p akt1 2 3  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p akt1 2 3
    SMOC2 potentiates BMP9-induced ectopic bone formation in MEF implantation in vivo, while knockdown of FAK inhibits bone formation. (a) Macrographic images of ectopic bone mass. MEFs were implanted subcutaneously after infection with the designed adenoviruses. Ectopic osseous masses were retrieved at 4 weeks. Representative images are shown. (b) Masson's trichrome staining results showed the effect of SMOC2 and FAK knockdown on BMP9-induced ectopic bone masses in MEFs (scale bar is 50 μ m for the panel). (c) Hematoxylin-eosin (H&E) staining results showed that the osteogenesis ability was affected by SMOC2 and/or FAK knockdown in MEFs (scale bar is 200 μ m for upper panel and 50 μ m for lower panel). (d) Immunohistochemical staining results showed the expression relationship between p-FAK and <t>p-AKT1/2/3.</t> Ectopic osseous masses were retrieved at 4 weeks. The expression of p-FAK and p-AKT1/2/3 was assessed by immunohistochemical staining analysis. Representative images are shown (scale bar is 50 μ m for the panel).
    P Akt1 2 3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Matricellular Protein SMOC2 Potentiates BMP9-Induced Osteogenic Differentiation in Mesenchymal Stem Cells through the Enhancement of FAK/PI3K/AKT Signaling"

    Article Title: Matricellular Protein SMOC2 Potentiates BMP9-Induced Osteogenic Differentiation in Mesenchymal Stem Cells through the Enhancement of FAK/PI3K/AKT Signaling

    Journal: Stem Cells International

    doi: 10.1155/2023/5915988

    SMOC2 potentiates BMP9-induced ectopic bone formation in MEF implantation in vivo, while knockdown of FAK inhibits bone formation. (a) Macrographic images of ectopic bone mass. MEFs were implanted subcutaneously after infection with the designed adenoviruses. Ectopic osseous masses were retrieved at 4 weeks. Representative images are shown. (b) Masson's trichrome staining results showed the effect of SMOC2 and FAK knockdown on BMP9-induced ectopic bone masses in MEFs (scale bar is 50 μ m for the panel). (c) Hematoxylin-eosin (H&E) staining results showed that the osteogenesis ability was affected by SMOC2 and/or FAK knockdown in MEFs (scale bar is 200 μ m for upper panel and 50 μ m for lower panel). (d) Immunohistochemical staining results showed the expression relationship between p-FAK and p-AKT1/2/3. Ectopic osseous masses were retrieved at 4 weeks. The expression of p-FAK and p-AKT1/2/3 was assessed by immunohistochemical staining analysis. Representative images are shown (scale bar is 50 μ m for the panel).
    Figure Legend Snippet: SMOC2 potentiates BMP9-induced ectopic bone formation in MEF implantation in vivo, while knockdown of FAK inhibits bone formation. (a) Macrographic images of ectopic bone mass. MEFs were implanted subcutaneously after infection with the designed adenoviruses. Ectopic osseous masses were retrieved at 4 weeks. Representative images are shown. (b) Masson's trichrome staining results showed the effect of SMOC2 and FAK knockdown on BMP9-induced ectopic bone masses in MEFs (scale bar is 50 μ m for the panel). (c) Hematoxylin-eosin (H&E) staining results showed that the osteogenesis ability was affected by SMOC2 and/or FAK knockdown in MEFs (scale bar is 200 μ m for upper panel and 50 μ m for lower panel). (d) Immunohistochemical staining results showed the expression relationship between p-FAK and p-AKT1/2/3. Ectopic osseous masses were retrieved at 4 weeks. The expression of p-FAK and p-AKT1/2/3 was assessed by immunohistochemical staining analysis. Representative images are shown (scale bar is 50 μ m for the panel).

    Techniques Used: In Vivo, Infection, Staining, Immunohistochemical staining, Expressing

    p akt1 2 3  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p akt1 2 3
    SMOC2 potentiates BMP9-induced ectopic bone formation in MEF implantation in vivo, while knockdown of FAK inhibits bone formation. (a) Macrographic images of ectopic bone mass. MEFs were implanted subcutaneously after infection with the designed adenoviruses. Ectopic osseous masses were retrieved at 4 weeks. Representative images are shown. (b) Masson's trichrome staining results showed the effect of SMOC2 and FAK knockdown on BMP9-induced ectopic bone masses in MEFs (scale bar is 50 μ m for the panel). (c) Hematoxylin-eosin (H&E) staining results showed that the osteogenesis ability was affected by SMOC2 and/or FAK knockdown in MEFs (scale bar is 200 μ m for upper panel and 50 μ m for lower panel). (d) Immunohistochemical staining results showed the expression relationship between p-FAK and <t>p-AKT1/2/3.</t> Ectopic osseous masses were retrieved at 4 weeks. The expression of p-FAK and p-AKT1/2/3 was assessed by immunohistochemical staining analysis. Representative images are shown (scale bar is 50 μ m for the panel).
    P Akt1 2 3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Matricellular Protein SMOC2 Potentiates BMP9-Induced Osteogenic Differentiation in Mesenchymal Stem Cells through the Enhancement of FAK/PI3K/AKT Signaling"

    Article Title: Matricellular Protein SMOC2 Potentiates BMP9-Induced Osteogenic Differentiation in Mesenchymal Stem Cells through the Enhancement of FAK/PI3K/AKT Signaling

    Journal: Stem Cells International

    doi: 10.1155/2023/5915988

    SMOC2 potentiates BMP9-induced ectopic bone formation in MEF implantation in vivo, while knockdown of FAK inhibits bone formation. (a) Macrographic images of ectopic bone mass. MEFs were implanted subcutaneously after infection with the designed adenoviruses. Ectopic osseous masses were retrieved at 4 weeks. Representative images are shown. (b) Masson's trichrome staining results showed the effect of SMOC2 and FAK knockdown on BMP9-induced ectopic bone masses in MEFs (scale bar is 50 μ m for the panel). (c) Hematoxylin-eosin (H&E) staining results showed that the osteogenesis ability was affected by SMOC2 and/or FAK knockdown in MEFs (scale bar is 200 μ m for upper panel and 50 μ m for lower panel). (d) Immunohistochemical staining results showed the expression relationship between p-FAK and p-AKT1/2/3. Ectopic osseous masses were retrieved at 4 weeks. The expression of p-FAK and p-AKT1/2/3 was assessed by immunohistochemical staining analysis. Representative images are shown (scale bar is 50 μ m for the panel).
    Figure Legend Snippet: SMOC2 potentiates BMP9-induced ectopic bone formation in MEF implantation in vivo, while knockdown of FAK inhibits bone formation. (a) Macrographic images of ectopic bone mass. MEFs were implanted subcutaneously after infection with the designed adenoviruses. Ectopic osseous masses were retrieved at 4 weeks. Representative images are shown. (b) Masson's trichrome staining results showed the effect of SMOC2 and FAK knockdown on BMP9-induced ectopic bone masses in MEFs (scale bar is 50 μ m for the panel). (c) Hematoxylin-eosin (H&E) staining results showed that the osteogenesis ability was affected by SMOC2 and/or FAK knockdown in MEFs (scale bar is 200 μ m for upper panel and 50 μ m for lower panel). (d) Immunohistochemical staining results showed the expression relationship between p-FAK and p-AKT1/2/3. Ectopic osseous masses were retrieved at 4 weeks. The expression of p-FAK and p-AKT1/2/3 was assessed by immunohistochemical staining analysis. Representative images are shown (scale bar is 50 μ m for the panel).

    Techniques Used: In Vivo, Infection, Staining, Immunohistochemical staining, Expressing

    p ser473 akt1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p ser473 akt1
    Changes in <t>Akt1</t> and CaMKII expression and phosphorylation in the PL. While we did not detect any time-dependent or group differences in the PL expression of total Akt1 (A) , both 2-h and Mixed rats exhibited a time-dependent increase total <t>p(Ser473)-Akt1</t> expression (B) and the 2-h rats exhibited a time-dependent increase in the relative expression of p(Ser473)-Akt1 (C) . (D) We detected no group or time-dependent changes in total CaMKII expression within the PL. However, the Mixed group demonstrated a significant time-dependent increase in both total (E) and relative (F) p(Thr286)-CaMKII expression. Data are normalized to the average protein densities of the Sham controls tested on WD3 and represented as means ± SEMs of the number of rats indicated. + p < 0.05, compared to WD3.
    P Ser473 Akt1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Profiling prefrontal cortex protein expression in rats exhibiting an incubation of cocaine craving following short-access self-administration procedures"

    Article Title: Profiling prefrontal cortex protein expression in rats exhibiting an incubation of cocaine craving following short-access self-administration procedures

    Journal: Frontiers in Psychiatry

    doi: 10.3389/fpsyt.2022.1031585

    Changes in Akt1 and CaMKII expression and phosphorylation in the PL. While we did not detect any time-dependent or group differences in the PL expression of total Akt1 (A) , both 2-h and Mixed rats exhibited a time-dependent increase total p(Ser473)-Akt1 expression (B) and the 2-h rats exhibited a time-dependent increase in the relative expression of p(Ser473)-Akt1 (C) . (D) We detected no group or time-dependent changes in total CaMKII expression within the PL. However, the Mixed group demonstrated a significant time-dependent increase in both total (E) and relative (F) p(Thr286)-CaMKII expression. Data are normalized to the average protein densities of the Sham controls tested on WD3 and represented as means ± SEMs of the number of rats indicated. + p < 0.05, compared to WD3.
    Figure Legend Snippet: Changes in Akt1 and CaMKII expression and phosphorylation in the PL. While we did not detect any time-dependent or group differences in the PL expression of total Akt1 (A) , both 2-h and Mixed rats exhibited a time-dependent increase total p(Ser473)-Akt1 expression (B) and the 2-h rats exhibited a time-dependent increase in the relative expression of p(Ser473)-Akt1 (C) . (D) We detected no group or time-dependent changes in total CaMKII expression within the PL. However, the Mixed group demonstrated a significant time-dependent increase in both total (E) and relative (F) p(Thr286)-CaMKII expression. Data are normalized to the average protein densities of the Sham controls tested on WD3 and represented as means ± SEMs of the number of rats indicated. + p < 0.05, compared to WD3.

    Techniques Used: Expressing

    Summary of the negative results from the immunoblotting study of the IL from Sham, 2-h- and Mixed-Access rats.
    Figure Legend Snippet: Summary of the negative results from the immunoblotting study of the IL from Sham, 2-h- and Mixed-Access rats.

    Techniques Used: Western Blot

    phosphorylated akt1 p akt1 ser473  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphorylated akt1 p akt1 ser473
    Effect of CIP2A knockdown on the expression level of PI3K/AKT/mTOR signaling components. The protein expression levels of nonphosphorylated and phosphorylated PI3K p85, <t>AKT1,</t> and mTOR in RPMI-8226 and NCI-H929 cells transfected with si-CIP2A or si-Scr were evaluated by western blotting, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as a loading control.
    Phosphorylated Akt1 P Akt1 Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Cancerous Inhibitor of PP2A Silencing Inhibits Proliferation and Promotes Apoptosis in Human Multiple Myeloma Cells"

    Article Title: Cancerous Inhibitor of PP2A Silencing Inhibits Proliferation and Promotes Apoptosis in Human Multiple Myeloma Cells

    Journal: BioMed Research International

    doi: 10.1155/2016/6864135

    Effect of CIP2A knockdown on the expression level of PI3K/AKT/mTOR signaling components. The protein expression levels of nonphosphorylated and phosphorylated PI3K p85, AKT1, and mTOR in RPMI-8226 and NCI-H929 cells transfected with si-CIP2A or si-Scr were evaluated by western blotting, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as a loading control.
    Figure Legend Snippet: Effect of CIP2A knockdown on the expression level of PI3K/AKT/mTOR signaling components. The protein expression levels of nonphosphorylated and phosphorylated PI3K p85, AKT1, and mTOR in RPMI-8226 and NCI-H929 cells transfected with si-CIP2A or si-Scr were evaluated by western blotting, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as a loading control.

    Techniques Used: Expressing, Transfection, Western Blot

    Effect of IGF-1 treatment on the expression level of PI3K/AKT/mTOR signaling components in RPMI-8226 and NCI-H929 cells that are knocked down by si-CIP2A. The protein expression levels of nonphosphorylated and phosphorylated PI3K p85, AKT1, and mTOR in RPMI-8226 and NCI-H929 cells that are knocked down by si-CIP2A treated with PBS or IGF-1 were evaluated by western blotting, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as a loading control.
    Figure Legend Snippet: Effect of IGF-1 treatment on the expression level of PI3K/AKT/mTOR signaling components in RPMI-8226 and NCI-H929 cells that are knocked down by si-CIP2A. The protein expression levels of nonphosphorylated and phosphorylated PI3K p85, AKT1, and mTOR in RPMI-8226 and NCI-H929 cells that are knocked down by si-CIP2A treated with PBS or IGF-1 were evaluated by western blotting, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as a loading control.

    Techniques Used: Expressing, Western Blot

    p akt1 2 3 ser473  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p akt1 2 3 ser473
    P Akt1 2 3 Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti p akt1 ser473  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti p akt1 ser473
    Anti P Akt1 Ser473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    p akt  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p akt
    P Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    antibodies recognized phospho p akt  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc antibodies recognized phospho p akt
    A–C: In total lung homogenates, mRNA expression of Ang-1, Ang-2 and Tie2 was determined by real time RT-PCR. Levels were normalized for expression of internal controls, i.e. the average value of β-actin and glyceraldehyde 3-phosphate dehydrogenase (GAPdH). No group differences in expression levels of β-actin and GAPdH were observed. D–E: In total lung homogenates, protein expression of Ang-1 and Ang-2 was determined by Western blotting. Membranes were reprobed with antibody recognizing total <t>Akt</t> (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western Blot depicting immunodetectable Ang-1 and Ang-2. F: In total lung homogenates, protein expression of Tie2 was determined by ELISA. Levels were normalized for total protein concentrations. Data are depicted relative to NVC and expressed as mean ± SEM of 6–16 animals for each group (** p<0.01, *** p<0.001). G: Lung sections of non-ventilated controls were stained with fluorescent antibody recognizing Tie2 to visualize the presence of Tie2 on pulmonary cells (isotype control was negative). Magnification ×200. NVC = non-ventilated controls; LV T , HV T = mice ventilated with low or high tidal volumes.
    Antibodies Recognized Phospho P Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Angiopoietin-1 Treatment Reduces Inflammation but Does Not Prevent Ventilator-Induced Lung Injury"

    Article Title: Angiopoietin-1 Treatment Reduces Inflammation but Does Not Prevent Ventilator-Induced Lung Injury

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0015653

    A–C: In total lung homogenates, mRNA expression of Ang-1, Ang-2 and Tie2 was determined by real time RT-PCR. Levels were normalized for expression of internal controls, i.e. the average value of β-actin and glyceraldehyde 3-phosphate dehydrogenase (GAPdH). No group differences in expression levels of β-actin and GAPdH were observed. D–E: In total lung homogenates, protein expression of Ang-1 and Ang-2 was determined by Western blotting. Membranes were reprobed with antibody recognizing total Akt (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western Blot depicting immunodetectable Ang-1 and Ang-2. F: In total lung homogenates, protein expression of Tie2 was determined by ELISA. Levels were normalized for total protein concentrations. Data are depicted relative to NVC and expressed as mean ± SEM of 6–16 animals for each group (** p<0.01, *** p<0.001). G: Lung sections of non-ventilated controls were stained with fluorescent antibody recognizing Tie2 to visualize the presence of Tie2 on pulmonary cells (isotype control was negative). Magnification ×200. NVC = non-ventilated controls; LV T , HV T = mice ventilated with low or high tidal volumes.
    Figure Legend Snippet: A–C: In total lung homogenates, mRNA expression of Ang-1, Ang-2 and Tie2 was determined by real time RT-PCR. Levels were normalized for expression of internal controls, i.e. the average value of β-actin and glyceraldehyde 3-phosphate dehydrogenase (GAPdH). No group differences in expression levels of β-actin and GAPdH were observed. D–E: In total lung homogenates, protein expression of Ang-1 and Ang-2 was determined by Western blotting. Membranes were reprobed with antibody recognizing total Akt (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western Blot depicting immunodetectable Ang-1 and Ang-2. F: In total lung homogenates, protein expression of Tie2 was determined by ELISA. Levels were normalized for total protein concentrations. Data are depicted relative to NVC and expressed as mean ± SEM of 6–16 animals for each group (** p<0.01, *** p<0.001). G: Lung sections of non-ventilated controls were stained with fluorescent antibody recognizing Tie2 to visualize the presence of Tie2 on pulmonary cells (isotype control was negative). Magnification ×200. NVC = non-ventilated controls; LV T , HV T = mice ventilated with low or high tidal volumes.

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Staining

    In total lung homogenates, protein expression of p-Akt was determined by Western blotting as an indirect measure of Tie2 signaling. Membranes were stripped and reprobed with antibody recognizing total Akt (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western blot depicting immunodetectable p-Akt. Data are depicted relative to NVC and expressed as mean ± SEM of 8–10 animals per group (* p<0.05, ** p<0.01). NVC = non-ventilated controls; HV T = mice ventilated with high tidal volumes; Veh, 1 µg, 4 µg = mice intravenously treated with either vehicle (sterile saline), Ang-1 (1 µg per animal), or Ang-1 (4 µg per animal).
    Figure Legend Snippet: In total lung homogenates, protein expression of p-Akt was determined by Western blotting as an indirect measure of Tie2 signaling. Membranes were stripped and reprobed with antibody recognizing total Akt (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western blot depicting immunodetectable p-Akt. Data are depicted relative to NVC and expressed as mean ± SEM of 8–10 animals per group (* p<0.05, ** p<0.01). NVC = non-ventilated controls; HV T = mice ventilated with high tidal volumes; Veh, 1 µg, 4 µg = mice intravenously treated with either vehicle (sterile saline), Ang-1 (1 µg per animal), or Ang-1 (4 µg per animal).

    Techniques Used: Expressing, Western Blot

    A: In total lung homogenates, mRNA expression of Ang-2 was determined by real time RT-PCR. Levels were normalized for expression of internal controls, i.e. the average value of β-actin and glyceraldehyde 3-phosphate dehydrogenase (GAPdH). No group differences in β-actin and GAPdH were observed. B: In total lung homogenates, protein expression of Ang-2 was determined by Western blotting. Membranes were reprobed with antibody recognizing total Akt (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western blot depicting immunodetectable Ang-2. Data are depicted relative to NVC and expressed as mean ± SEM of 7–16 animals per group (** p<0.01, *** p<0.001). NVC = non-ventilated controls; HV T = mice ventilated with high tidal volumes; Veh, 1 µg, 4 µg = mice intravenously treated with either vehicle (sterile saline), Ang-1 (1 µg per animal), or Ang-1 (4 µg per animal).
    Figure Legend Snippet: A: In total lung homogenates, mRNA expression of Ang-2 was determined by real time RT-PCR. Levels were normalized for expression of internal controls, i.e. the average value of β-actin and glyceraldehyde 3-phosphate dehydrogenase (GAPdH). No group differences in β-actin and GAPdH were observed. B: In total lung homogenates, protein expression of Ang-2 was determined by Western blotting. Membranes were reprobed with antibody recognizing total Akt (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western blot depicting immunodetectable Ang-2. Data are depicted relative to NVC and expressed as mean ± SEM of 7–16 animals per group (** p<0.01, *** p<0.001). NVC = non-ventilated controls; HV T = mice ventilated with high tidal volumes; Veh, 1 µg, 4 µg = mice intravenously treated with either vehicle (sterile saline), Ang-1 (1 µg per animal), or Ang-1 (4 µg per animal).

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

    anti human p akt  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti human p akt
    Anti Human P Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti human p akt/product/Cell Signaling Technology Inc
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    pathscan p akt1 s473 sandwich elisa  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc pathscan p akt1 s473 sandwich elisa
    (a) A time course of cell growth activity in BT474 cells in the presence of 100 nM trastuzumab, 100 nM bis-Fab 1325, or 10 nM heregulin. BT474 were cultured in media containing 10% fetal bovine serum for up to 84 hours. At 12-hour intervals total number of cells were determined; three plates from each treatment group were counted for the total number of cells and plotted as the mean cell count. The error bars indicate standard deviation from the mean. At approximately 60 hours (indicated by the arrow) the cells reached confluence in the agonist treatment groups. (b) BT474 cells were treated with 100 nM of trastuzumab, 100 nM of bis-Fab 1325, or 100 nM of bis-Fab 1329 for 10, 30 and 120 minutes. At times indicated, cell lysates were prepared and analyzed by immunoblotting using phospho-specific antibodies for HER3, AKT, and MAPK as well as antibodies recognizing total protein. Data are representative of three independent experiments. (c) Quantification of AKT phosphorylation after treatment with 100 nM bis-Fab 1325, 100 nM trastuzumab, 2 nM heregulin and a non-specific control antibody (anti-gD) by PathScan <t>p-AKT1</t> <t>(S473)</t> <t>ELISA.</t> All data points were collected in triplicates and the mean of the triplicate absorbance values were used to calculate the percent change in pAKT compared to untreated control group. The error bars indicate standard deviation from the mean. Data are representative of three independent experiments. (d) A model for the HER2 dimerization patterns induced by either the agonist antibody-analogs or trastuzumab. The diagram depicts three potential dimer conformations; 1) the basal state induced by high cell surface density, 2) the activated state induced by the bis-Fab agonist, and 3) the inhibited state stabilized by trastuzumab. The cell growth activity of agonist bis-Fabs may be due to stabilization of an allosterically activated conformation between HER2–HER2 dimers. Trastuzumab's antagonistic activity may arise from dimer orientations that favor the inactive allosteric interactions between kinases. A non-stabilized dimer may represent the basal state where interactions between the juxtamembrane (black line) loop of the activator kinase and the C-terminal lobe of the receiver kinase are not fully stabilized without agonist binding.
    Pathscan P Akt1 S473 Sandwich Elisa, 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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    Images

    1) Product Images from "Reorienting the Fab Domains of Trastuzumab Results in Potent HER2 Activators"

    Article Title: Reorienting the Fab Domains of Trastuzumab Results in Potent HER2 Activators

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0051817

    (a) A time course of cell growth activity in BT474 cells in the presence of 100 nM trastuzumab, 100 nM bis-Fab 1325, or 10 nM heregulin. BT474 were cultured in media containing 10% fetal bovine serum for up to 84 hours. At 12-hour intervals total number of cells were determined; three plates from each treatment group were counted for the total number of cells and plotted as the mean cell count. The error bars indicate standard deviation from the mean. At approximately 60 hours (indicated by the arrow) the cells reached confluence in the agonist treatment groups. (b) BT474 cells were treated with 100 nM of trastuzumab, 100 nM of bis-Fab 1325, or 100 nM of bis-Fab 1329 for 10, 30 and 120 minutes. At times indicated, cell lysates were prepared and analyzed by immunoblotting using phospho-specific antibodies for HER3, AKT, and MAPK as well as antibodies recognizing total protein. Data are representative of three independent experiments. (c) Quantification of AKT phosphorylation after treatment with 100 nM bis-Fab 1325, 100 nM trastuzumab, 2 nM heregulin and a non-specific control antibody (anti-gD) by PathScan p-AKT1 (S473) ELISA. All data points were collected in triplicates and the mean of the triplicate absorbance values were used to calculate the percent change in pAKT compared to untreated control group. The error bars indicate standard deviation from the mean. Data are representative of three independent experiments. (d) A model for the HER2 dimerization patterns induced by either the agonist antibody-analogs or trastuzumab. The diagram depicts three potential dimer conformations; 1) the basal state induced by high cell surface density, 2) the activated state induced by the bis-Fab agonist, and 3) the inhibited state stabilized by trastuzumab. The cell growth activity of agonist bis-Fabs may be due to stabilization of an allosterically activated conformation between HER2–HER2 dimers. Trastuzumab's antagonistic activity may arise from dimer orientations that favor the inactive allosteric interactions between kinases. A non-stabilized dimer may represent the basal state where interactions between the juxtamembrane (black line) loop of the activator kinase and the C-terminal lobe of the receiver kinase are not fully stabilized without agonist binding.
    Figure Legend Snippet: (a) A time course of cell growth activity in BT474 cells in the presence of 100 nM trastuzumab, 100 nM bis-Fab 1325, or 10 nM heregulin. BT474 were cultured in media containing 10% fetal bovine serum for up to 84 hours. At 12-hour intervals total number of cells were determined; three plates from each treatment group were counted for the total number of cells and plotted as the mean cell count. The error bars indicate standard deviation from the mean. At approximately 60 hours (indicated by the arrow) the cells reached confluence in the agonist treatment groups. (b) BT474 cells were treated with 100 nM of trastuzumab, 100 nM of bis-Fab 1325, or 100 nM of bis-Fab 1329 for 10, 30 and 120 minutes. At times indicated, cell lysates were prepared and analyzed by immunoblotting using phospho-specific antibodies for HER3, AKT, and MAPK as well as antibodies recognizing total protein. Data are representative of three independent experiments. (c) Quantification of AKT phosphorylation after treatment with 100 nM bis-Fab 1325, 100 nM trastuzumab, 2 nM heregulin and a non-specific control antibody (anti-gD) by PathScan p-AKT1 (S473) ELISA. All data points were collected in triplicates and the mean of the triplicate absorbance values were used to calculate the percent change in pAKT compared to untreated control group. The error bars indicate standard deviation from the mean. Data are representative of three independent experiments. (d) A model for the HER2 dimerization patterns induced by either the agonist antibody-analogs or trastuzumab. The diagram depicts three potential dimer conformations; 1) the basal state induced by high cell surface density, 2) the activated state induced by the bis-Fab agonist, and 3) the inhibited state stabilized by trastuzumab. The cell growth activity of agonist bis-Fabs may be due to stabilization of an allosterically activated conformation between HER2–HER2 dimers. Trastuzumab's antagonistic activity may arise from dimer orientations that favor the inactive allosteric interactions between kinases. A non-stabilized dimer may represent the basal state where interactions between the juxtamembrane (black line) loop of the activator kinase and the C-terminal lobe of the receiver kinase are not fully stabilized without agonist binding.

    Techniques Used: Activity Assay, Cell Culture, Cell Counting, Standard Deviation, Western Blot, Enzyme-linked Immunosorbent Assay, Binding Assay

    phosphospecific antibodies against p akt  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphospecific antibodies against p akt
    Phosphospecific Antibodies Against P Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc p akt1 2 3
    SMOC2 potentiates BMP9-induced ectopic bone formation in MEF implantation in vivo, while knockdown of FAK inhibits bone formation. (a) Macrographic images of ectopic bone mass. MEFs were implanted subcutaneously after infection with the designed adenoviruses. Ectopic osseous masses were retrieved at 4 weeks. Representative images are shown. (b) Masson's trichrome staining results showed the effect of SMOC2 and FAK knockdown on BMP9-induced ectopic bone masses in MEFs (scale bar is 50 μ m for the panel). (c) Hematoxylin-eosin (H&E) staining results showed that the osteogenesis ability was affected by SMOC2 and/or FAK knockdown in MEFs (scale bar is 200 μ m for upper panel and 50 μ m for lower panel). (d) Immunohistochemical staining results showed the expression relationship between p-FAK and <t>p-AKT1/2/3.</t> Ectopic osseous masses were retrieved at 4 weeks. The expression of p-FAK and p-AKT1/2/3 was assessed by immunohistochemical staining analysis. Representative images are shown (scale bar is 50 μ m for the panel).
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    Changes in <t>Akt1</t> and CaMKII expression and phosphorylation in the PL. While we did not detect any time-dependent or group differences in the PL expression of total Akt1 (A) , both 2-h and Mixed rats exhibited a time-dependent increase total <t>p(Ser473)-Akt1</t> expression (B) and the 2-h rats exhibited a time-dependent increase in the relative expression of p(Ser473)-Akt1 (C) . (D) We detected no group or time-dependent changes in total CaMKII expression within the PL. However, the Mixed group demonstrated a significant time-dependent increase in both total (E) and relative (F) p(Thr286)-CaMKII expression. Data are normalized to the average protein densities of the Sham controls tested on WD3 and represented as means ± SEMs of the number of rats indicated. + p < 0.05, compared to WD3.
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    Cell Signaling Technology Inc phosphorylated akt1 p akt1 ser473
    Effect of CIP2A knockdown on the expression level of PI3K/AKT/mTOR signaling components. The protein expression levels of nonphosphorylated and phosphorylated PI3K p85, <t>AKT1,</t> and mTOR in RPMI-8226 and NCI-H929 cells transfected with si-CIP2A or si-Scr were evaluated by western blotting, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as a loading control.
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    Cell Signaling Technology Inc p akt1 2 3 ser473
    Effect of CIP2A knockdown on the expression level of PI3K/AKT/mTOR signaling components. The protein expression levels of nonphosphorylated and phosphorylated PI3K p85, <t>AKT1,</t> and mTOR in RPMI-8226 and NCI-H929 cells transfected with si-CIP2A or si-Scr were evaluated by western blotting, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as a loading control.
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    Effect of CIP2A knockdown on the expression level of PI3K/AKT/mTOR signaling components. The protein expression levels of nonphosphorylated and phosphorylated PI3K p85, <t>AKT1,</t> and mTOR in RPMI-8226 and NCI-H929 cells transfected with si-CIP2A or si-Scr were evaluated by western blotting, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as a loading control.
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    Cell Signaling Technology Inc p akt
    Effect of CIP2A knockdown on the expression level of PI3K/AKT/mTOR signaling components. The protein expression levels of nonphosphorylated and phosphorylated PI3K p85, <t>AKT1,</t> and mTOR in RPMI-8226 and NCI-H929 cells transfected with si-CIP2A or si-Scr were evaluated by western blotting, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as a loading control.
    P Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc antibodies recognized phospho p akt
    A–C: In total lung homogenates, mRNA expression of Ang-1, Ang-2 and Tie2 was determined by real time RT-PCR. Levels were normalized for expression of internal controls, i.e. the average value of β-actin and glyceraldehyde 3-phosphate dehydrogenase (GAPdH). No group differences in expression levels of β-actin and GAPdH were observed. D–E: In total lung homogenates, protein expression of Ang-1 and Ang-2 was determined by Western blotting. Membranes were reprobed with antibody recognizing total <t>Akt</t> (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western Blot depicting immunodetectable Ang-1 and Ang-2. F: In total lung homogenates, protein expression of Tie2 was determined by ELISA. Levels were normalized for total protein concentrations. Data are depicted relative to NVC and expressed as mean ± SEM of 6–16 animals for each group (** p<0.01, *** p<0.001). G: Lung sections of non-ventilated controls were stained with fluorescent antibody recognizing Tie2 to visualize the presence of Tie2 on pulmonary cells (isotype control was negative). Magnification ×200. NVC = non-ventilated controls; LV T , HV T = mice ventilated with low or high tidal volumes.
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    Cell Signaling Technology Inc anti human p akt
    A–C: In total lung homogenates, mRNA expression of Ang-1, Ang-2 and Tie2 was determined by real time RT-PCR. Levels were normalized for expression of internal controls, i.e. the average value of β-actin and glyceraldehyde 3-phosphate dehydrogenase (GAPdH). No group differences in expression levels of β-actin and GAPdH were observed. D–E: In total lung homogenates, protein expression of Ang-1 and Ang-2 was determined by Western blotting. Membranes were reprobed with antibody recognizing total <t>Akt</t> (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western Blot depicting immunodetectable Ang-1 and Ang-2. F: In total lung homogenates, protein expression of Tie2 was determined by ELISA. Levels were normalized for total protein concentrations. Data are depicted relative to NVC and expressed as mean ± SEM of 6–16 animals for each group (** p<0.01, *** p<0.001). G: Lung sections of non-ventilated controls were stained with fluorescent antibody recognizing Tie2 to visualize the presence of Tie2 on pulmonary cells (isotype control was negative). Magnification ×200. NVC = non-ventilated controls; LV T , HV T = mice ventilated with low or high tidal volumes.
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    Cell Signaling Technology Inc pathscan p akt1 s473 sandwich elisa
    (a) A time course of cell growth activity in BT474 cells in the presence of 100 nM trastuzumab, 100 nM bis-Fab 1325, or 10 nM heregulin. BT474 were cultured in media containing 10% fetal bovine serum for up to 84 hours. At 12-hour intervals total number of cells were determined; three plates from each treatment group were counted for the total number of cells and plotted as the mean cell count. The error bars indicate standard deviation from the mean. At approximately 60 hours (indicated by the arrow) the cells reached confluence in the agonist treatment groups. (b) BT474 cells were treated with 100 nM of trastuzumab, 100 nM of bis-Fab 1325, or 100 nM of bis-Fab 1329 for 10, 30 and 120 minutes. At times indicated, cell lysates were prepared and analyzed by immunoblotting using phospho-specific antibodies for HER3, AKT, and MAPK as well as antibodies recognizing total protein. Data are representative of three independent experiments. (c) Quantification of AKT phosphorylation after treatment with 100 nM bis-Fab 1325, 100 nM trastuzumab, 2 nM heregulin and a non-specific control antibody (anti-gD) by PathScan <t>p-AKT1</t> <t>(S473)</t> <t>ELISA.</t> All data points were collected in triplicates and the mean of the triplicate absorbance values were used to calculate the percent change in pAKT compared to untreated control group. The error bars indicate standard deviation from the mean. Data are representative of three independent experiments. (d) A model for the HER2 dimerization patterns induced by either the agonist antibody-analogs or trastuzumab. The diagram depicts three potential dimer conformations; 1) the basal state induced by high cell surface density, 2) the activated state induced by the bis-Fab agonist, and 3) the inhibited state stabilized by trastuzumab. The cell growth activity of agonist bis-Fabs may be due to stabilization of an allosterically activated conformation between HER2–HER2 dimers. Trastuzumab's antagonistic activity may arise from dimer orientations that favor the inactive allosteric interactions between kinases. A non-stabilized dimer may represent the basal state where interactions between the juxtamembrane (black line) loop of the activator kinase and the C-terminal lobe of the receiver kinase are not fully stabilized without agonist binding.
    Pathscan P Akt1 S473 Sandwich Elisa, 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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    Cell Signaling Technology Inc phosphospecific antibodies against p akt
    (a) A time course of cell growth activity in BT474 cells in the presence of 100 nM trastuzumab, 100 nM bis-Fab 1325, or 10 nM heregulin. BT474 were cultured in media containing 10% fetal bovine serum for up to 84 hours. At 12-hour intervals total number of cells were determined; three plates from each treatment group were counted for the total number of cells and plotted as the mean cell count. The error bars indicate standard deviation from the mean. At approximately 60 hours (indicated by the arrow) the cells reached confluence in the agonist treatment groups. (b) BT474 cells were treated with 100 nM of trastuzumab, 100 nM of bis-Fab 1325, or 100 nM of bis-Fab 1329 for 10, 30 and 120 minutes. At times indicated, cell lysates were prepared and analyzed by immunoblotting using phospho-specific antibodies for HER3, AKT, and MAPK as well as antibodies recognizing total protein. Data are representative of three independent experiments. (c) Quantification of AKT phosphorylation after treatment with 100 nM bis-Fab 1325, 100 nM trastuzumab, 2 nM heregulin and a non-specific control antibody (anti-gD) by PathScan <t>p-AKT1</t> <t>(S473)</t> <t>ELISA.</t> All data points were collected in triplicates and the mean of the triplicate absorbance values were used to calculate the percent change in pAKT compared to untreated control group. The error bars indicate standard deviation from the mean. Data are representative of three independent experiments. (d) A model for the HER2 dimerization patterns induced by either the agonist antibody-analogs or trastuzumab. The diagram depicts three potential dimer conformations; 1) the basal state induced by high cell surface density, 2) the activated state induced by the bis-Fab agonist, and 3) the inhibited state stabilized by trastuzumab. The cell growth activity of agonist bis-Fabs may be due to stabilization of an allosterically activated conformation between HER2–HER2 dimers. Trastuzumab's antagonistic activity may arise from dimer orientations that favor the inactive allosteric interactions between kinases. A non-stabilized dimer may represent the basal state where interactions between the juxtamembrane (black line) loop of the activator kinase and the C-terminal lobe of the receiver kinase are not fully stabilized without agonist binding.
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    Image Search Results


    SMOC2 potentiates BMP9-induced ectopic bone formation in MEF implantation in vivo, while knockdown of FAK inhibits bone formation. (a) Macrographic images of ectopic bone mass. MEFs were implanted subcutaneously after infection with the designed adenoviruses. Ectopic osseous masses were retrieved at 4 weeks. Representative images are shown. (b) Masson's trichrome staining results showed the effect of SMOC2 and FAK knockdown on BMP9-induced ectopic bone masses in MEFs (scale bar is 50 μ m for the panel). (c) Hematoxylin-eosin (H&E) staining results showed that the osteogenesis ability was affected by SMOC2 and/or FAK knockdown in MEFs (scale bar is 200 μ m for upper panel and 50 μ m for lower panel). (d) Immunohistochemical staining results showed the expression relationship between p-FAK and p-AKT1/2/3. Ectopic osseous masses were retrieved at 4 weeks. The expression of p-FAK and p-AKT1/2/3 was assessed by immunohistochemical staining analysis. Representative images are shown (scale bar is 50 μ m for the panel).

    Journal: Stem Cells International

    Article Title: Matricellular Protein SMOC2 Potentiates BMP9-Induced Osteogenic Differentiation in Mesenchymal Stem Cells through the Enhancement of FAK/PI3K/AKT Signaling

    doi: 10.1155/2023/5915988

    Figure Lengend Snippet: SMOC2 potentiates BMP9-induced ectopic bone formation in MEF implantation in vivo, while knockdown of FAK inhibits bone formation. (a) Macrographic images of ectopic bone mass. MEFs were implanted subcutaneously after infection with the designed adenoviruses. Ectopic osseous masses were retrieved at 4 weeks. Representative images are shown. (b) Masson's trichrome staining results showed the effect of SMOC2 and FAK knockdown on BMP9-induced ectopic bone masses in MEFs (scale bar is 50 μ m for the panel). (c) Hematoxylin-eosin (H&E) staining results showed that the osteogenesis ability was affected by SMOC2 and/or FAK knockdown in MEFs (scale bar is 200 μ m for upper panel and 50 μ m for lower panel). (d) Immunohistochemical staining results showed the expression relationship between p-FAK and p-AKT1/2/3. Ectopic osseous masses were retrieved at 4 weeks. The expression of p-FAK and p-AKT1/2/3 was assessed by immunohistochemical staining analysis. Representative images are shown (scale bar is 50 μ m for the panel).

    Article Snippet: Primary antibodies against RUNX2 (12556S), p-AKT1/2/3 (4060S), and AKT1/2/3 (9272) were purchased from Cell Signaling Technology (Shanghai, China).

    Techniques: In Vivo, Infection, Staining, Immunohistochemical staining, Expressing

    Changes in Akt1 and CaMKII expression and phosphorylation in the PL. While we did not detect any time-dependent or group differences in the PL expression of total Akt1 (A) , both 2-h and Mixed rats exhibited a time-dependent increase total p(Ser473)-Akt1 expression (B) and the 2-h rats exhibited a time-dependent increase in the relative expression of p(Ser473)-Akt1 (C) . (D) We detected no group or time-dependent changes in total CaMKII expression within the PL. However, the Mixed group demonstrated a significant time-dependent increase in both total (E) and relative (F) p(Thr286)-CaMKII expression. Data are normalized to the average protein densities of the Sham controls tested on WD3 and represented as means ± SEMs of the number of rats indicated. + p < 0.05, compared to WD3.

    Journal: Frontiers in Psychiatry

    Article Title: Profiling prefrontal cortex protein expression in rats exhibiting an incubation of cocaine craving following short-access self-administration procedures

    doi: 10.3389/fpsyt.2022.1031585

    Figure Lengend Snippet: Changes in Akt1 and CaMKII expression and phosphorylation in the PL. While we did not detect any time-dependent or group differences in the PL expression of total Akt1 (A) , both 2-h and Mixed rats exhibited a time-dependent increase total p(Ser473)-Akt1 expression (B) and the 2-h rats exhibited a time-dependent increase in the relative expression of p(Ser473)-Akt1 (C) . (D) We detected no group or time-dependent changes in total CaMKII expression within the PL. However, the Mixed group demonstrated a significant time-dependent increase in both total (E) and relative (F) p(Thr286)-CaMKII expression. Data are normalized to the average protein densities of the Sham controls tested on WD3 and represented as means ± SEMs of the number of rats indicated. + p < 0.05, compared to WD3.

    Article Snippet: The following mouse primary antibodies were also employed: Homer1b/c (1:1,000 dilution; Santa Cruz Biotechnology; sc-25271), mGlu1 (1:1,000 dilution; BD Biosciences; 610965), p(Ser473)-Akt1 (1:1,000 dilution; Cell Signaling Technology; 4051), GluN2b (1:500 dilution; Invitrogen; MA1-2014), GluA2 (1:500 dilution; Synaptic Systems; 182 111), and CaMKII (1:500 dilution; Millipore; 05-532).

    Techniques: Expressing

    Summary of the negative results from the immunoblotting study of the IL from Sham, 2-h- and Mixed-Access rats.

    Journal: Frontiers in Psychiatry

    Article Title: Profiling prefrontal cortex protein expression in rats exhibiting an incubation of cocaine craving following short-access self-administration procedures

    doi: 10.3389/fpsyt.2022.1031585

    Figure Lengend Snippet: Summary of the negative results from the immunoblotting study of the IL from Sham, 2-h- and Mixed-Access rats.

    Article Snippet: The following mouse primary antibodies were also employed: Homer1b/c (1:1,000 dilution; Santa Cruz Biotechnology; sc-25271), mGlu1 (1:1,000 dilution; BD Biosciences; 610965), p(Ser473)-Akt1 (1:1,000 dilution; Cell Signaling Technology; 4051), GluN2b (1:500 dilution; Invitrogen; MA1-2014), GluA2 (1:500 dilution; Synaptic Systems; 182 111), and CaMKII (1:500 dilution; Millipore; 05-532).

    Techniques: Western Blot

    Effect of CIP2A knockdown on the expression level of PI3K/AKT/mTOR signaling components. The protein expression levels of nonphosphorylated and phosphorylated PI3K p85, AKT1, and mTOR in RPMI-8226 and NCI-H929 cells transfected with si-CIP2A or si-Scr were evaluated by western blotting, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as a loading control.

    Journal: BioMed Research International

    Article Title: Cancerous Inhibitor of PP2A Silencing Inhibits Proliferation and Promotes Apoptosis in Human Multiple Myeloma Cells

    doi: 10.1155/2016/6864135

    Figure Lengend Snippet: Effect of CIP2A knockdown on the expression level of PI3K/AKT/mTOR signaling components. The protein expression levels of nonphosphorylated and phosphorylated PI3K p85, AKT1, and mTOR in RPMI-8226 and NCI-H929 cells transfected with si-CIP2A or si-Scr were evaluated by western blotting, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as a loading control.

    Article Snippet: Nonspecific binding was blocked with 5% milk in tris-buffered saline with Tween 20, and membranes were incubated overnight at 4°C with primary antibodies against the following proteins: CIP2A (1 : 1000), AKT1 (1 : 2000), phosphorylated AKT1 (p-AKT1) (Ser473) (1 : 1500), PI3K p85 (1 : 500), p-PI3K p85 (Tyr458) (1 : 1000), mTOR (1 : 1000), p-mTOR (Ser2448) (1 : 2000), and poly(ADP-ribose) polymerase (PARP, 1 : 1500) (all from Cell Signaling Technology, Danvers, MA, USA).

    Techniques: Expressing, Transfection, Western Blot

    Effect of IGF-1 treatment on the expression level of PI3K/AKT/mTOR signaling components in RPMI-8226 and NCI-H929 cells that are knocked down by si-CIP2A. The protein expression levels of nonphosphorylated and phosphorylated PI3K p85, AKT1, and mTOR in RPMI-8226 and NCI-H929 cells that are knocked down by si-CIP2A treated with PBS or IGF-1 were evaluated by western blotting, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as a loading control.

    Journal: BioMed Research International

    Article Title: Cancerous Inhibitor of PP2A Silencing Inhibits Proliferation and Promotes Apoptosis in Human Multiple Myeloma Cells

    doi: 10.1155/2016/6864135

    Figure Lengend Snippet: Effect of IGF-1 treatment on the expression level of PI3K/AKT/mTOR signaling components in RPMI-8226 and NCI-H929 cells that are knocked down by si-CIP2A. The protein expression levels of nonphosphorylated and phosphorylated PI3K p85, AKT1, and mTOR in RPMI-8226 and NCI-H929 cells that are knocked down by si-CIP2A treated with PBS or IGF-1 were evaluated by western blotting, with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) used as a loading control.

    Article Snippet: Nonspecific binding was blocked with 5% milk in tris-buffered saline with Tween 20, and membranes were incubated overnight at 4°C with primary antibodies against the following proteins: CIP2A (1 : 1000), AKT1 (1 : 2000), phosphorylated AKT1 (p-AKT1) (Ser473) (1 : 1500), PI3K p85 (1 : 500), p-PI3K p85 (Tyr458) (1 : 1000), mTOR (1 : 1000), p-mTOR (Ser2448) (1 : 2000), and poly(ADP-ribose) polymerase (PARP, 1 : 1500) (all from Cell Signaling Technology, Danvers, MA, USA).

    Techniques: Expressing, Western Blot

    A–C: In total lung homogenates, mRNA expression of Ang-1, Ang-2 and Tie2 was determined by real time RT-PCR. Levels were normalized for expression of internal controls, i.e. the average value of β-actin and glyceraldehyde 3-phosphate dehydrogenase (GAPdH). No group differences in expression levels of β-actin and GAPdH were observed. D–E: In total lung homogenates, protein expression of Ang-1 and Ang-2 was determined by Western blotting. Membranes were reprobed with antibody recognizing total Akt (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western Blot depicting immunodetectable Ang-1 and Ang-2. F: In total lung homogenates, protein expression of Tie2 was determined by ELISA. Levels were normalized for total protein concentrations. Data are depicted relative to NVC and expressed as mean ± SEM of 6–16 animals for each group (** p<0.01, *** p<0.001). G: Lung sections of non-ventilated controls were stained with fluorescent antibody recognizing Tie2 to visualize the presence of Tie2 on pulmonary cells (isotype control was negative). Magnification ×200. NVC = non-ventilated controls; LV T , HV T = mice ventilated with low or high tidal volumes.

    Journal: PLoS ONE

    Article Title: Angiopoietin-1 Treatment Reduces Inflammation but Does Not Prevent Ventilator-Induced Lung Injury

    doi: 10.1371/journal.pone.0015653

    Figure Lengend Snippet: A–C: In total lung homogenates, mRNA expression of Ang-1, Ang-2 and Tie2 was determined by real time RT-PCR. Levels were normalized for expression of internal controls, i.e. the average value of β-actin and glyceraldehyde 3-phosphate dehydrogenase (GAPdH). No group differences in expression levels of β-actin and GAPdH were observed. D–E: In total lung homogenates, protein expression of Ang-1 and Ang-2 was determined by Western blotting. Membranes were reprobed with antibody recognizing total Akt (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western Blot depicting immunodetectable Ang-1 and Ang-2. F: In total lung homogenates, protein expression of Tie2 was determined by ELISA. Levels were normalized for total protein concentrations. Data are depicted relative to NVC and expressed as mean ± SEM of 6–16 animals for each group (** p<0.01, *** p<0.001). G: Lung sections of non-ventilated controls were stained with fluorescent antibody recognizing Tie2 to visualize the presence of Tie2 on pulmonary cells (isotype control was negative). Magnification ×200. NVC = non-ventilated controls; LV T , HV T = mice ventilated with low or high tidal volumes.

    Article Snippet: Antibodies recognized phospho (p)-Akt (Ser473; Cell Signaling, Danvers, MA), Ang-1 or Ang-2 (both Alpha Diagnostic, San Antonio, TX).

    Techniques: Expressing, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Staining

    In total lung homogenates, protein expression of p-Akt was determined by Western blotting as an indirect measure of Tie2 signaling. Membranes were stripped and reprobed with antibody recognizing total Akt (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western blot depicting immunodetectable p-Akt. Data are depicted relative to NVC and expressed as mean ± SEM of 8–10 animals per group (* p<0.05, ** p<0.01). NVC = non-ventilated controls; HV T = mice ventilated with high tidal volumes; Veh, 1 µg, 4 µg = mice intravenously treated with either vehicle (sterile saline), Ang-1 (1 µg per animal), or Ang-1 (4 µg per animal).

    Journal: PLoS ONE

    Article Title: Angiopoietin-1 Treatment Reduces Inflammation but Does Not Prevent Ventilator-Induced Lung Injury

    doi: 10.1371/journal.pone.0015653

    Figure Lengend Snippet: In total lung homogenates, protein expression of p-Akt was determined by Western blotting as an indirect measure of Tie2 signaling. Membranes were stripped and reprobed with antibody recognizing total Akt (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western blot depicting immunodetectable p-Akt. Data are depicted relative to NVC and expressed as mean ± SEM of 8–10 animals per group (* p<0.05, ** p<0.01). NVC = non-ventilated controls; HV T = mice ventilated with high tidal volumes; Veh, 1 µg, 4 µg = mice intravenously treated with either vehicle (sterile saline), Ang-1 (1 µg per animal), or Ang-1 (4 µg per animal).

    Article Snippet: Antibodies recognized phospho (p)-Akt (Ser473; Cell Signaling, Danvers, MA), Ang-1 or Ang-2 (both Alpha Diagnostic, San Antonio, TX).

    Techniques: Expressing, Western Blot

    A: In total lung homogenates, mRNA expression of Ang-2 was determined by real time RT-PCR. Levels were normalized for expression of internal controls, i.e. the average value of β-actin and glyceraldehyde 3-phosphate dehydrogenase (GAPdH). No group differences in β-actin and GAPdH were observed. B: In total lung homogenates, protein expression of Ang-2 was determined by Western blotting. Membranes were reprobed with antibody recognizing total Akt (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western blot depicting immunodetectable Ang-2. Data are depicted relative to NVC and expressed as mean ± SEM of 7–16 animals per group (** p<0.01, *** p<0.001). NVC = non-ventilated controls; HV T = mice ventilated with high tidal volumes; Veh, 1 µg, 4 µg = mice intravenously treated with either vehicle (sterile saline), Ang-1 (1 µg per animal), or Ang-1 (4 µg per animal).

    Journal: PLoS ONE

    Article Title: Angiopoietin-1 Treatment Reduces Inflammation but Does Not Prevent Ventilator-Induced Lung Injury

    doi: 10.1371/journal.pone.0015653

    Figure Lengend Snippet: A: In total lung homogenates, mRNA expression of Ang-2 was determined by real time RT-PCR. Levels were normalized for expression of internal controls, i.e. the average value of β-actin and glyceraldehyde 3-phosphate dehydrogenase (GAPdH). No group differences in β-actin and GAPdH were observed. B: In total lung homogenates, protein expression of Ang-2 was determined by Western blotting. Membranes were reprobed with antibody recognizing total Akt (Akt1/PKBα) to control for equal loading. No group differences in total Akt were observed. Inset: representative Western blot depicting immunodetectable Ang-2. Data are depicted relative to NVC and expressed as mean ± SEM of 7–16 animals per group (** p<0.01, *** p<0.001). NVC = non-ventilated controls; HV T = mice ventilated with high tidal volumes; Veh, 1 µg, 4 µg = mice intravenously treated with either vehicle (sterile saline), Ang-1 (1 µg per animal), or Ang-1 (4 µg per animal).

    Article Snippet: Antibodies recognized phospho (p)-Akt (Ser473; Cell Signaling, Danvers, MA), Ang-1 or Ang-2 (both Alpha Diagnostic, San Antonio, TX).

    Techniques: Expressing, Quantitative RT-PCR, Western Blot

    (a) A time course of cell growth activity in BT474 cells in the presence of 100 nM trastuzumab, 100 nM bis-Fab 1325, or 10 nM heregulin. BT474 were cultured in media containing 10% fetal bovine serum for up to 84 hours. At 12-hour intervals total number of cells were determined; three plates from each treatment group were counted for the total number of cells and plotted as the mean cell count. The error bars indicate standard deviation from the mean. At approximately 60 hours (indicated by the arrow) the cells reached confluence in the agonist treatment groups. (b) BT474 cells were treated with 100 nM of trastuzumab, 100 nM of bis-Fab 1325, or 100 nM of bis-Fab 1329 for 10, 30 and 120 minutes. At times indicated, cell lysates were prepared and analyzed by immunoblotting using phospho-specific antibodies for HER3, AKT, and MAPK as well as antibodies recognizing total protein. Data are representative of three independent experiments. (c) Quantification of AKT phosphorylation after treatment with 100 nM bis-Fab 1325, 100 nM trastuzumab, 2 nM heregulin and a non-specific control antibody (anti-gD) by PathScan p-AKT1 (S473) ELISA. All data points were collected in triplicates and the mean of the triplicate absorbance values were used to calculate the percent change in pAKT compared to untreated control group. The error bars indicate standard deviation from the mean. Data are representative of three independent experiments. (d) A model for the HER2 dimerization patterns induced by either the agonist antibody-analogs or trastuzumab. The diagram depicts three potential dimer conformations; 1) the basal state induced by high cell surface density, 2) the activated state induced by the bis-Fab agonist, and 3) the inhibited state stabilized by trastuzumab. The cell growth activity of agonist bis-Fabs may be due to stabilization of an allosterically activated conformation between HER2–HER2 dimers. Trastuzumab's antagonistic activity may arise from dimer orientations that favor the inactive allosteric interactions between kinases. A non-stabilized dimer may represent the basal state where interactions between the juxtamembrane (black line) loop of the activator kinase and the C-terminal lobe of the receiver kinase are not fully stabilized without agonist binding.

    Journal: PLoS ONE

    Article Title: Reorienting the Fab Domains of Trastuzumab Results in Potent HER2 Activators

    doi: 10.1371/journal.pone.0051817

    Figure Lengend Snippet: (a) A time course of cell growth activity in BT474 cells in the presence of 100 nM trastuzumab, 100 nM bis-Fab 1325, or 10 nM heregulin. BT474 were cultured in media containing 10% fetal bovine serum for up to 84 hours. At 12-hour intervals total number of cells were determined; three plates from each treatment group were counted for the total number of cells and plotted as the mean cell count. The error bars indicate standard deviation from the mean. At approximately 60 hours (indicated by the arrow) the cells reached confluence in the agonist treatment groups. (b) BT474 cells were treated with 100 nM of trastuzumab, 100 nM of bis-Fab 1325, or 100 nM of bis-Fab 1329 for 10, 30 and 120 minutes. At times indicated, cell lysates were prepared and analyzed by immunoblotting using phospho-specific antibodies for HER3, AKT, and MAPK as well as antibodies recognizing total protein. Data are representative of three independent experiments. (c) Quantification of AKT phosphorylation after treatment with 100 nM bis-Fab 1325, 100 nM trastuzumab, 2 nM heregulin and a non-specific control antibody (anti-gD) by PathScan p-AKT1 (S473) ELISA. All data points were collected in triplicates and the mean of the triplicate absorbance values were used to calculate the percent change in pAKT compared to untreated control group. The error bars indicate standard deviation from the mean. Data are representative of three independent experiments. (d) A model for the HER2 dimerization patterns induced by either the agonist antibody-analogs or trastuzumab. The diagram depicts three potential dimer conformations; 1) the basal state induced by high cell surface density, 2) the activated state induced by the bis-Fab agonist, and 3) the inhibited state stabilized by trastuzumab. The cell growth activity of agonist bis-Fabs may be due to stabilization of an allosterically activated conformation between HER2–HER2 dimers. Trastuzumab's antagonistic activity may arise from dimer orientations that favor the inactive allosteric interactions between kinases. A non-stabilized dimer may represent the basal state where interactions between the juxtamembrane (black line) loop of the activator kinase and the C-terminal lobe of the receiver kinase are not fully stabilized without agonist binding.

    Article Snippet: The cell lysates described above were also evaluated with PathScan p-AKT1 (S473) Sandwich ELISA (Cat#7160, Cell Signaling Technology).

    Techniques: Activity Assay, Cell Culture, Cell Counting, Standard Deviation, Western Blot, Enzyme-linked Immunosorbent Assay, Binding Assay