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ppar adipor1  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology ppar adipor1
    Figure 4. Induction of proprotein convertase subtilisin kexin type 9 (PCSK9) expression by ADP355 (ADP) and AdipoRon (AR) is related to activation of AMP-activated protein kinase α (AMPKα). A, Expression of <t>AdipoR1</t> and AdipoR2 in the stable AdipoR1 and AdipoR2 knockdown HepG2 (shAR1i and shAR2i) cells was determined by real-time RT-PCR. **P<0.01 vs control (shNSi) cells (n=3). B, shNSi, shAR1i, or shAR2i cells received indicated treatment overnight. Expression of PCSK9, LDLR (low-density lipoprotein receptor), AMP- activated protein kinase α (AMPKα), and π-AMPKα was determined by Western blot. C and D, HepG2 cells were treated with ADP355 and AR at the indicated concentrations overnight. Expression of AMPKα and π-AMPKα was determined by Western blot. AICAR was used as a positive control. E, HepG2 cells were treated with AICAR or metformin (Met) at the indicated concentrations overnight followed by determination of PCSK9, AMPKα, π-AMPKα and PPARγ protein expression. F, CRISPR-Ctrl (clustered regulatory interspaced short palindromic repeat-associated 9) and CRISPR-AMPKα1 HepG2 cells were treated with ADP at the indicated concentrations overnight followed by determination of AMPKα1, PPARγ, and PCSK9 protein expression. G and H, Primary hepatocytes isolated from PPARγfl/fl and HepPPARγ KO mice were treated with AICAR or Met at the indicated concentrations overnight. Expression of PCSK9 protein (G) and mRNA (H) was determined by Western blot and real-time RT-PCR, respectively. *P<0.05 vs control (n=3).
    Ppar Adipor1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 27 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ppar adipor1/product/Santa Cruz Biotechnology
    Average 93 stars, based on 27 article reviews
    ppar adipor1 - by Bioz Stars, 2026-03
    93/100 stars

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    1) Product Images from "Activation of Adiponectin Receptor Regulates Proprotein Convertase Subtilisin/Kexin Type 9 Expression and Inhibits Lesions in ApoE-Deficient Mice."

    Article Title: Activation of Adiponectin Receptor Regulates Proprotein Convertase Subtilisin/Kexin Type 9 Expression and Inhibits Lesions in ApoE-Deficient Mice.

    Journal: Arteriosclerosis, thrombosis, and vascular biology

    doi: 10.1161/ATVBAHA.117.309630

    Figure 4. Induction of proprotein convertase subtilisin kexin type 9 (PCSK9) expression by ADP355 (ADP) and AdipoRon (AR) is related to activation of AMP-activated protein kinase α (AMPKα). A, Expression of AdipoR1 and AdipoR2 in the stable AdipoR1 and AdipoR2 knockdown HepG2 (shAR1i and shAR2i) cells was determined by real-time RT-PCR. **P<0.01 vs control (shNSi) cells (n=3). B, shNSi, shAR1i, or shAR2i cells received indicated treatment overnight. Expression of PCSK9, LDLR (low-density lipoprotein receptor), AMP- activated protein kinase α (AMPKα), and π-AMPKα was determined by Western blot. C and D, HepG2 cells were treated with ADP355 and AR at the indicated concentrations overnight. Expression of AMPKα and π-AMPKα was determined by Western blot. AICAR was used as a positive control. E, HepG2 cells were treated with AICAR or metformin (Met) at the indicated concentrations overnight followed by determination of PCSK9, AMPKα, π-AMPKα and PPARγ protein expression. F, CRISPR-Ctrl (clustered regulatory interspaced short palindromic repeat-associated 9) and CRISPR-AMPKα1 HepG2 cells were treated with ADP at the indicated concentrations overnight followed by determination of AMPKα1, PPARγ, and PCSK9 protein expression. G and H, Primary hepatocytes isolated from PPARγfl/fl and HepPPARγ KO mice were treated with AICAR or Met at the indicated concentrations overnight. Expression of PCSK9 protein (G) and mRNA (H) was determined by Western blot and real-time RT-PCR, respectively. *P<0.05 vs control (n=3).
    Figure Legend Snippet: Figure 4. Induction of proprotein convertase subtilisin kexin type 9 (PCSK9) expression by ADP355 (ADP) and AdipoRon (AR) is related to activation of AMP-activated protein kinase α (AMPKα). A, Expression of AdipoR1 and AdipoR2 in the stable AdipoR1 and AdipoR2 knockdown HepG2 (shAR1i and shAR2i) cells was determined by real-time RT-PCR. **P<0.01 vs control (shNSi) cells (n=3). B, shNSi, shAR1i, or shAR2i cells received indicated treatment overnight. Expression of PCSK9, LDLR (low-density lipoprotein receptor), AMP- activated protein kinase α (AMPKα), and π-AMPKα was determined by Western blot. C and D, HepG2 cells were treated with ADP355 and AR at the indicated concentrations overnight. Expression of AMPKα and π-AMPKα was determined by Western blot. AICAR was used as a positive control. E, HepG2 cells were treated with AICAR or metformin (Met) at the indicated concentrations overnight followed by determination of PCSK9, AMPKα, π-AMPKα and PPARγ protein expression. F, CRISPR-Ctrl (clustered regulatory interspaced short palindromic repeat-associated 9) and CRISPR-AMPKα1 HepG2 cells were treated with ADP at the indicated concentrations overnight followed by determination of AMPKα1, PPARγ, and PCSK9 protein expression. G and H, Primary hepatocytes isolated from PPARγfl/fl and HepPPARγ KO mice were treated with AICAR or Met at the indicated concentrations overnight. Expression of PCSK9 protein (G) and mRNA (H) was determined by Western blot and real-time RT-PCR, respectively. *P<0.05 vs control (n=3).

    Techniques Used: Expressing, Activation Assay, Knockdown, Quantitative RT-PCR, Control, Western Blot, Positive Control, CRISPR, Isolation



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    Santa Cruz Biotechnology ppar adipor1
    Figure 4. Induction of proprotein convertase subtilisin kexin type 9 (PCSK9) expression by ADP355 (ADP) and AdipoRon (AR) is related to activation of AMP-activated protein kinase α (AMPKα). A, Expression of <t>AdipoR1</t> and AdipoR2 in the stable AdipoR1 and AdipoR2 knockdown HepG2 (shAR1i and shAR2i) cells was determined by real-time RT-PCR. **P<0.01 vs control (shNSi) cells (n=3). B, shNSi, shAR1i, or shAR2i cells received indicated treatment overnight. Expression of PCSK9, LDLR (low-density lipoprotein receptor), AMP- activated protein kinase α (AMPKα), and π-AMPKα was determined by Western blot. C and D, HepG2 cells were treated with ADP355 and AR at the indicated concentrations overnight. Expression of AMPKα and π-AMPKα was determined by Western blot. AICAR was used as a positive control. E, HepG2 cells were treated with AICAR or metformin (Met) at the indicated concentrations overnight followed by determination of PCSK9, AMPKα, π-AMPKα and PPARγ protein expression. F, CRISPR-Ctrl (clustered regulatory interspaced short palindromic repeat-associated 9) and CRISPR-AMPKα1 HepG2 cells were treated with ADP at the indicated concentrations overnight followed by determination of AMPKα1, PPARγ, and PCSK9 protein expression. G and H, Primary hepatocytes isolated from PPARγfl/fl and HepPPARγ KO mice were treated with AICAR or Met at the indicated concentrations overnight. Expression of PCSK9 protein (G) and mRNA (H) was determined by Western blot and real-time RT-PCR, respectively. *P<0.05 vs control (n=3).
    Ppar Adipor1, 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/ppar adipor1/product/Santa Cruz Biotechnology
    Average 93 stars, based on 1 article reviews
    ppar adipor1 - by Bioz Stars, 2026-03
    93/100 stars
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    Figure 4. Induction of proprotein convertase subtilisin kexin type 9 (PCSK9) expression by ADP355 (ADP) and AdipoRon (AR) is related to activation of AMP-activated protein kinase α (AMPKα). A, Expression of AdipoR1 and AdipoR2 in the stable AdipoR1 and AdipoR2 knockdown HepG2 (shAR1i and shAR2i) cells was determined by real-time RT-PCR. **P<0.01 vs control (shNSi) cells (n=3). B, shNSi, shAR1i, or shAR2i cells received indicated treatment overnight. Expression of PCSK9, LDLR (low-density lipoprotein receptor), AMP- activated protein kinase α (AMPKα), and π-AMPKα was determined by Western blot. C and D, HepG2 cells were treated with ADP355 and AR at the indicated concentrations overnight. Expression of AMPKα and π-AMPKα was determined by Western blot. AICAR was used as a positive control. E, HepG2 cells were treated with AICAR or metformin (Met) at the indicated concentrations overnight followed by determination of PCSK9, AMPKα, π-AMPKα and PPARγ protein expression. F, CRISPR-Ctrl (clustered regulatory interspaced short palindromic repeat-associated 9) and CRISPR-AMPKα1 HepG2 cells were treated with ADP at the indicated concentrations overnight followed by determination of AMPKα1, PPARγ, and PCSK9 protein expression. G and H, Primary hepatocytes isolated from PPARγfl/fl and HepPPARγ KO mice were treated with AICAR or Met at the indicated concentrations overnight. Expression of PCSK9 protein (G) and mRNA (H) was determined by Western blot and real-time RT-PCR, respectively. *P<0.05 vs control (n=3).

    Journal: Arteriosclerosis, thrombosis, and vascular biology

    Article Title: Activation of Adiponectin Receptor Regulates Proprotein Convertase Subtilisin/Kexin Type 9 Expression and Inhibits Lesions in ApoE-Deficient Mice.

    doi: 10.1161/ATVBAHA.117.309630

    Figure Lengend Snippet: Figure 4. Induction of proprotein convertase subtilisin kexin type 9 (PCSK9) expression by ADP355 (ADP) and AdipoRon (AR) is related to activation of AMP-activated protein kinase α (AMPKα). A, Expression of AdipoR1 and AdipoR2 in the stable AdipoR1 and AdipoR2 knockdown HepG2 (shAR1i and shAR2i) cells was determined by real-time RT-PCR. **P<0.01 vs control (shNSi) cells (n=3). B, shNSi, shAR1i, or shAR2i cells received indicated treatment overnight. Expression of PCSK9, LDLR (low-density lipoprotein receptor), AMP- activated protein kinase α (AMPKα), and π-AMPKα was determined by Western blot. C and D, HepG2 cells were treated with ADP355 and AR at the indicated concentrations overnight. Expression of AMPKα and π-AMPKα was determined by Western blot. AICAR was used as a positive control. E, HepG2 cells were treated with AICAR or metformin (Met) at the indicated concentrations overnight followed by determination of PCSK9, AMPKα, π-AMPKα and PPARγ protein expression. F, CRISPR-Ctrl (clustered regulatory interspaced short palindromic repeat-associated 9) and CRISPR-AMPKα1 HepG2 cells were treated with ADP at the indicated concentrations overnight followed by determination of AMPKα1, PPARγ, and PCSK9 protein expression. G and H, Primary hepatocytes isolated from PPARγfl/fl and HepPPARγ KO mice were treated with AICAR or Met at the indicated concentrations overnight. Expression of PCSK9 protein (G) and mRNA (H) was determined by Western blot and real-time RT-PCR, respectively. *P<0.05 vs control (n=3).

    Article Snippet: 4 Inhibition of PPAR AdipoR1 and AdipoR2 expression by siRNA The siRNA was purchased from Santa Cruz Biotechnology (Dallas, TX).

    Techniques: Expressing, Activation Assay, Knockdown, Quantitative RT-PCR, Control, Western Blot, Positive Control, CRISPR, Isolation