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dominant negative s6k  (Addgene inc)


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    Addgene inc dominant negative s6k
    Dominant Negative S6k, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/dominant negative s6k/product/Addgene inc
    Average 93 stars, based on 14 article reviews
    dominant negative s6k - by Bioz Stars, 2026-02
    93/100 stars

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    dominant negative s6k  (Addgene inc)
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    prk7-ha-s6k1-kr plasmid dominant-negative s6k  (Addgene inc)
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    Addgene inc prk7-ha-s6k1-kr plasmid dominant-negative s6k
    Mammalian target of rapamycin (mTOR) in PDGF-induced tube formation. The role of <t>mTOR/S6K</t> in PDGF-induced tube formation was tested with mTOR inhibitor (rapamycin) and protein synthesis inhibitor cycloheximide (CHX). A: representative images of tube formation in the presence of rapamycin and CHX. Insulin was used as a positive control in induction of mTOR activation. Rapamycin (200 nM) and CHX (20 ng/ml) were used to pretreat cells for 30 min, followed by treatment of PDGF (50 ng/ml) or insulin (100 nM) for 10 h. B: quantification of tube formation. C: representative Western blots for mTOR/S6K signaling pathway in endothelial cells. Phosphorylation of S6K was determined in SVEC4-10 cells after treatment with PDGF or insulin. D: quantification of Western blot signals. In this figure, all experiments were repeated 3 times with consistent results. Each data point represents mean ± SE (n = 3 experiments).
    Prk7 Ha S6k1 Kr Plasmid Dominant Negative S6k, supplied by Addgene inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Mammalian target of rapamycin (mTOR) in PDGF-induced tube formation. The role of mTOR/S6K in PDGF-induced tube formation was tested with mTOR inhibitor (rapamycin) and protein synthesis inhibitor cycloheximide (CHX). A: representative images of tube formation in the presence of rapamycin and CHX. Insulin was used as a positive control in induction of mTOR activation. Rapamycin (200 nM) and CHX (20 ng/ml) were used to pretreat cells for 30 min, followed by treatment of PDGF (50 ng/ml) or insulin (100 nM) for 10 h. B: quantification of tube formation. C: representative Western blots for mTOR/S6K signaling pathway in endothelial cells. Phosphorylation of S6K was determined in SVEC4-10 cells after treatment with PDGF or insulin. D: quantification of Western blot signals. In this figure, all experiments were repeated 3 times with consistent results. Each data point represents mean ± SE (n = 3 experiments).

    Journal:

    Article Title: Macrophage infiltration into adipose tissue may promote angiogenesis for adipose tissue remodeling in obesity

    doi: 10.1152/ajpendo.90296.2008

    Figure Lengend Snippet: Mammalian target of rapamycin (mTOR) in PDGF-induced tube formation. The role of mTOR/S6K in PDGF-induced tube formation was tested with mTOR inhibitor (rapamycin) and protein synthesis inhibitor cycloheximide (CHX). A: representative images of tube formation in the presence of rapamycin and CHX. Insulin was used as a positive control in induction of mTOR activation. Rapamycin (200 nM) and CHX (20 ng/ml) were used to pretreat cells for 30 min, followed by treatment of PDGF (50 ng/ml) or insulin (100 nM) for 10 h. B: quantification of tube formation. C: representative Western blots for mTOR/S6K signaling pathway in endothelial cells. Phosphorylation of S6K was determined in SVEC4-10 cells after treatment with PDGF or insulin. D: quantification of Western blot signals. In this figure, all experiments were repeated 3 times with consistent results. Each data point represents mean ± SE (n = 3 experiments).

    Article Snippet: The SVEC4-10 endothelial cells were cotransfected with 3 μg of pRK7-HA-S6K1-KR plasmid for dominant-negative S6K (8985, Addgene) and 0.5 μg of pcDNA3.1 plasmid for neomycin resistance.

    Techniques: Positive Control, Activation Assay, Western Blot

    S6K in PDGF-induced tube formation. A: expression of dominant-negative S6K (S6K-DN) in stable cells. B: inhibition of S6K activity by S6K-DN mutant. C: tube formation in stable cells in response to PDGF. D: quantification of tube formation. In this figure, all experiments were repeated 3 times with consistent results. Each data point represents mean ± SE (n = 3 experiments).

    Journal:

    Article Title: Macrophage infiltration into adipose tissue may promote angiogenesis for adipose tissue remodeling in obesity

    doi: 10.1152/ajpendo.90296.2008

    Figure Lengend Snippet: S6K in PDGF-induced tube formation. A: expression of dominant-negative S6K (S6K-DN) in stable cells. B: inhibition of S6K activity by S6K-DN mutant. C: tube formation in stable cells in response to PDGF. D: quantification of tube formation. In this figure, all experiments were repeated 3 times with consistent results. Each data point represents mean ± SE (n = 3 experiments).

    Article Snippet: The SVEC4-10 endothelial cells were cotransfected with 3 μg of pRK7-HA-S6K1-KR plasmid for dominant-negative S6K (8985, Addgene) and 0.5 μg of pcDNA3.1 plasmid for neomycin resistance.

    Techniques: Expressing, Dominant Negative Mutation, Inhibition, Activity Assay, Mutagenesis

    S6K in tube formation induced by albumin. A: Induction of phosphorylation of S6K by albumin. Phosphorylation of S6K was examined in whole cell lysate in Western blot. B: BSA-stimulated tube formation and inhibition by rapamycin (200 nM). C: quantification of tube formation. D: cell viability after rapamycin treatment. Cell viability was determined with MTT assay at 24 h after cell exposure to rapamycin. In this figure, all experiments were repeated 3 times with consistent results. Each data points represents mean ± SE (n = 3 experiments).

    Journal:

    Article Title: Macrophage infiltration into adipose tissue may promote angiogenesis for adipose tissue remodeling in obesity

    doi: 10.1152/ajpendo.90296.2008

    Figure Lengend Snippet: S6K in tube formation induced by albumin. A: Induction of phosphorylation of S6K by albumin. Phosphorylation of S6K was examined in whole cell lysate in Western blot. B: BSA-stimulated tube formation and inhibition by rapamycin (200 nM). C: quantification of tube formation. D: cell viability after rapamycin treatment. Cell viability was determined with MTT assay at 24 h after cell exposure to rapamycin. In this figure, all experiments were repeated 3 times with consistent results. Each data points represents mean ± SE (n = 3 experiments).

    Article Snippet: The SVEC4-10 endothelial cells were cotransfected with 3 μg of pRK7-HA-S6K1-KR plasmid for dominant-negative S6K (8985, Addgene) and 0.5 μg of pcDNA3.1 plasmid for neomycin resistance.

    Techniques: Western Blot, Inhibition, MTT Assay