akt2 levels  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc akt2 levels
    Akt2 Levels, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    akt2 levels  (Thermo Fisher)


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    Thermo Fisher akt2 levels
    Akt2 Levels, supplied by Thermo Fisher, 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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    Average 86 stars, based on 1 article reviews
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    86/100 stars

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    akt2 levels  (Thermo Fisher)


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    Thermo Fisher akt2 levels
    ( A ) Schematic indicating the experimental setup to potentiate insulin response in functional assays. hPSCs are differentiated into adipocytes using a published protocol, after which an additional step was added and optimized to sensitize adipocytes. ( B and C ) Phosphorylation of <t>AKT2</t> normalized to total AKT2 (B) and glucose uptake (C) after 100 nM insulin stimulation measured for all the medium compositions from our DoE model and the medium from a previously published protocol. RLU, relative light unit. ( D and E ) The parameter coefficient of each factor in our DoE model indicating its contribution to the AKT2 phosphorylation (D) and glucose uptake (E). ( F ) Time course of sensitization with the DoE-optimized media measuring glucose uptake at baseline and after insulin stimulation. Results are normalized to total protein for each sample. All bar graphs depict the mean with error bars representing SD, n = 2 biological replicates. OD 450 , optical density at 450 nm.
    Akt2 Levels, supplied by Thermo Fisher, 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/akt2 levels/product/Thermo Fisher
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    akt2 levels - by Bioz Stars, 2024-09
    86/100 stars

    Images

    1) Product Images from "Development of a physiological insulin resistance model in human stem cell–derived adipocytes"

    Article Title: Development of a physiological insulin resistance model in human stem cell–derived adipocytes

    Journal: Science Advances

    doi: 10.1126/sciadv.abn7298

    ( A ) Schematic indicating the experimental setup to potentiate insulin response in functional assays. hPSCs are differentiated into adipocytes using a published protocol, after which an additional step was added and optimized to sensitize adipocytes. ( B and C ) Phosphorylation of AKT2 normalized to total AKT2 (B) and glucose uptake (C) after 100 nM insulin stimulation measured for all the medium compositions from our DoE model and the medium from a previously published protocol. RLU, relative light unit. ( D and E ) The parameter coefficient of each factor in our DoE model indicating its contribution to the AKT2 phosphorylation (D) and glucose uptake (E). ( F ) Time course of sensitization with the DoE-optimized media measuring glucose uptake at baseline and after insulin stimulation. Results are normalized to total protein for each sample. All bar graphs depict the mean with error bars representing SD, n = 2 biological replicates. OD 450 , optical density at 450 nm.
    Figure Legend Snippet: ( A ) Schematic indicating the experimental setup to potentiate insulin response in functional assays. hPSCs are differentiated into adipocytes using a published protocol, after which an additional step was added and optimized to sensitize adipocytes. ( B and C ) Phosphorylation of AKT2 normalized to total AKT2 (B) and glucose uptake (C) after 100 nM insulin stimulation measured for all the medium compositions from our DoE model and the medium from a previously published protocol. RLU, relative light unit. ( D and E ) The parameter coefficient of each factor in our DoE model indicating its contribution to the AKT2 phosphorylation (D) and glucose uptake (E). ( F ) Time course of sensitization with the DoE-optimized media measuring glucose uptake at baseline and after insulin stimulation. Results are normalized to total protein for each sample. All bar graphs depict the mean with error bars representing SD, n = 2 biological replicates. OD 450 , optical density at 450 nm.

    Techniques Used: Functional Assay

    ( A ) Schematic indicating the experimental setup to measure insulin dose-response and induction of insulin resistance. ( B ) Insulin dose-response curve showing fold change in AKT2 phosphorylation compared to the unstimulated state. ( C ) Representative images of GLUT4 translocation to the cell membrane upon insulin stimulation. ( D ) TIRF measurement of GLUT4 signal intensity at the adipocyte cell membrane (** P < 0.01, unpaired two-tailed t test). ( E ) Insulin dose-response curve showing AKT2 phosphorylation fold change in three insulin preexposure conditions. Results are normalized to total AKT2 and plotted as fold change to unstimulated cells in that condition. ( F ) Insulin dose-response curve showing glucose uptake for sensitized and hyperinsulinemia-exposed adipocytes. Results are normalized to total protein content and plotted as fold change to unstimulated cells. ( G ) Glycerol release into the medium for published, sensitized, and hyperinsulinemia-exposed adipocytes showing basal or insulin-suppressed lipolysis, normalized to total protein. Bar graphs depict the mean with error bars representing SD, dose-response curves depict a nonlinear fit curve with error bars representing SD, and the scatterplot depicts individual cell values with mean and 95% confidence interval (CI) overlaid; n = 3 biological replicates unless otherwise indicated.
    Figure Legend Snippet: ( A ) Schematic indicating the experimental setup to measure insulin dose-response and induction of insulin resistance. ( B ) Insulin dose-response curve showing fold change in AKT2 phosphorylation compared to the unstimulated state. ( C ) Representative images of GLUT4 translocation to the cell membrane upon insulin stimulation. ( D ) TIRF measurement of GLUT4 signal intensity at the adipocyte cell membrane (** P < 0.01, unpaired two-tailed t test). ( E ) Insulin dose-response curve showing AKT2 phosphorylation fold change in three insulin preexposure conditions. Results are normalized to total AKT2 and plotted as fold change to unstimulated cells in that condition. ( F ) Insulin dose-response curve showing glucose uptake for sensitized and hyperinsulinemia-exposed adipocytes. Results are normalized to total protein content and plotted as fold change to unstimulated cells. ( G ) Glycerol release into the medium for published, sensitized, and hyperinsulinemia-exposed adipocytes showing basal or insulin-suppressed lipolysis, normalized to total protein. Bar graphs depict the mean with error bars representing SD, dose-response curves depict a nonlinear fit curve with error bars representing SD, and the scatterplot depicts individual cell values with mean and 95% confidence interval (CI) overlaid; n = 3 biological replicates unless otherwise indicated.

    Techniques Used: Translocation Assay, Two Tailed Test

    ( A ) Phosphorylated AKT2 measurements as a fraction of total AKT2 normalized to total protein per well for brown hPSC adipocytes, mouse 3T3-L1 differentiated adipocytes, and primary human SVF adipocytes. ( B ) Glucose uptake measurements normalized to total protein per well and displayed as fold change in glucose uptake versus the unstimulated condition for brown hPSC adipocytes, mouse 3T3-L1 differentiated adipocytes, and primary human SVF adipocytes. All bar graphs depict the mean with error bars representing SD, n = 4 biological replicates.
    Figure Legend Snippet: ( A ) Phosphorylated AKT2 measurements as a fraction of total AKT2 normalized to total protein per well for brown hPSC adipocytes, mouse 3T3-L1 differentiated adipocytes, and primary human SVF adipocytes. ( B ) Glucose uptake measurements normalized to total protein per well and displayed as fold change in glucose uptake versus the unstimulated condition for brown hPSC adipocytes, mouse 3T3-L1 differentiated adipocytes, and primary human SVF adipocytes. All bar graphs depict the mean with error bars representing SD, n = 4 biological replicates.

    Techniques Used:

    akt2 levels  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Cell Signaling Technology Inc akt2 levels
    ( A ) Schematic indicating the experimental setup to potentiate insulin response in functional assays. hPSCs are differentiated into adipocytes using a published protocol, after which an additional step was added and optimized to sensitize adipocytes. ( B and C ) Phosphorylation of <t>AKT2</t> normalized to total AKT2 (B) and glucose uptake (C) after 100 nM insulin stimulation measured for all the medium compositions from our DoE model and the medium from a previously published protocol. RLU, relative light unit. ( D and E ) The parameter coefficient of each factor in our DoE model indicating its contribution to the AKT2 phosphorylation (D) and glucose uptake (E). ( F ) Time course of sensitization with the DoE-optimized media measuring glucose uptake at baseline and after insulin stimulation. Results are normalized to total protein for each sample. All bar graphs depict the mean with error bars representing SD, n = 2 biological replicates. OD 450 , optical density at 450 nm.
    Akt2 Levels, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/akt2 levels/product/Cell Signaling Technology Inc
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    akt2 levels - by Bioz Stars, 2024-09
    93/100 stars

    Images

    1) Product Images from "Development of a physiological insulin resistance model in human stem cell–derived adipocytes"

    Article Title: Development of a physiological insulin resistance model in human stem cell–derived adipocytes

    Journal: Science Advances

    doi: 10.1126/sciadv.abn7298

    ( A ) Schematic indicating the experimental setup to potentiate insulin response in functional assays. hPSCs are differentiated into adipocytes using a published protocol, after which an additional step was added and optimized to sensitize adipocytes. ( B and C ) Phosphorylation of AKT2 normalized to total AKT2 (B) and glucose uptake (C) after 100 nM insulin stimulation measured for all the medium compositions from our DoE model and the medium from a previously published protocol. RLU, relative light unit. ( D and E ) The parameter coefficient of each factor in our DoE model indicating its contribution to the AKT2 phosphorylation (D) and glucose uptake (E). ( F ) Time course of sensitization with the DoE-optimized media measuring glucose uptake at baseline and after insulin stimulation. Results are normalized to total protein for each sample. All bar graphs depict the mean with error bars representing SD, n = 2 biological replicates. OD 450 , optical density at 450 nm.
    Figure Legend Snippet: ( A ) Schematic indicating the experimental setup to potentiate insulin response in functional assays. hPSCs are differentiated into adipocytes using a published protocol, after which an additional step was added and optimized to sensitize adipocytes. ( B and C ) Phosphorylation of AKT2 normalized to total AKT2 (B) and glucose uptake (C) after 100 nM insulin stimulation measured for all the medium compositions from our DoE model and the medium from a previously published protocol. RLU, relative light unit. ( D and E ) The parameter coefficient of each factor in our DoE model indicating its contribution to the AKT2 phosphorylation (D) and glucose uptake (E). ( F ) Time course of sensitization with the DoE-optimized media measuring glucose uptake at baseline and after insulin stimulation. Results are normalized to total protein for each sample. All bar graphs depict the mean with error bars representing SD, n = 2 biological replicates. OD 450 , optical density at 450 nm.

    Techniques Used: Functional Assay

    ( A ) Schematic indicating the experimental setup to measure insulin dose-response and induction of insulin resistance. ( B ) Insulin dose-response curve showing fold change in AKT2 phosphorylation compared to the unstimulated state. ( C ) Representative images of GLUT4 translocation to the cell membrane upon insulin stimulation. ( D ) TIRF measurement of GLUT4 signal intensity at the adipocyte cell membrane (** P < 0.01, unpaired two-tailed t test). ( E ) Insulin dose-response curve showing AKT2 phosphorylation fold change in three insulin preexposure conditions. Results are normalized to total AKT2 and plotted as fold change to unstimulated cells in that condition. ( F ) Insulin dose-response curve showing glucose uptake for sensitized and hyperinsulinemia-exposed adipocytes. Results are normalized to total protein content and plotted as fold change to unstimulated cells. ( G ) Glycerol release into the medium for published, sensitized, and hyperinsulinemia-exposed adipocytes showing basal or insulin-suppressed lipolysis, normalized to total protein. Bar graphs depict the mean with error bars representing SD, dose-response curves depict a nonlinear fit curve with error bars representing SD, and the scatterplot depicts individual cell values with mean and 95% confidence interval (CI) overlaid; n = 3 biological replicates unless otherwise indicated.
    Figure Legend Snippet: ( A ) Schematic indicating the experimental setup to measure insulin dose-response and induction of insulin resistance. ( B ) Insulin dose-response curve showing fold change in AKT2 phosphorylation compared to the unstimulated state. ( C ) Representative images of GLUT4 translocation to the cell membrane upon insulin stimulation. ( D ) TIRF measurement of GLUT4 signal intensity at the adipocyte cell membrane (** P < 0.01, unpaired two-tailed t test). ( E ) Insulin dose-response curve showing AKT2 phosphorylation fold change in three insulin preexposure conditions. Results are normalized to total AKT2 and plotted as fold change to unstimulated cells in that condition. ( F ) Insulin dose-response curve showing glucose uptake for sensitized and hyperinsulinemia-exposed adipocytes. Results are normalized to total protein content and plotted as fold change to unstimulated cells. ( G ) Glycerol release into the medium for published, sensitized, and hyperinsulinemia-exposed adipocytes showing basal or insulin-suppressed lipolysis, normalized to total protein. Bar graphs depict the mean with error bars representing SD, dose-response curves depict a nonlinear fit curve with error bars representing SD, and the scatterplot depicts individual cell values with mean and 95% confidence interval (CI) overlaid; n = 3 biological replicates unless otherwise indicated.

    Techniques Used: Translocation Assay, Two Tailed Test

    ( A ) Phosphorylated AKT2 measurements as a fraction of total AKT2 normalized to total protein per well for brown hPSC adipocytes, mouse 3T3-L1 differentiated adipocytes, and primary human SVF adipocytes. ( B ) Glucose uptake measurements normalized to total protein per well and displayed as fold change in glucose uptake versus the unstimulated condition for brown hPSC adipocytes, mouse 3T3-L1 differentiated adipocytes, and primary human SVF adipocytes. All bar graphs depict the mean with error bars representing SD, n = 4 biological replicates.
    Figure Legend Snippet: ( A ) Phosphorylated AKT2 measurements as a fraction of total AKT2 normalized to total protein per well for brown hPSC adipocytes, mouse 3T3-L1 differentiated adipocytes, and primary human SVF adipocytes. ( B ) Glucose uptake measurements normalized to total protein per well and displayed as fold change in glucose uptake versus the unstimulated condition for brown hPSC adipocytes, mouse 3T3-L1 differentiated adipocytes, and primary human SVF adipocytes. All bar graphs depict the mean with error bars representing SD, n = 4 biological replicates.

    Techniques Used:

    akt2 levels  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Cell Signaling Technology Inc akt2 levels
    Generation of an insulin-sensitive human adipocyte model. A, Schematic indicating the experimental setup to potentiate insulin response in functional assays. hPSCs are differentiated into adipocytes using a published protocol, after which an additional step was added and optimized to sensitize adipocytes. B-C, Phosphorylation of <t>AKT2</t> normalized to total AKT2 (B) and glucose uptake (C) after 100nM insulin stimulation measured for all the medium compositions from our DoE model and the medium from a previously published protocol. D-E, The parameter coefficient of each factor in our DoE model indicating its contribution to the AKT2 phosphorylation (D) and glucose uptake (E). F, Timecourse of sensitization with the DoE-optimized media measuring glucose uptake at baseline and after insulin stimulation. Results are normalized to total protein for each sample. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates.
    Akt2 Levels, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/akt2 levels/product/Cell Signaling Technology Inc
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    akt2 levels - by Bioz Stars, 2024-09
    93/100 stars

    Images

    1) Product Images from "Development of a physiological insulin resistance model in human stem cell-derived adipocytes"

    Article Title: Development of a physiological insulin resistance model in human stem cell-derived adipocytes

    Journal: bioRxiv

    doi: 10.1101/2022.02.22.481495

    Generation of an insulin-sensitive human adipocyte model. A, Schematic indicating the experimental setup to potentiate insulin response in functional assays. hPSCs are differentiated into adipocytes using a published protocol, after which an additional step was added and optimized to sensitize adipocytes. B-C, Phosphorylation of AKT2 normalized to total AKT2 (B) and glucose uptake (C) after 100nM insulin stimulation measured for all the medium compositions from our DoE model and the medium from a previously published protocol. D-E, The parameter coefficient of each factor in our DoE model indicating its contribution to the AKT2 phosphorylation (D) and glucose uptake (E). F, Timecourse of sensitization with the DoE-optimized media measuring glucose uptake at baseline and after insulin stimulation. Results are normalized to total protein for each sample. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates.
    Figure Legend Snippet: Generation of an insulin-sensitive human adipocyte model. A, Schematic indicating the experimental setup to potentiate insulin response in functional assays. hPSCs are differentiated into adipocytes using a published protocol, after which an additional step was added and optimized to sensitize adipocytes. B-C, Phosphorylation of AKT2 normalized to total AKT2 (B) and glucose uptake (C) after 100nM insulin stimulation measured for all the medium compositions from our DoE model and the medium from a previously published protocol. D-E, The parameter coefficient of each factor in our DoE model indicating its contribution to the AKT2 phosphorylation (D) and glucose uptake (E). F, Timecourse of sensitization with the DoE-optimized media measuring glucose uptake at baseline and after insulin stimulation. Results are normalized to total protein for each sample. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates.

    Techniques Used: Functional Assay

    A, Total protein content of samples used in the DoE screen and the published protocol medium. B, Total AKT2 ELISA measurement of samples in the DoE screen. C, Profile curves for each factor illustrating the influence on glucose uptake and phosphorylation of AKT2 throughout the experimental space of the DoE. D, t-Ratio p-values indicating the significance of each factor in the DoE screen for phosphorylated AKT2 (left) and glucose uptake (right). E, Timecourse of sensitization with the DoE-optimized media measuring phosphorylation of AKT2 at baseline and after insulin stimulation. Results are normalized to total AKT2 for each sample. F, Total protein content of each sample during the glucose uptake timecourse . G, Total protein content of each sample during the AKT2 timecourse . H, Quantification of adipocyte marker CEBPA-positive nuclei per area in published and sensitized-protocol adipocytes. I, Triglyceride content per sample of published and sensitized adipocytes in several cell lines. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates for A-G, n=3 for H,I.
    Figure Legend Snippet: A, Total protein content of samples used in the DoE screen and the published protocol medium. B, Total AKT2 ELISA measurement of samples in the DoE screen. C, Profile curves for each factor illustrating the influence on glucose uptake and phosphorylation of AKT2 throughout the experimental space of the DoE. D, t-Ratio p-values indicating the significance of each factor in the DoE screen for phosphorylated AKT2 (left) and glucose uptake (right). E, Timecourse of sensitization with the DoE-optimized media measuring phosphorylation of AKT2 at baseline and after insulin stimulation. Results are normalized to total AKT2 for each sample. F, Total protein content of each sample during the glucose uptake timecourse . G, Total protein content of each sample during the AKT2 timecourse . H, Quantification of adipocyte marker CEBPA-positive nuclei per area in published and sensitized-protocol adipocytes. I, Triglyceride content per sample of published and sensitized adipocytes in several cell lines. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates for A-G, n=3 for H,I.

    Techniques Used: Enzyme-linked Immunosorbent Assay, Marker

    Physiological insulin levels induce insulin response and resistance. A, Schematic indicating the experimental setup to measure insulin dose-response and induction of insulin resistance. B, Insulin dose-response curve showing fold change in AKT2 phosphorylation compared to the unstimulated state. C, Representative images of GLUT4 translocation to the cell membrane upon insulin stimulation. D, TIRF measurement of GLUT4 signal intensity at the adipocyte cell membrane (**=p<0.01, unpaired two-tailed T-test). E, AKT2 phosphorylation in basal and insulin-stimulated state after increasing exposure to higher insulin levels during the sensitization period. Results are normalized to total AKT2 and plotted as fold change compared to the sensitized basal state. F, Insulin dose-response curve showing AKT2 phosphorylation fold change in three insulin pre-exposure conditions. Results are normalized to total AKT2 and plotted as fold change to unstimulated cells in that condition. G, Insulin dose-response curve showing glucose uptake for sensitized and hyperinsulinemia-exposed adipocytes. Results are normalized to total protein content and plotted as fold change to unstimulated cells. Bar graphs depict the mean with error bars representing s.d., dose-response curves depict a nonlinear fit curve with error bars representing s.d., scatterplot depicts individual cell values with mean and 95% CI overlaid, n=3 biological replicates unless otherwise indicated.
    Figure Legend Snippet: Physiological insulin levels induce insulin response and resistance. A, Schematic indicating the experimental setup to measure insulin dose-response and induction of insulin resistance. B, Insulin dose-response curve showing fold change in AKT2 phosphorylation compared to the unstimulated state. C, Representative images of GLUT4 translocation to the cell membrane upon insulin stimulation. D, TIRF measurement of GLUT4 signal intensity at the adipocyte cell membrane (**=p<0.01, unpaired two-tailed T-test). E, AKT2 phosphorylation in basal and insulin-stimulated state after increasing exposure to higher insulin levels during the sensitization period. Results are normalized to total AKT2 and plotted as fold change compared to the sensitized basal state. F, Insulin dose-response curve showing AKT2 phosphorylation fold change in three insulin pre-exposure conditions. Results are normalized to total AKT2 and plotted as fold change to unstimulated cells in that condition. G, Insulin dose-response curve showing glucose uptake for sensitized and hyperinsulinemia-exposed adipocytes. Results are normalized to total protein content and plotted as fold change to unstimulated cells. Bar graphs depict the mean with error bars representing s.d., dose-response curves depict a nonlinear fit curve with error bars representing s.d., scatterplot depicts individual cell values with mean and 95% CI overlaid, n=3 biological replicates unless otherwise indicated.

    Techniques Used: Translocation Assay, Two Tailed Test

    A, Representive images of the TIRF quantification in . For each condition, the three cells closest to the mean are shown. B, Full panel of pre-treatment insulin exposure concentrations and acute stimulation dose-response measuring phosphorylated AKT2 normalized to total AKT2, related to . C, As in B but measuring glucose uptake normalized to total protein, related to . D, Phosphorylated AKT2 measurements normalized to total AKT2 for 3 additional hPSC lines. E, As in D but measuring glucose uptake normalized to total protein. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates for B,C, n=3 for D,E.
    Figure Legend Snippet: A, Representive images of the TIRF quantification in . For each condition, the three cells closest to the mean are shown. B, Full panel of pre-treatment insulin exposure concentrations and acute stimulation dose-response measuring phosphorylated AKT2 normalized to total AKT2, related to . C, As in B but measuring glucose uptake normalized to total protein, related to . D, Phosphorylated AKT2 measurements normalized to total AKT2 for 3 additional hPSC lines. E, As in D but measuring glucose uptake normalized to total protein. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates for B,C, n=3 for D,E.

    Techniques Used:

    akt2 levels  (Thermo Fisher)


    Bioz Verified Symbol Thermo Fisher is a verified supplier
    Bioz Manufacturer Symbol Thermo Fisher manufactures this product  
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    Thermo Fisher akt2 levels
    Generation of an insulin-sensitive human adipocyte model. A, Schematic indicating the experimental setup to potentiate insulin response in functional assays. hPSCs are differentiated into adipocytes using a published protocol, after which an additional step was added and optimized to sensitize adipocytes. B-C, Phosphorylation of <t>AKT2</t> normalized to total AKT2 (B) and glucose uptake (C) after 100nM insulin stimulation measured for all the medium compositions from our DoE model and the medium from a previously published protocol. D-E, The parameter coefficient of each factor in our DoE model indicating its contribution to the AKT2 phosphorylation (D) and glucose uptake (E). F, Timecourse of sensitization with the DoE-optimized media measuring glucose uptake at baseline and after insulin stimulation. Results are normalized to total protein for each sample. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates.
    Akt2 Levels, supplied by Thermo Fisher, 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/akt2 levels/product/Thermo Fisher
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    akt2 levels - by Bioz Stars, 2024-09
    86/100 stars

    Images

    1) Product Images from "Development of a physiological insulin resistance model in human stem cell-derived adipocytes"

    Article Title: Development of a physiological insulin resistance model in human stem cell-derived adipocytes

    Journal: bioRxiv

    doi: 10.1101/2022.02.22.481495

    Generation of an insulin-sensitive human adipocyte model. A, Schematic indicating the experimental setup to potentiate insulin response in functional assays. hPSCs are differentiated into adipocytes using a published protocol, after which an additional step was added and optimized to sensitize adipocytes. B-C, Phosphorylation of AKT2 normalized to total AKT2 (B) and glucose uptake (C) after 100nM insulin stimulation measured for all the medium compositions from our DoE model and the medium from a previously published protocol. D-E, The parameter coefficient of each factor in our DoE model indicating its contribution to the AKT2 phosphorylation (D) and glucose uptake (E). F, Timecourse of sensitization with the DoE-optimized media measuring glucose uptake at baseline and after insulin stimulation. Results are normalized to total protein for each sample. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates.
    Figure Legend Snippet: Generation of an insulin-sensitive human adipocyte model. A, Schematic indicating the experimental setup to potentiate insulin response in functional assays. hPSCs are differentiated into adipocytes using a published protocol, after which an additional step was added and optimized to sensitize adipocytes. B-C, Phosphorylation of AKT2 normalized to total AKT2 (B) and glucose uptake (C) after 100nM insulin stimulation measured for all the medium compositions from our DoE model and the medium from a previously published protocol. D-E, The parameter coefficient of each factor in our DoE model indicating its contribution to the AKT2 phosphorylation (D) and glucose uptake (E). F, Timecourse of sensitization with the DoE-optimized media measuring glucose uptake at baseline and after insulin stimulation. Results are normalized to total protein for each sample. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates.

    Techniques Used: Functional Assay

    A, Total protein content of samples used in the DoE screen and the published protocol medium. B, Total AKT2 ELISA measurement of samples in the DoE screen. C, Profile curves for each factor illustrating the influence on glucose uptake and phosphorylation of AKT2 throughout the experimental space of the DoE. D, t-Ratio p-values indicating the significance of each factor in the DoE screen for phosphorylated AKT2 (left) and glucose uptake (right). E, Timecourse of sensitization with the DoE-optimized media measuring phosphorylation of AKT2 at baseline and after insulin stimulation. Results are normalized to total AKT2 for each sample. F, Total protein content of each sample during the glucose uptake timecourse . G, Total protein content of each sample during the AKT2 timecourse . H, Quantification of adipocyte marker CEBPA-positive nuclei per area in published and sensitized-protocol adipocytes. I, Triglyceride content per sample of published and sensitized adipocytes in several cell lines. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates for A-G, n=3 for H,I.
    Figure Legend Snippet: A, Total protein content of samples used in the DoE screen and the published protocol medium. B, Total AKT2 ELISA measurement of samples in the DoE screen. C, Profile curves for each factor illustrating the influence on glucose uptake and phosphorylation of AKT2 throughout the experimental space of the DoE. D, t-Ratio p-values indicating the significance of each factor in the DoE screen for phosphorylated AKT2 (left) and glucose uptake (right). E, Timecourse of sensitization with the DoE-optimized media measuring phosphorylation of AKT2 at baseline and after insulin stimulation. Results are normalized to total AKT2 for each sample. F, Total protein content of each sample during the glucose uptake timecourse . G, Total protein content of each sample during the AKT2 timecourse . H, Quantification of adipocyte marker CEBPA-positive nuclei per area in published and sensitized-protocol adipocytes. I, Triglyceride content per sample of published and sensitized adipocytes in several cell lines. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates for A-G, n=3 for H,I.

    Techniques Used: Enzyme-linked Immunosorbent Assay, Marker

    Physiological insulin levels induce insulin response and resistance. A, Schematic indicating the experimental setup to measure insulin dose-response and induction of insulin resistance. B, Insulin dose-response curve showing fold change in AKT2 phosphorylation compared to the unstimulated state. C, Representative images of GLUT4 translocation to the cell membrane upon insulin stimulation. D, TIRF measurement of GLUT4 signal intensity at the adipocyte cell membrane (**=p<0.01, unpaired two-tailed T-test). E, AKT2 phosphorylation in basal and insulin-stimulated state after increasing exposure to higher insulin levels during the sensitization period. Results are normalized to total AKT2 and plotted as fold change compared to the sensitized basal state. F, Insulin dose-response curve showing AKT2 phosphorylation fold change in three insulin pre-exposure conditions. Results are normalized to total AKT2 and plotted as fold change to unstimulated cells in that condition. G, Insulin dose-response curve showing glucose uptake for sensitized and hyperinsulinemia-exposed adipocytes. Results are normalized to total protein content and plotted as fold change to unstimulated cells. Bar graphs depict the mean with error bars representing s.d., dose-response curves depict a nonlinear fit curve with error bars representing s.d., scatterplot depicts individual cell values with mean and 95% CI overlaid, n=3 biological replicates unless otherwise indicated.
    Figure Legend Snippet: Physiological insulin levels induce insulin response and resistance. A, Schematic indicating the experimental setup to measure insulin dose-response and induction of insulin resistance. B, Insulin dose-response curve showing fold change in AKT2 phosphorylation compared to the unstimulated state. C, Representative images of GLUT4 translocation to the cell membrane upon insulin stimulation. D, TIRF measurement of GLUT4 signal intensity at the adipocyte cell membrane (**=p<0.01, unpaired two-tailed T-test). E, AKT2 phosphorylation in basal and insulin-stimulated state after increasing exposure to higher insulin levels during the sensitization period. Results are normalized to total AKT2 and plotted as fold change compared to the sensitized basal state. F, Insulin dose-response curve showing AKT2 phosphorylation fold change in three insulin pre-exposure conditions. Results are normalized to total AKT2 and plotted as fold change to unstimulated cells in that condition. G, Insulin dose-response curve showing glucose uptake for sensitized and hyperinsulinemia-exposed adipocytes. Results are normalized to total protein content and plotted as fold change to unstimulated cells. Bar graphs depict the mean with error bars representing s.d., dose-response curves depict a nonlinear fit curve with error bars representing s.d., scatterplot depicts individual cell values with mean and 95% CI overlaid, n=3 biological replicates unless otherwise indicated.

    Techniques Used: Translocation Assay, Two Tailed Test

    A, Representive images of the TIRF quantification in . For each condition, the three cells closest to the mean are shown. B, Full panel of pre-treatment insulin exposure concentrations and acute stimulation dose-response measuring phosphorylated AKT2 normalized to total AKT2, related to . C, As in B but measuring glucose uptake normalized to total protein, related to . D, Phosphorylated AKT2 measurements normalized to total AKT2 for 3 additional hPSC lines. E, As in D but measuring glucose uptake normalized to total protein. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates for B,C, n=3 for D,E.
    Figure Legend Snippet: A, Representive images of the TIRF quantification in . For each condition, the three cells closest to the mean are shown. B, Full panel of pre-treatment insulin exposure concentrations and acute stimulation dose-response measuring phosphorylated AKT2 normalized to total AKT2, related to . C, As in B but measuring glucose uptake normalized to total protein, related to . D, Phosphorylated AKT2 measurements normalized to total AKT2 for 3 additional hPSC lines. E, As in D but measuring glucose uptake normalized to total protein. All bar graphs depict the mean with error bars representing s.d., n=2 biological replicates for B,C, n=3 for D,E.

    Techniques Used:


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    Sangon Biotech akt2 expression levels
    Akt2 Expression Levels, supplied by Sangon Biotech, 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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    akt2 mrna levels  (Vazyme Biotech Co)


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    Vazyme Biotech Co akt2 mrna levels
    <t>AKT2</t> is a direct target of miR-497. (A) Putative seed-matching sites or mutant sites (red) between miR-497 and 3’-UTR of AKT2. (B) Reporter assay of miR-497 targeting AKT2. Luciferase activities of reporter constructs containing wild-type (WT) or mutant (MT) 3’-UTR of AKT2 were assayed and normalized to those of renilla activities (internal control). (C) Suppression of AKT2 protein levels by miR-497. Total proteins were subjected to western blotting and detected for AKT2 expression levels.
    Akt2 Mrna Levels, supplied by Vazyme Biotech Co, 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/akt2 mrna levels/product/Vazyme Biotech Co
    Average 86 stars, based on 1 article reviews
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    akt2 mrna levels - by Bioz Stars, 2024-09
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    1) Product Images from "Regulation of MicroRNA-497-Targeting AKT2 Influences Tumor Growth and Chemoresistance to Cisplatin in Lung Cancer"

    Article Title: Regulation of MicroRNA-497-Targeting AKT2 Influences Tumor Growth and Chemoresistance to Cisplatin in Lung Cancer

    Journal: Frontiers in Cell and Developmental Biology

    doi: 10.3389/fcell.2020.00840

    AKT2 is a direct target of miR-497. (A) Putative seed-matching sites or mutant sites (red) between miR-497 and 3’-UTR of AKT2. (B) Reporter assay of miR-497 targeting AKT2. Luciferase activities of reporter constructs containing wild-type (WT) or mutant (MT) 3’-UTR of AKT2 were assayed and normalized to those of renilla activities (internal control). (C) Suppression of AKT2 protein levels by miR-497. Total proteins were subjected to western blotting and detected for AKT2 expression levels.
    Figure Legend Snippet: AKT2 is a direct target of miR-497. (A) Putative seed-matching sites or mutant sites (red) between miR-497 and 3’-UTR of AKT2. (B) Reporter assay of miR-497 targeting AKT2. Luciferase activities of reporter constructs containing wild-type (WT) or mutant (MT) 3’-UTR of AKT2 were assayed and normalized to those of renilla activities (internal control). (C) Suppression of AKT2 protein levels by miR-497. Total proteins were subjected to western blotting and detected for AKT2 expression levels.

    Techniques Used: Mutagenesis, Reporter Assay, Luciferase, Construct, Western Blot, Expressing

    Lung cancer tissues exhibits higher levels of AKT2 which are inversely correlated with miR-497 expression. (A) The expression levels of AKT2 in normal tissues and human NSCLC specimens were determined by qRT-PCR analysis and fold changes were obtained by the ratios of AKT2 to GAPDH levels. (B) Pearson’s correlation analysis was used to determine the correlation between the expression levels of AKT2 and miR-497 in human NSCLC specimens. Data were presented by mean ± SD. of 3 replicates. **indicated P < 0.01.
    Figure Legend Snippet: Lung cancer tissues exhibits higher levels of AKT2 which are inversely correlated with miR-497 expression. (A) The expression levels of AKT2 in normal tissues and human NSCLC specimens were determined by qRT-PCR analysis and fold changes were obtained by the ratios of AKT2 to GAPDH levels. (B) Pearson’s correlation analysis was used to determine the correlation between the expression levels of AKT2 and miR-497 in human NSCLC specimens. Data were presented by mean ± SD. of 3 replicates. **indicated P < 0.01.

    Techniques Used: Expressing, Quantitative RT-PCR

    Overexpression of AKT2 reverses the inhibitory effects of miR-497. (A) The expression of AKT2 was rescued by transfection of pCMV-AKT2 for 48 h. (B) Overexpression of miR-497 arrested cell proliferation, but this was rescued upon coexpression of exogenous AKT2 in H1299 cells. (C) MiR-497 overexpression decreased cell migration by its target AKT2 in H1299 cells. (D) Overexpression of AKT2 restored miR-497-inhibited colony formation. Data were presented by mean ± SD of 3 replicates. *or # indicated P < 0.05. *indicates significant difference compared to control; # indicates significant difference compared to miR-497 treatment plus AKT2.
    Figure Legend Snippet: Overexpression of AKT2 reverses the inhibitory effects of miR-497. (A) The expression of AKT2 was rescued by transfection of pCMV-AKT2 for 48 h. (B) Overexpression of miR-497 arrested cell proliferation, but this was rescued upon coexpression of exogenous AKT2 in H1299 cells. (C) MiR-497 overexpression decreased cell migration by its target AKT2 in H1299 cells. (D) Overexpression of AKT2 restored miR-497-inhibited colony formation. Data were presented by mean ± SD of 3 replicates. *or # indicated P < 0.05. *indicates significant difference compared to control; # indicates significant difference compared to miR-497 treatment plus AKT2.

    Techniques Used: Over Expression, Expressing, Transfection, Migration

    MiR-497 sensitizes lung cancer cells to CDDP treatment by suppressing AKT2. (A) H1299 cells stably expressing miR-NC or miR-497 were treated with different concentrations of CDDP for 48 h, and cell viability was analyzed using CCK-8 assay. (B) H1299 cells stably expressing miR-NC, miR-497, or miR-497 in combination with AKT2 overexpression were treated with 5 μM of CDDP for indicated time points. Cell viability was analyzed by CCK-8 assay. (C,D) Cell apoptosis was analyzed by flow cytometry and by caspase-3 assay. Data represent mean ± SD from three replicates. *, # indicates P < 0.05; **indicates P < 0.01, *indicates P < 0.05 compared to miR-NC control. # indicates P < 0.05 compared to miR-497 and AKT2 overexpression group.
    Figure Legend Snippet: MiR-497 sensitizes lung cancer cells to CDDP treatment by suppressing AKT2. (A) H1299 cells stably expressing miR-NC or miR-497 were treated with different concentrations of CDDP for 48 h, and cell viability was analyzed using CCK-8 assay. (B) H1299 cells stably expressing miR-NC, miR-497, or miR-497 in combination with AKT2 overexpression were treated with 5 μM of CDDP for indicated time points. Cell viability was analyzed by CCK-8 assay. (C,D) Cell apoptosis was analyzed by flow cytometry and by caspase-3 assay. Data represent mean ± SD from three replicates. *, # indicates P < 0.05; **indicates P < 0.01, *indicates P < 0.05 compared to miR-NC control. # indicates P < 0.05 compared to miR-497 and AKT2 overexpression group.

    Techniques Used: Stable Transfection, Expressing, CCK-8 Assay, Over Expression, Flow Cytometry, Caspase-3 Assay

    MiR-497 inhibits tumorigenesis in vivo . (A,B) Tumor growth assay in nude mice. Tumor growth curve, representative pictures and average weight of xenograft tumors between the groups of miR-NC and miR-497. Bar: 2 mm. (C) Protein levels of AKT2 in xenograft tumors. (D) The expression levels of AKT2 were analyzed by qRT-PCR. Data were presented by mean ± SD. of 3 replicates. *indicated P < 0.05; **indicates P < 0.01.
    Figure Legend Snippet: MiR-497 inhibits tumorigenesis in vivo . (A,B) Tumor growth assay in nude mice. Tumor growth curve, representative pictures and average weight of xenograft tumors between the groups of miR-NC and miR-497. Bar: 2 mm. (C) Protein levels of AKT2 in xenograft tumors. (D) The expression levels of AKT2 were analyzed by qRT-PCR. Data were presented by mean ± SD. of 3 replicates. *indicated P < 0.05; **indicates P < 0.01.

    Techniques Used: In Vivo, Growth Assay, Expressing, Quantitative RT-PCR


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    Abcam akt2 levels
    Akt2 Levels, supplied by Abcam, 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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    Abcam akt2 levels
    Akt2 Levels, supplied by Abcam, 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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    Vazyme Biotech Co akt2 mrna levels
    <t>AKT2</t> is a direct target of miR-497. (A) Putative seed-matching sites or mutant sites (red) between miR-497 and 3’-UTR of AKT2. (B) Reporter assay of miR-497 targeting AKT2. Luciferase activities of reporter constructs containing wild-type (WT) or mutant (MT) 3’-UTR of AKT2 were assayed and normalized to those of renilla activities (internal control). (C) Suppression of AKT2 protein levels by miR-497. Total proteins were subjected to western blotting and detected for AKT2 expression levels.
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    Abcam akt2 levels
    <t>AKT2</t> is a direct target of miR-497. (A) Putative seed-matching sites or mutant sites (red) between miR-497 and 3’-UTR of AKT2. (B) Reporter assay of miR-497 targeting AKT2. Luciferase activities of reporter constructs containing wild-type (WT) or mutant (MT) 3’-UTR of AKT2 were assayed and normalized to those of renilla activities (internal control). (C) Suppression of AKT2 protein levels by miR-497. Total proteins were subjected to western blotting and detected for AKT2 expression levels.
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    AKT2 is a direct target of miR-497. (A) Putative seed-matching sites or mutant sites (red) between miR-497 and 3’-UTR of AKT2. (B) Reporter assay of miR-497 targeting AKT2. Luciferase activities of reporter constructs containing wild-type (WT) or mutant (MT) 3’-UTR of AKT2 were assayed and normalized to those of renilla activities (internal control). (C) Suppression of AKT2 protein levels by miR-497. Total proteins were subjected to western blotting and detected for AKT2 expression levels.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Regulation of MicroRNA-497-Targeting AKT2 Influences Tumor Growth and Chemoresistance to Cisplatin in Lung Cancer

    doi: 10.3389/fcell.2020.00840

    Figure Lengend Snippet: AKT2 is a direct target of miR-497. (A) Putative seed-matching sites or mutant sites (red) between miR-497 and 3’-UTR of AKT2. (B) Reporter assay of miR-497 targeting AKT2. Luciferase activities of reporter constructs containing wild-type (WT) or mutant (MT) 3’-UTR of AKT2 were assayed and normalized to those of renilla activities (internal control). (C) Suppression of AKT2 protein levels by miR-497. Total proteins were subjected to western blotting and detected for AKT2 expression levels.

    Article Snippet: To quantify AKT2 mRNA levels, oligo dT primer were used for transcription with RT Kit (Vazyme, China).

    Techniques: Mutagenesis, Reporter Assay, Luciferase, Construct, Western Blot, Expressing

    Lung cancer tissues exhibits higher levels of AKT2 which are inversely correlated with miR-497 expression. (A) The expression levels of AKT2 in normal tissues and human NSCLC specimens were determined by qRT-PCR analysis and fold changes were obtained by the ratios of AKT2 to GAPDH levels. (B) Pearson’s correlation analysis was used to determine the correlation between the expression levels of AKT2 and miR-497 in human NSCLC specimens. Data were presented by mean ± SD. of 3 replicates. **indicated P < 0.01.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Regulation of MicroRNA-497-Targeting AKT2 Influences Tumor Growth and Chemoresistance to Cisplatin in Lung Cancer

    doi: 10.3389/fcell.2020.00840

    Figure Lengend Snippet: Lung cancer tissues exhibits higher levels of AKT2 which are inversely correlated with miR-497 expression. (A) The expression levels of AKT2 in normal tissues and human NSCLC specimens were determined by qRT-PCR analysis and fold changes were obtained by the ratios of AKT2 to GAPDH levels. (B) Pearson’s correlation analysis was used to determine the correlation between the expression levels of AKT2 and miR-497 in human NSCLC specimens. Data were presented by mean ± SD. of 3 replicates. **indicated P < 0.01.

    Article Snippet: To quantify AKT2 mRNA levels, oligo dT primer were used for transcription with RT Kit (Vazyme, China).

    Techniques: Expressing, Quantitative RT-PCR

    Overexpression of AKT2 reverses the inhibitory effects of miR-497. (A) The expression of AKT2 was rescued by transfection of pCMV-AKT2 for 48 h. (B) Overexpression of miR-497 arrested cell proliferation, but this was rescued upon coexpression of exogenous AKT2 in H1299 cells. (C) MiR-497 overexpression decreased cell migration by its target AKT2 in H1299 cells. (D) Overexpression of AKT2 restored miR-497-inhibited colony formation. Data were presented by mean ± SD of 3 replicates. *or # indicated P < 0.05. *indicates significant difference compared to control; # indicates significant difference compared to miR-497 treatment plus AKT2.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Regulation of MicroRNA-497-Targeting AKT2 Influences Tumor Growth and Chemoresistance to Cisplatin in Lung Cancer

    doi: 10.3389/fcell.2020.00840

    Figure Lengend Snippet: Overexpression of AKT2 reverses the inhibitory effects of miR-497. (A) The expression of AKT2 was rescued by transfection of pCMV-AKT2 for 48 h. (B) Overexpression of miR-497 arrested cell proliferation, but this was rescued upon coexpression of exogenous AKT2 in H1299 cells. (C) MiR-497 overexpression decreased cell migration by its target AKT2 in H1299 cells. (D) Overexpression of AKT2 restored miR-497-inhibited colony formation. Data were presented by mean ± SD of 3 replicates. *or # indicated P < 0.05. *indicates significant difference compared to control; # indicates significant difference compared to miR-497 treatment plus AKT2.

    Article Snippet: To quantify AKT2 mRNA levels, oligo dT primer were used for transcription with RT Kit (Vazyme, China).

    Techniques: Over Expression, Expressing, Transfection, Migration

    MiR-497 sensitizes lung cancer cells to CDDP treatment by suppressing AKT2. (A) H1299 cells stably expressing miR-NC or miR-497 were treated with different concentrations of CDDP for 48 h, and cell viability was analyzed using CCK-8 assay. (B) H1299 cells stably expressing miR-NC, miR-497, or miR-497 in combination with AKT2 overexpression were treated with 5 μM of CDDP for indicated time points. Cell viability was analyzed by CCK-8 assay. (C,D) Cell apoptosis was analyzed by flow cytometry and by caspase-3 assay. Data represent mean ± SD from three replicates. *, # indicates P < 0.05; **indicates P < 0.01, *indicates P < 0.05 compared to miR-NC control. # indicates P < 0.05 compared to miR-497 and AKT2 overexpression group.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Regulation of MicroRNA-497-Targeting AKT2 Influences Tumor Growth and Chemoresistance to Cisplatin in Lung Cancer

    doi: 10.3389/fcell.2020.00840

    Figure Lengend Snippet: MiR-497 sensitizes lung cancer cells to CDDP treatment by suppressing AKT2. (A) H1299 cells stably expressing miR-NC or miR-497 were treated with different concentrations of CDDP for 48 h, and cell viability was analyzed using CCK-8 assay. (B) H1299 cells stably expressing miR-NC, miR-497, or miR-497 in combination with AKT2 overexpression were treated with 5 μM of CDDP for indicated time points. Cell viability was analyzed by CCK-8 assay. (C,D) Cell apoptosis was analyzed by flow cytometry and by caspase-3 assay. Data represent mean ± SD from three replicates. *, # indicates P < 0.05; **indicates P < 0.01, *indicates P < 0.05 compared to miR-NC control. # indicates P < 0.05 compared to miR-497 and AKT2 overexpression group.

    Article Snippet: To quantify AKT2 mRNA levels, oligo dT primer were used for transcription with RT Kit (Vazyme, China).

    Techniques: Stable Transfection, Expressing, CCK-8 Assay, Over Expression, Flow Cytometry, Caspase-3 Assay

    MiR-497 inhibits tumorigenesis in vivo . (A,B) Tumor growth assay in nude mice. Tumor growth curve, representative pictures and average weight of xenograft tumors between the groups of miR-NC and miR-497. Bar: 2 mm. (C) Protein levels of AKT2 in xenograft tumors. (D) The expression levels of AKT2 were analyzed by qRT-PCR. Data were presented by mean ± SD. of 3 replicates. *indicated P < 0.05; **indicates P < 0.01.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Regulation of MicroRNA-497-Targeting AKT2 Influences Tumor Growth and Chemoresistance to Cisplatin in Lung Cancer

    doi: 10.3389/fcell.2020.00840

    Figure Lengend Snippet: MiR-497 inhibits tumorigenesis in vivo . (A,B) Tumor growth assay in nude mice. Tumor growth curve, representative pictures and average weight of xenograft tumors between the groups of miR-NC and miR-497. Bar: 2 mm. (C) Protein levels of AKT2 in xenograft tumors. (D) The expression levels of AKT2 were analyzed by qRT-PCR. Data were presented by mean ± SD. of 3 replicates. *indicated P < 0.05; **indicates P < 0.01.

    Article Snippet: To quantify AKT2 mRNA levels, oligo dT primer were used for transcription with RT Kit (Vazyme, China).

    Techniques: In Vivo, Growth Assay, Expressing, Quantitative RT-PCR