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U73122 PLC g15
βE2 treatment prevented the PCSK9-mediated LDLR degradation by activating GPR30. (A) βE2-treated cells for 4 h with and without <t>G15</t> were visualized for the internalization of AF− PCSK9 (25 μg/mL) by fluorescence microscopy. (B,C) Immunofluorescence staining of LDLR and clathrin, and the intensity of which was quantified in βE2-treated cells treated with and without G15, respectively. (D) After 4 h, the cells were exposed to BODIPY-labeled LDL, and then, the uptake was visualized through fluorescence microscopy. Fluorescence intensity was quantified with a SpectraMax M5 reader. Values represent the means ± SEM, n = 3, * P
G15, supplied by U73122 PLC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "17β-Estradiol Inhibits PCSK9-Mediated LDLR Degradation Through GPER/PLC Activation in HepG2 Cells"

Article Title: 17β-Estradiol Inhibits PCSK9-Mediated LDLR Degradation Through GPER/PLC Activation in HepG2 Cells

Journal: Frontiers in Endocrinology

doi: 10.3389/fendo.2019.00930

βE2 treatment prevented the PCSK9-mediated LDLR degradation by activating GPR30. (A) βE2-treated cells for 4 h with and without G15 were visualized for the internalization of AF− PCSK9 (25 μg/mL) by fluorescence microscopy. (B,C) Immunofluorescence staining of LDLR and clathrin, and the intensity of which was quantified in βE2-treated cells treated with and without G15, respectively. (D) After 4 h, the cells were exposed to BODIPY-labeled LDL, and then, the uptake was visualized through fluorescence microscopy. Fluorescence intensity was quantified with a SpectraMax M5 reader. Values represent the means ± SEM, n = 3, * P
Figure Legend Snippet: βE2 treatment prevented the PCSK9-mediated LDLR degradation by activating GPR30. (A) βE2-treated cells for 4 h with and without G15 were visualized for the internalization of AF− PCSK9 (25 μg/mL) by fluorescence microscopy. (B,C) Immunofluorescence staining of LDLR and clathrin, and the intensity of which was quantified in βE2-treated cells treated with and without G15, respectively. (D) After 4 h, the cells were exposed to BODIPY-labeled LDL, and then, the uptake was visualized through fluorescence microscopy. Fluorescence intensity was quantified with a SpectraMax M5 reader. Values represent the means ± SEM, n = 3, * P

Techniques Used: Fluorescence, Microscopy, Immunofluorescence, Staining, Labeling

Related Articles

Incubation:

Article Title: 17β-Estradiol Inhibits PCSK9-Mediated LDLR Degradation Through GPER/PLC Activation in HepG2 Cells
Article Snippet: .. The effects of βE2 can be blocked by G15 and U73122 (PLC inhibitor) pretreatment of cells ( ) for 15 min. Phospholipase C-γ (PLCγ), in the Ca2+ signaling pathway, was also activated after a 5 min βE2 incubation. .. The effect of βE2 can be blocked by G15 pretreatment , indicating the rapid activation of PLCγ through GPER stimulation.

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    U73122 PLC g15
    βE2 treatment prevented the PCSK9-mediated LDLR degradation by activating GPR30. (A) βE2-treated cells for 4 h with and without <t>G15</t> were visualized for the internalization of AF− PCSK9 (25 μg/mL) by fluorescence microscopy. (B,C) Immunofluorescence staining of LDLR and clathrin, and the intensity of which was quantified in βE2-treated cells treated with and without G15, respectively. (D) After 4 h, the cells were exposed to BODIPY-labeled LDL, and then, the uptake was visualized through fluorescence microscopy. Fluorescence intensity was quantified with a SpectraMax M5 reader. Values represent the means ± SEM, n = 3, * P
    G15, supplied by U73122 PLC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/g15/product/U73122 PLC
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    g15 - by Bioz Stars, 2020-11
    94/100 stars
      Buy from Supplier

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    βE2 treatment prevented the PCSK9-mediated LDLR degradation by activating GPR30. (A) βE2-treated cells for 4 h with and without G15 were visualized for the internalization of AF− PCSK9 (25 μg/mL) by fluorescence microscopy. (B,C) Immunofluorescence staining of LDLR and clathrin, and the intensity of which was quantified in βE2-treated cells treated with and without G15, respectively. (D) After 4 h, the cells were exposed to BODIPY-labeled LDL, and then, the uptake was visualized through fluorescence microscopy. Fluorescence intensity was quantified with a SpectraMax M5 reader. Values represent the means ± SEM, n = 3, * P

    Journal: Frontiers in Endocrinology

    Article Title: 17β-Estradiol Inhibits PCSK9-Mediated LDLR Degradation Through GPER/PLC Activation in HepG2 Cells

    doi: 10.3389/fendo.2019.00930

    Figure Lengend Snippet: βE2 treatment prevented the PCSK9-mediated LDLR degradation by activating GPR30. (A) βE2-treated cells for 4 h with and without G15 were visualized for the internalization of AF− PCSK9 (25 μg/mL) by fluorescence microscopy. (B,C) Immunofluorescence staining of LDLR and clathrin, and the intensity of which was quantified in βE2-treated cells treated with and without G15, respectively. (D) After 4 h, the cells were exposed to BODIPY-labeled LDL, and then, the uptake was visualized through fluorescence microscopy. Fluorescence intensity was quantified with a SpectraMax M5 reader. Values represent the means ± SEM, n = 3, * P

    Article Snippet: The effects of βE2 can be blocked by G15 and U73122 (PLC inhibitor) pretreatment of cells ( ) for 15 min. Phospholipase C-γ (PLCγ), in the Ca2+ signaling pathway, was also activated after a 5 min βE2 incubation.

    Techniques: Fluorescence, Microscopy, Immunofluorescence, Staining, Labeling