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recombinant mouse fetuin a  (R&D Systems)


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    Structured Review

    R&D Systems recombinant mouse fetuin a
    Recombinant Mouse Fetuin A, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant mouse fetuin a/product/R&D Systems
    Average 92 stars, based on 4 article reviews
    recombinant mouse fetuin a - by Bioz Stars, 2026-03
    92/100 stars

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    R&D Systems recombinant fetuin a protein
    Expression of <t>fetuin</t> <t>B</t> in HepG2 cells and mice. The levels of fetuin B mRNA and protein in HepG2 cells and cell culture supernatants increased with FFAs compared with controls. The levels of fetuin B mRNA and protein in mice increased in the HFD group compared with the SCD group. A: The mRNA levels: Control vs. FFAs (P < 0.001); B: The protein expression of fetuin B in HepG2 cells; C: The protein levels in the culture supernatants of HepG2 cells (P < 0.001); (HepG2 experiment) Results are the mean ± SD of three independent experiments, each repeated in triplicate. D: The hepatic mRNA level: SCD vs. HFD (P < 0.001); E: The hepatic protein expression; F: The serum levels (SCD vs. HFD, P = 0.010); (Mouse experiment) Results are the mean ± SD of three independent experiments (n = 6, each group).
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    Image Search Results


    Expression of fetuin B in HepG2 cells and mice. The levels of fetuin B mRNA and protein in HepG2 cells and cell culture supernatants increased with FFAs compared with controls. The levels of fetuin B mRNA and protein in mice increased in the HFD group compared with the SCD group. A: The mRNA levels: Control vs. FFAs (P < 0.001); B: The protein expression of fetuin B in HepG2 cells; C: The protein levels in the culture supernatants of HepG2 cells (P < 0.001); (HepG2 experiment) Results are the mean ± SD of three independent experiments, each repeated in triplicate. D: The hepatic mRNA level: SCD vs. HFD (P < 0.001); E: The hepatic protein expression; F: The serum levels (SCD vs. HFD, P = 0.010); (Mouse experiment) Results are the mean ± SD of three independent experiments (n = 6, each group).

    Journal: American Journal of Translational Research

    Article Title: Fetuin B aggravates liver X receptor-mediated hepatic steatosis through AMPK in HepG2 cells and mice

    doi:

    Figure Lengend Snippet: Expression of fetuin B in HepG2 cells and mice. The levels of fetuin B mRNA and protein in HepG2 cells and cell culture supernatants increased with FFAs compared with controls. The levels of fetuin B mRNA and protein in mice increased in the HFD group compared with the SCD group. A: The mRNA levels: Control vs. FFAs (P < 0.001); B: The protein expression of fetuin B in HepG2 cells; C: The protein levels in the culture supernatants of HepG2 cells (P < 0.001); (HepG2 experiment) Results are the mean ± SD of three independent experiments, each repeated in triplicate. D: The hepatic mRNA level: SCD vs. HFD (P < 0.001); E: The hepatic protein expression; F: The serum levels (SCD vs. HFD, P = 0.010); (Mouse experiment) Results are the mean ± SD of three independent experiments (n = 6, each group).

    Article Snippet: Vehicle (20 mM Tris-HCL, Invitrogen, Carlsbad, CA) or recombinant mouse fetuin B (RPB860Mu0, Cloud-Clone Corp., Houston, TX) was infused using s.c. implanted osmotic pumps (Alzet #1002, Durect Corp., CA) for the 10-day duration.

    Techniques: Expressing, Cell Culture

    Recombinant fetuin B aggravated hepatic lipid accumulation in HepG2 cells. Hepatocellular lipid accumulation and AMPK-/LXR-pathways were evaluated after the administration of recombinant fetuin B in HepG2 cells exposed to FFAs. A: Oil Red O staining: FFA vs. FFA + Rec FetB (200 × and 400 ×); B: Intercellular TG content (FFA vs. FFA + Rec FetB, P = 0.001); C: The expression of key proteins in the AMPK and LXR pathways; D: The mRNA levels of lipid metabolic enzymes; Rec FetB, Recombinant fetuin B. Results are the mean ± SD of three independent experiments, each repeated in triplicate.

    Journal: American Journal of Translational Research

    Article Title: Fetuin B aggravates liver X receptor-mediated hepatic steatosis through AMPK in HepG2 cells and mice

    doi:

    Figure Lengend Snippet: Recombinant fetuin B aggravated hepatic lipid accumulation in HepG2 cells. Hepatocellular lipid accumulation and AMPK-/LXR-pathways were evaluated after the administration of recombinant fetuin B in HepG2 cells exposed to FFAs. A: Oil Red O staining: FFA vs. FFA + Rec FetB (200 × and 400 ×); B: Intercellular TG content (FFA vs. FFA + Rec FetB, P = 0.001); C: The expression of key proteins in the AMPK and LXR pathways; D: The mRNA levels of lipid metabolic enzymes; Rec FetB, Recombinant fetuin B. Results are the mean ± SD of three independent experiments, each repeated in triplicate.

    Article Snippet: Vehicle (20 mM Tris-HCL, Invitrogen, Carlsbad, CA) or recombinant mouse fetuin B (RPB860Mu0, Cloud-Clone Corp., Houston, TX) was infused using s.c. implanted osmotic pumps (Alzet #1002, Durect Corp., CA) for the 10-day duration.

    Techniques: Recombinant, Staining, Expressing

    LXR is a downstream target of AMPK. To clarify the relation between AMPK and LXR, pretreatment with LXR siRNA was applied in HepG2 cells exposed to FFA + recombinant fetuin B. Pretreatment with AMPK agonist (AICAR, 1 mM) was applied to HepG2 cells exposed to FFA + recombinant fetuin B. A: Intercellular TG content: FFA + Rec vs. FFA + Rec + siLXR (P = 0.003); B: The expression of key proteins in the AMPK and LXR pathways; C: The mRNA levels of lipid metabolic enzymes; D: Intercellular TG content: FFA + Rec FetB vs. FFA + Rec FetB + AICAR (P < 0.001); E: The expression of key proteins in the AMPK AND LXR pathways; F: The mRNA levels of lipid metabolic enzymes; Rec, Recombinant fetuin B; siLXR, siRNA LXR. Results are the mean ± SD of three independent experiments, each repeated in triplicate.

    Journal: American Journal of Translational Research

    Article Title: Fetuin B aggravates liver X receptor-mediated hepatic steatosis through AMPK in HepG2 cells and mice

    doi:

    Figure Lengend Snippet: LXR is a downstream target of AMPK. To clarify the relation between AMPK and LXR, pretreatment with LXR siRNA was applied in HepG2 cells exposed to FFA + recombinant fetuin B. Pretreatment with AMPK agonist (AICAR, 1 mM) was applied to HepG2 cells exposed to FFA + recombinant fetuin B. A: Intercellular TG content: FFA + Rec vs. FFA + Rec + siLXR (P = 0.003); B: The expression of key proteins in the AMPK and LXR pathways; C: The mRNA levels of lipid metabolic enzymes; D: Intercellular TG content: FFA + Rec FetB vs. FFA + Rec FetB + AICAR (P < 0.001); E: The expression of key proteins in the AMPK AND LXR pathways; F: The mRNA levels of lipid metabolic enzymes; Rec, Recombinant fetuin B; siLXR, siRNA LXR. Results are the mean ± SD of three independent experiments, each repeated in triplicate.

    Article Snippet: Vehicle (20 mM Tris-HCL, Invitrogen, Carlsbad, CA) or recombinant mouse fetuin B (RPB860Mu0, Cloud-Clone Corp., Houston, TX) was infused using s.c. implanted osmotic pumps (Alzet #1002, Durect Corp., CA) for the 10-day duration.

    Techniques: Recombinant, Expressing

    Fetuin B knockdown attenuated hepatic lipid accumulation in HepG2 cells. Hepatocellular lipid accumulation and the AMPK-/LXR-pathways were evaluated after fetuin B knockdown in HepG2 cells exposed to FFAs. A: Oil Red O staining: FFA vs. FFA + siFetB (200 × and 400 ×); B: Intercellular TG content (P = 0.004); C: The expression of key proteins in the AMPK and LXR pathways; D: The mRNA levels of lipid metabolic enzymes; siFetB, siRNA fetuin B. Results are the mean ± SD of three independent experiments, each repeated in triplicate.

    Journal: American Journal of Translational Research

    Article Title: Fetuin B aggravates liver X receptor-mediated hepatic steatosis through AMPK in HepG2 cells and mice

    doi:

    Figure Lengend Snippet: Fetuin B knockdown attenuated hepatic lipid accumulation in HepG2 cells. Hepatocellular lipid accumulation and the AMPK-/LXR-pathways were evaluated after fetuin B knockdown in HepG2 cells exposed to FFAs. A: Oil Red O staining: FFA vs. FFA + siFetB (200 × and 400 ×); B: Intercellular TG content (P = 0.004); C: The expression of key proteins in the AMPK and LXR pathways; D: The mRNA levels of lipid metabolic enzymes; siFetB, siRNA fetuin B. Results are the mean ± SD of three independent experiments, each repeated in triplicate.

    Article Snippet: Vehicle (20 mM Tris-HCL, Invitrogen, Carlsbad, CA) or recombinant mouse fetuin B (RPB860Mu0, Cloud-Clone Corp., Houston, TX) was infused using s.c. implanted osmotic pumps (Alzet #1002, Durect Corp., CA) for the 10-day duration.

    Techniques: Staining, Expressing

    LXR is a downstream target of AMPK. To confirm that LXR is a downstream target of AMPK, pretreatment with LXR agonist (GW3965, 5 μM) was applied to HepG2 cells exposed to FFA + Fetuin B siRNA. A: Intercellular TG content: FFA + Rec FetB vs. FFA + siFetB + GW3965 (P = 0.005); B: The expression of key proteins in the AMPK and LXR pathways; C: The mRNA levels of lipid metabolic enzymes; siFetB, siRNA fetuin B. Results are the mean ± SD of three independent experiments, each repeated in triplicate.

    Journal: American Journal of Translational Research

    Article Title: Fetuin B aggravates liver X receptor-mediated hepatic steatosis through AMPK in HepG2 cells and mice

    doi:

    Figure Lengend Snippet: LXR is a downstream target of AMPK. To confirm that LXR is a downstream target of AMPK, pretreatment with LXR agonist (GW3965, 5 μM) was applied to HepG2 cells exposed to FFA + Fetuin B siRNA. A: Intercellular TG content: FFA + Rec FetB vs. FFA + siFetB + GW3965 (P = 0.005); B: The expression of key proteins in the AMPK and LXR pathways; C: The mRNA levels of lipid metabolic enzymes; siFetB, siRNA fetuin B. Results are the mean ± SD of three independent experiments, each repeated in triplicate.

    Article Snippet: Vehicle (20 mM Tris-HCL, Invitrogen, Carlsbad, CA) or recombinant mouse fetuin B (RPB860Mu0, Cloud-Clone Corp., Houston, TX) was infused using s.c. implanted osmotic pumps (Alzet #1002, Durect Corp., CA) for the 10-day duration.

    Techniques: Expressing

    Fetuin B knockdown attenuated hepatic lipogenesis in mice fed a HFD. Hepatic lipid accumulation and the AMPK-/LXR-pathways were evaluated after fetuin B knockdown in mice exposed to a HFD. A: H&E staining and Oil Red O staining: HFD vs. HFD + shRNA (400 ×); B: Intrahepatic TG content (P < 0.001); C: Serum TG (P = 0.003); D: Liver enzymes; E: Key protein expression of the AMPK and LXR pathways in mouse liver; F: The mRNA levels of lipid metabolic enzymes; ALT, alanine transaminase; AST, aspartate transaminase. Results are the mean ± SD of three independent experiments (n = 6, each group).

    Journal: American Journal of Translational Research

    Article Title: Fetuin B aggravates liver X receptor-mediated hepatic steatosis through AMPK in HepG2 cells and mice

    doi:

    Figure Lengend Snippet: Fetuin B knockdown attenuated hepatic lipogenesis in mice fed a HFD. Hepatic lipid accumulation and the AMPK-/LXR-pathways were evaluated after fetuin B knockdown in mice exposed to a HFD. A: H&E staining and Oil Red O staining: HFD vs. HFD + shRNA (400 ×); B: Intrahepatic TG content (P < 0.001); C: Serum TG (P = 0.003); D: Liver enzymes; E: Key protein expression of the AMPK and LXR pathways in mouse liver; F: The mRNA levels of lipid metabolic enzymes; ALT, alanine transaminase; AST, aspartate transaminase. Results are the mean ± SD of three independent experiments (n = 6, each group).

    Article Snippet: Vehicle (20 mM Tris-HCL, Invitrogen, Carlsbad, CA) or recombinant mouse fetuin B (RPB860Mu0, Cloud-Clone Corp., Houston, TX) was infused using s.c. implanted osmotic pumps (Alzet #1002, Durect Corp., CA) for the 10-day duration.

    Techniques: Staining, shRNA, Expressing

    Recombinant fetuin B aggravated hepatic lipogenesis in HFD-fed mice. Hepatic lipid accumulation and the AMPK-/LXR-pathways were evaluated after the administration of recombinant fetuin B in mice exposed to a HFD. A: H&E staining and Oil Red O staining: HFD vs. HFD + Rec (400 ×); B: Intrahepatic TG content (P = 0.026); C: Serum TG (P = 0.011); D: Liver enzymes; E: Key protein expression of the AMPK and LXR pathways in mouse liver; F: The mRNA levels of lipid metabolic enzymes; ALT, alanine transaminase; AST, aspartate transaminase; Rec, Recombinant fetuin B. Results are the mean ± SD of three independent experiments (n = 6, each group).

    Journal: American Journal of Translational Research

    Article Title: Fetuin B aggravates liver X receptor-mediated hepatic steatosis through AMPK in HepG2 cells and mice

    doi:

    Figure Lengend Snippet: Recombinant fetuin B aggravated hepatic lipogenesis in HFD-fed mice. Hepatic lipid accumulation and the AMPK-/LXR-pathways were evaluated after the administration of recombinant fetuin B in mice exposed to a HFD. A: H&E staining and Oil Red O staining: HFD vs. HFD + Rec (400 ×); B: Intrahepatic TG content (P = 0.026); C: Serum TG (P = 0.011); D: Liver enzymes; E: Key protein expression of the AMPK and LXR pathways in mouse liver; F: The mRNA levels of lipid metabolic enzymes; ALT, alanine transaminase; AST, aspartate transaminase; Rec, Recombinant fetuin B. Results are the mean ± SD of three independent experiments (n = 6, each group).

    Article Snippet: Vehicle (20 mM Tris-HCL, Invitrogen, Carlsbad, CA) or recombinant mouse fetuin B (RPB860Mu0, Cloud-Clone Corp., Houston, TX) was infused using s.c. implanted osmotic pumps (Alzet #1002, Durect Corp., CA) for the 10-day duration.

    Techniques: Recombinant, Staining, Expressing