mab7419 Wb Mouse, supplied by R&D Systems, used in various techniques. Bioz Stars score: 88/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+anti+human+pakt/Human+Phospho-Akt1+(T308)+Antibody/pmc12453065__iovs-66-12-45_s001-42-121-122
    Average 88 stars, based on 10 article reviews
    pakt r d systems mab7419 wb mouse - by Bioz Stars, 2026-11
    88/100 stars

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    other:

    Article Title: Hyaluronic acid restored protein permeability across injured human lung microvascular endothelial cells.
    Article Snippet: For the primary antibodies, rat anti- human/mouse CD44 (#14- 0441- 85, Thermo Fischer Scientific), rabbit anti- human ZO- 1 (#5406, Cell Signaling Technology), rabbit anti- human VE- cadherin (#2158, Cell Signaling Technology), rabbit anti- human HMGA2 (#5269, Cell Signaling Technology), mouse anti- human pAKT (#MAB887, R&D Systems), mouse anti- human AKT (# MAB2055, R&D Systems), mouse anti- human caspase- 3 (#31A1067, Novus Biologicals, LLC), and mouse antihuman GAPDH (#MAB5718, R&D Systems) were used.



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    The figure illustrates the inhibitory effects of AMD3100 and A1 on CXCL12-induced AKT phosphorylation in CT-26 treated cells. In panel ( A ), representative Western blot images depict the expression of phosphorylated AKT <t>(pAKT)</t> <t>and</t> <t>Actin-β</t> (as a loading control) in cells subjected to 100 ng/mL of CXCL12 alongside increasing concentrations of either AMD3100 or A1 (0, 5, and 10 µM). The treatment with AMD3100 and A1 resulted in a noticeable reduction in pAKT levels compared to the control group. Panels ( B ) and ( C ) quantify the relative pAKT expression normalized to Actin-β for AMD3100 and A1, respectively. In panel ( B ), cells treated with 10 µM AMD3100 exhibited a statistically significant decrease in pAKT levels compared to both the control (***p < 0.001) and the 5 µM groups (**p < 0.01). Conversely, the difference between the control and the 5 µM groups was not statistically significant. In panel (C), A1 treatment demonstrated a significant reduction in pAKT levels in both the 5 µM (****p < 0.0001) and 10 µM (***p < 0.001) groups in comparison to the control, with the 10 µM group exhibiting a further reduction relative to the 5 µM group (****p < 0.0001). Statistical analysis was performed utilizing one-way ANOVA followed by Tukey’s post hoc test, and the data are presented as mean ± SEM from three independent experiments
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    The figure illustrates the inhibitory effects of AMD3100 and A1 on CXCL12-induced AKT phosphorylation in CT-26 treated cells. In panel ( A ), representative Western blot images depict the expression of phosphorylated AKT <t>(pAKT)</t> <t>and</t> <t>Actin-β</t> (as a loading control) in cells subjected to 100 ng/mL of CXCL12 alongside increasing concentrations of either AMD3100 or A1 (0, 5, and 10 µM). The treatment with AMD3100 and A1 resulted in a noticeable reduction in pAKT levels compared to the control group. Panels ( B ) and ( C ) quantify the relative pAKT expression normalized to Actin-β for AMD3100 and A1, respectively. In panel ( B ), cells treated with 10 µM AMD3100 exhibited a statistically significant decrease in pAKT levels compared to both the control (***p < 0.001) and the 5 µM groups (**p < 0.01). Conversely, the difference between the control and the 5 µM groups was not statistically significant. In panel (C), A1 treatment demonstrated a significant reduction in pAKT levels in both the 5 µM (****p < 0.0001) and 10 µM (***p < 0.001) groups in comparison to the control, with the 10 µM group exhibiting a further reduction relative to the 5 µM group (****p < 0.0001). Statistical analysis was performed utilizing one-way ANOVA followed by Tukey’s post hoc test, and the data are presented as mean ± SEM from three independent experiments
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    The figure illustrates the inhibitory effects of AMD3100 and A1 on CXCL12-induced AKT phosphorylation in CT-26 treated cells. In panel ( A ), representative Western blot images depict the expression of phosphorylated AKT <t>(pAKT)</t> <t>and</t> <t>Actin-β</t> (as a loading control) in cells subjected to 100 ng/mL of CXCL12 alongside increasing concentrations of either AMD3100 or A1 (0, 5, and 10 µM). The treatment with AMD3100 and A1 resulted in a noticeable reduction in pAKT levels compared to the control group. Panels ( B ) and ( C ) quantify the relative pAKT expression normalized to Actin-β for AMD3100 and A1, respectively. In panel ( B ), cells treated with 10 µM AMD3100 exhibited a statistically significant decrease in pAKT levels compared to both the control (***p < 0.001) and the 5 µM groups (**p < 0.01). Conversely, the difference between the control and the 5 µM groups was not statistically significant. In panel (C), A1 treatment demonstrated a significant reduction in pAKT levels in both the 5 µM (****p < 0.0001) and 10 µM (***p < 0.001) groups in comparison to the control, with the 10 µM group exhibiting a further reduction relative to the 5 µM group (****p < 0.0001). Statistical analysis was performed utilizing one-way ANOVA followed by Tukey’s post hoc test, and the data are presented as mean ± SEM from three independent experiments
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    The figure illustrates the inhibitory effects of AMD3100 and A1 on CXCL12-induced AKT phosphorylation in CT-26 treated cells. In panel ( A ), representative Western blot images depict the expression of phosphorylated AKT <t>(pAKT)</t> <t>and</t> <t>Actin-β</t> (as a loading control) in cells subjected to 100 ng/mL of CXCL12 alongside increasing concentrations of either AMD3100 or A1 (0, 5, and 10 µM). The treatment with AMD3100 and A1 resulted in a noticeable reduction in pAKT levels compared to the control group. Panels ( B ) and ( C ) quantify the relative pAKT expression normalized to Actin-β for AMD3100 and A1, respectively. In panel ( B ), cells treated with 10 µM AMD3100 exhibited a statistically significant decrease in pAKT levels compared to both the control (***p < 0.001) and the 5 µM groups (**p < 0.01). Conversely, the difference between the control and the 5 µM groups was not statistically significant. In panel (C), A1 treatment demonstrated a significant reduction in pAKT levels in both the 5 µM (****p < 0.0001) and 10 µM (***p < 0.001) groups in comparison to the control, with the 10 µM group exhibiting a further reduction relative to the 5 µM group (****p < 0.0001). Statistical analysis was performed utilizing one-way ANOVA followed by Tukey’s post hoc test, and the data are presented as mean ± SEM from three independent experiments
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    fluidigm anti human mouse pakt
    The figure illustrates the inhibitory effects of AMD3100 and A1 on CXCL12-induced AKT phosphorylation in CT-26 treated cells. In panel ( A ), representative Western blot images depict the expression of phosphorylated AKT <t>(pAKT)</t> <t>and</t> <t>Actin-β</t> (as a loading control) in cells subjected to 100 ng/mL of CXCL12 alongside increasing concentrations of either AMD3100 or A1 (0, 5, and 10 µM). The treatment with AMD3100 and A1 resulted in a noticeable reduction in pAKT levels compared to the control group. Panels ( B ) and ( C ) quantify the relative pAKT expression normalized to Actin-β for AMD3100 and A1, respectively. In panel ( B ), cells treated with 10 µM AMD3100 exhibited a statistically significant decrease in pAKT levels compared to both the control (***p < 0.001) and the 5 µM groups (**p < 0.01). Conversely, the difference between the control and the 5 µM groups was not statistically significant. In panel (C), A1 treatment demonstrated a significant reduction in pAKT levels in both the 5 µM (****p < 0.0001) and 10 µM (***p < 0.001) groups in comparison to the control, with the 10 µM group exhibiting a further reduction relative to the 5 µM group (****p < 0.0001). Statistical analysis was performed utilizing one-way ANOVA followed by Tukey’s post hoc test, and the data are presented as mean ± SEM from three independent experiments
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    Cell Signaling Technology Inc anti human mouse pakt t308 clone d25e6

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    Image Search Results


    The figure illustrates the inhibitory effects of AMD3100 and A1 on CXCL12-induced AKT phosphorylation in CT-26 treated cells. In panel ( A ), representative Western blot images depict the expression of phosphorylated AKT (pAKT) and Actin-β (as a loading control) in cells subjected to 100 ng/mL of CXCL12 alongside increasing concentrations of either AMD3100 or A1 (0, 5, and 10 µM). The treatment with AMD3100 and A1 resulted in a noticeable reduction in pAKT levels compared to the control group. Panels ( B ) and ( C ) quantify the relative pAKT expression normalized to Actin-β for AMD3100 and A1, respectively. In panel ( B ), cells treated with 10 µM AMD3100 exhibited a statistically significant decrease in pAKT levels compared to both the control (***p < 0.001) and the 5 µM groups (**p < 0.01). Conversely, the difference between the control and the 5 µM groups was not statistically significant. In panel (C), A1 treatment demonstrated a significant reduction in pAKT levels in both the 5 µM (****p < 0.0001) and 10 µM (***p < 0.001) groups in comparison to the control, with the 10 µM group exhibiting a further reduction relative to the 5 µM group (****p < 0.0001). Statistical analysis was performed utilizing one-way ANOVA followed by Tukey’s post hoc test, and the data are presented as mean ± SEM from three independent experiments

    Journal: Cancer Cell International

    Article Title: A1, an innovative fluorinated CXCR4 inhibitor, redefines the therapeutic landscape in colorectal cancer

    doi: 10.1186/s12935-024-03584-y

    Figure Lengend Snippet: The figure illustrates the inhibitory effects of AMD3100 and A1 on CXCL12-induced AKT phosphorylation in CT-26 treated cells. In panel ( A ), representative Western blot images depict the expression of phosphorylated AKT (pAKT) and Actin-β (as a loading control) in cells subjected to 100 ng/mL of CXCL12 alongside increasing concentrations of either AMD3100 or A1 (0, 5, and 10 µM). The treatment with AMD3100 and A1 resulted in a noticeable reduction in pAKT levels compared to the control group. Panels ( B ) and ( C ) quantify the relative pAKT expression normalized to Actin-β for AMD3100 and A1, respectively. In panel ( B ), cells treated with 10 µM AMD3100 exhibited a statistically significant decrease in pAKT levels compared to both the control (***p < 0.001) and the 5 µM groups (**p < 0.01). Conversely, the difference between the control and the 5 µM groups was not statistically significant. In panel (C), A1 treatment demonstrated a significant reduction in pAKT levels in both the 5 µM (****p < 0.0001) and 10 µM (***p < 0.001) groups in comparison to the control, with the 10 µM group exhibiting a further reduction relative to the 5 µM group (****p < 0.0001). Statistical analysis was performed utilizing one-way ANOVA followed by Tukey’s post hoc test, and the data are presented as mean ± SEM from three independent experiments

    Article Snippet: Subsequently, proteins were separated by SDS-PAGE electrophoresis, transferred onto membranes, and immunoblotted with mouse anti-pAKT antibodies (R&D System, MAB887-SP) along with anti-actin β antibodies (R&D System, MAB8929-SP) for normalization.

    Techniques: Phospho-proteomics, Western Blot, Expressing, Control, Comparison

    Journal: Cancer Cell

    Article Title: Single-cell analysis defines a pancreatic fibroblast lineage that supports anti-tumor immunity

    doi: 10.1016/j.ccell.2021.06.017

    Figure Lengend Snippet:

    Article Snippet: Anti-human/mouse pAKT [T308] clone D25E6 , Cell Signaling Technology , 13038.

    Techniques: Blocking Assay, Virus, Recombinant, Plasmid Preparation, Saline, Lysis, Staining, Reverse Transcription, In Vivo, Electroporation, Mass Cytometry, Conjugation Assay, Illumina Sequencing, Library Quantification, In Vitro, Quantitative RT-PCR, Software, Real-time Polymerase Chain Reaction, Cytometry, Microscopy, Imaging, Spectrophotometry