antibodies against phosphor 4e bp1 ser65 thr70  (Santa Cruz Biotechnology)

 
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    Santa Cruz Biotechnology antibodies against phosphor 4e bp1 ser65 thr70
    Angiogenesis-related proteins are affected by TF3 treatment in OVCAR-3 cells. Western blot analysis revealed that TF3 decreased the protein level of p-Akt, p-mTOR, <t>p-p70S6K,</t> <t>p-4E-BP1,</t> Notch-1 (NICD), c-Myc and HIF-1α in OVCAR-3 cells. TF3 had no impact on the protein level of p-ERK1/2, ERK1/2, JNK, p38 and p-FoxO 1. GAPDH served as the loading control.
    Antibodies Against Phosphor 4e Bp1 Ser65 Thr70, supplied by Santa Cruz Biotechnology, 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/antibodies against phosphor 4e bp1 ser65 thr70/product/Santa Cruz Biotechnology
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies against phosphor 4e bp1 ser65 thr70 - by Bioz Stars, 2023-09
    93/100 stars

    Images

    1) Product Images from "Theaflavin-3, 3′-digallate decreases human ovarian carcinoma OVCAR-3 cell-induced angiogenesis via Akt and Notch-1 pathways, not via MAPK pathways"

    Article Title: Theaflavin-3, 3′-digallate decreases human ovarian carcinoma OVCAR-3 cell-induced angiogenesis via Akt and Notch-1 pathways, not via MAPK pathways

    Journal: International Journal of Oncology

    doi: 10.3892/ijo.2015.3257

    Angiogenesis-related proteins are affected by TF3 treatment in OVCAR-3 cells. Western blot analysis revealed that TF3 decreased the protein level of p-Akt, p-mTOR, p-p70S6K, p-4E-BP1, Notch-1 (NICD), c-Myc and HIF-1α in OVCAR-3 cells. TF3 had no impact on the protein level of p-ERK1/2, ERK1/2, JNK, p38 and p-FoxO 1. GAPDH served as the loading control.
    Figure Legend Snippet: Angiogenesis-related proteins are affected by TF3 treatment in OVCAR-3 cells. Western blot analysis revealed that TF3 decreased the protein level of p-Akt, p-mTOR, p-p70S6K, p-4E-BP1, Notch-1 (NICD), c-Myc and HIF-1α in OVCAR-3 cells. TF3 had no impact on the protein level of p-ERK1/2, ERK1/2, JNK, p38 and p-FoxO 1. GAPDH served as the loading control.

    Techniques Used: Western Blot

    Akt/mTOR/p70S6k/4E-BP1 pathway and Akt/c-Myc pathway are involved in TF3-induced inhibition of HIF-1α and VEGF. (A) Western blot analysis showed that 100 nM wortmannin, 10 μM TF3 and 100 nM wortmannin+10 μM TF3 decreased the phosphorylation of Akt, mTOR, p70S6K and 4E-BP1, and expression of c-Myc and HIF-1α. TF3+wortmannin exhibited the strongest effect among them. GAPDH served as the loading control. (B) Luciferase reporter assay and (C) VEGF ELISA showed 100 nM wortmannin, 10 μM TF3 and 100 nM wortmannin+10 μM TF3 suppressed the transcriptional activity of VEGF promoter and VEGF secretion, respectively. TF3+wortmannin elicited strongest effect among them. (D) Overexpression of active Akt attenuated the 15 μM TF3-induced decrease of phosphorylation of Akt, mTOR, p70S6K and 4E-BP1, and expression of c-Myc and HIF-1α. Overexpression of Akt, mTOR, p70S6K or 4E-BP1 attenuated TF3-induced inhibition of transcriptional activity of VEGF promoter (E) and HIF-1α promoter (F). (G) Overexpression of active Akt reversed the 15 μM TF3-induced reduction of VEGF secretion. The data are presented as the mean ± standard error of mean. * P<0.05 compared with control or between specific groups.
    Figure Legend Snippet: Akt/mTOR/p70S6k/4E-BP1 pathway and Akt/c-Myc pathway are involved in TF3-induced inhibition of HIF-1α and VEGF. (A) Western blot analysis showed that 100 nM wortmannin, 10 μM TF3 and 100 nM wortmannin+10 μM TF3 decreased the phosphorylation of Akt, mTOR, p70S6K and 4E-BP1, and expression of c-Myc and HIF-1α. TF3+wortmannin exhibited the strongest effect among them. GAPDH served as the loading control. (B) Luciferase reporter assay and (C) VEGF ELISA showed 100 nM wortmannin, 10 μM TF3 and 100 nM wortmannin+10 μM TF3 suppressed the transcriptional activity of VEGF promoter and VEGF secretion, respectively. TF3+wortmannin elicited strongest effect among them. (D) Overexpression of active Akt attenuated the 15 μM TF3-induced decrease of phosphorylation of Akt, mTOR, p70S6K and 4E-BP1, and expression of c-Myc and HIF-1α. Overexpression of Akt, mTOR, p70S6K or 4E-BP1 attenuated TF3-induced inhibition of transcriptional activity of VEGF promoter (E) and HIF-1α promoter (F). (G) Overexpression of active Akt reversed the 15 μM TF3-induced reduction of VEGF secretion. The data are presented as the mean ± standard error of mean. * P<0.05 compared with control or between specific groups.

    Techniques Used: Inhibition, Western Blot, Expressing, Luciferase, Reporter Assay, Enzyme-linked Immunosorbent Assay, Activity Assay, Over Expression

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    • antibodies against phosphor 4e bp1 ser65 thr70  (Santa Cruz Biotechnology)
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    Santa Cruz Biotechnology antibodies against phosphor 4e bp1 ser65 thr70
    Angiogenesis-related proteins are affected by TF3 treatment in OVCAR-3 cells. Western blot analysis revealed that TF3 decreased the protein level of p-Akt, p-mTOR, <t>p-p70S6K,</t> <t>p-4E-BP1,</t> Notch-1 (NICD), c-Myc and HIF-1α in OVCAR-3 cells. TF3 had no impact on the protein level of p-ERK1/2, ERK1/2, JNK, p38 and p-FoxO 1. GAPDH served as the loading control.
    Antibodies Against Phosphor 4e Bp1 Ser65 Thr70, supplied by Santa Cruz Biotechnology, 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/antibodies against phosphor 4e bp1 ser65 thr70/product/Santa Cruz Biotechnology
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies against phosphor 4e bp1 ser65 thr70 - by Bioz Stars, 2023-09
    93/100 stars
    		  Buy from Supplier

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    Angiogenesis-related proteins are affected by TF3 treatment in OVCAR-3 cells. Western blot analysis revealed that TF3 decreased the protein level of p-Akt, p-mTOR, p-p70S6K, p-4E-BP1, Notch-1 (NICD), c-Myc and HIF-1α in OVCAR-3 cells. TF3 had no impact on the protein level of p-ERK1/2, ERK1/2, JNK, p38 and p-FoxO 1. GAPDH served as the loading control.

    Journal: International Journal of Oncology

    Article Title: Theaflavin-3, 3′-digallate decreases human ovarian carcinoma OVCAR-3 cell-induced angiogenesis via Akt and Notch-1 pathways, not via MAPK pathways

    doi: 10.3892/ijo.2015.3257

    Figure Lengend Snippet: Angiogenesis-related proteins are affected by TF3 treatment in OVCAR-3 cells. Western blot analysis revealed that TF3 decreased the protein level of p-Akt, p-mTOR, p-p70S6K, p-4E-BP1, Notch-1 (NICD), c-Myc and HIF-1α in OVCAR-3 cells. TF3 had no impact on the protein level of p-ERK1/2, ERK1/2, JNK, p38 and p-FoxO 1. GAPDH served as the loading control.

    Article Snippet: Antibodies against phosphor-4E-BP1 (Ser65/Thr70) (p-4E-BP1), c-Myc, phosphor-extracellular signal-regulated kinases 1/2 (Thr202/Tyr204) (p-ERK1/2), ERK1/2 and GAPDH were purchased from Santa Cruz Biotechnology Inc. (Santa Cruz).

    Techniques: Western Blot

    Akt/mTOR/p70S6k/4E-BP1 pathway and Akt/c-Myc pathway are involved in TF3-induced inhibition of HIF-1α and VEGF. (A) Western blot analysis showed that 100 nM wortmannin, 10 μM TF3 and 100 nM wortmannin+10 μM TF3 decreased the phosphorylation of Akt, mTOR, p70S6K and 4E-BP1, and expression of c-Myc and HIF-1α. TF3+wortmannin exhibited the strongest effect among them. GAPDH served as the loading control. (B) Luciferase reporter assay and (C) VEGF ELISA showed 100 nM wortmannin, 10 μM TF3 and 100 nM wortmannin+10 μM TF3 suppressed the transcriptional activity of VEGF promoter and VEGF secretion, respectively. TF3+wortmannin elicited strongest effect among them. (D) Overexpression of active Akt attenuated the 15 μM TF3-induced decrease of phosphorylation of Akt, mTOR, p70S6K and 4E-BP1, and expression of c-Myc and HIF-1α. Overexpression of Akt, mTOR, p70S6K or 4E-BP1 attenuated TF3-induced inhibition of transcriptional activity of VEGF promoter (E) and HIF-1α promoter (F). (G) Overexpression of active Akt reversed the 15 μM TF3-induced reduction of VEGF secretion. The data are presented as the mean ± standard error of mean. * P<0.05 compared with control or between specific groups.

    Journal: International Journal of Oncology

    Article Title: Theaflavin-3, 3′-digallate decreases human ovarian carcinoma OVCAR-3 cell-induced angiogenesis via Akt and Notch-1 pathways, not via MAPK pathways

    doi: 10.3892/ijo.2015.3257

    Figure Lengend Snippet: Akt/mTOR/p70S6k/4E-BP1 pathway and Akt/c-Myc pathway are involved in TF3-induced inhibition of HIF-1α and VEGF. (A) Western blot analysis showed that 100 nM wortmannin, 10 μM TF3 and 100 nM wortmannin+10 μM TF3 decreased the phosphorylation of Akt, mTOR, p70S6K and 4E-BP1, and expression of c-Myc and HIF-1α. TF3+wortmannin exhibited the strongest effect among them. GAPDH served as the loading control. (B) Luciferase reporter assay and (C) VEGF ELISA showed 100 nM wortmannin, 10 μM TF3 and 100 nM wortmannin+10 μM TF3 suppressed the transcriptional activity of VEGF promoter and VEGF secretion, respectively. TF3+wortmannin elicited strongest effect among them. (D) Overexpression of active Akt attenuated the 15 μM TF3-induced decrease of phosphorylation of Akt, mTOR, p70S6K and 4E-BP1, and expression of c-Myc and HIF-1α. Overexpression of Akt, mTOR, p70S6K or 4E-BP1 attenuated TF3-induced inhibition of transcriptional activity of VEGF promoter (E) and HIF-1α promoter (F). (G) Overexpression of active Akt reversed the 15 μM TF3-induced reduction of VEGF secretion. The data are presented as the mean ± standard error of mean. * P<0.05 compared with control or between specific groups.

    Article Snippet: Antibodies against phosphor-4E-BP1 (Ser65/Thr70) (p-4E-BP1), c-Myc, phosphor-extracellular signal-regulated kinases 1/2 (Thr202/Tyr204) (p-ERK1/2), ERK1/2 and GAPDH were purchased from Santa Cruz Biotechnology Inc. (Santa Cruz).

    Techniques: Inhibition, Western Blot, Expressing, Luciferase, Reporter Assay, Enzyme-linked Immunosorbent Assay, Activity Assay, Over Expression