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serum pcsk9 levels  (R&D Systems)


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    R&D Systems serum pcsk9 levels
    Serum Pcsk9 Levels, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 81 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/serum+pcsk9+levels/Mouse+Proprotein+Convertase+9%2FPCSK9+Quantikine+ELISA+Kit/pm40335752-674-0-16
    Average 95 stars, based on 81 article reviews
    serum pcsk9 levels - by Bioz Stars, 2026-09
    95/100 stars

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    Related Articles

    Clinical Proteomics:

    Article Title: Identification of a Variant in APOB Gene as a Major Cause of Hypobetalipoproteinemia in Lebanese Families
    Article Snippet: .. We measured plasma and serum PCSK9 levels using a commercial ELISA kit (Human Proprotein Convertase 9/PCSK9 Duoset catalogue no. DY3888; R&D Systems, Minneapolis, MN, USA) and the Bio-Plex Pro assay technology (Luminex Corporation, Austin, TX, USA) as previously described [ ]. ..

    Enzyme-linked Immunosorbent Assay:

    Article Title: Identification of a Variant in APOB Gene as a Major Cause of Hypobetalipoproteinemia in Lebanese Families
    Article Snippet: .. We measured plasma and serum PCSK9 levels using a commercial ELISA kit (Human Proprotein Convertase 9/PCSK9 Duoset catalogue no. DY3888; R&D Systems, Minneapolis, MN, USA) and the Bio-Plex Pro assay technology (Luminex Corporation, Austin, TX, USA) as previously described [ ]. ..

    Article Title: Macrophage AMPK β1 activation by PF-06409577 reduces the inflammatory response, cholesterol synthesis, and atherosclerosis in mice
    Article Snippet: .. Serum PCSK9 levels were analysed using a murine PCSK9 ELISA (Cat# MPC900, R&D Systems) as per the manufacturer’s instructions. .. RNA was isolated using RNEasy Columns (Qiagen) with on column DNase treatment, RT-q-PCR was performed as previously described.

    Article Title: Macrophage AMPK β1 activation by PF-06409577 reduces the inflammatory response, cholesterol synthesis, and atherosclerosis in mice.
    Article Snippet: .. Serum PCSK9 levels were analysed using a murine PCSK9 ELISA (Cat# MPC900, R&D Systems) as per the manufacturer’s instructions. .. RNA was isolated using RNEasy Columns (Qiagen) with on column DNase treatment, RT-q-PCR was performed as previously described.21 All Taqman primers were purchased from Invitrogen, and relative gene expression was calculated using (2–DCT) method.

    Article Title: Evolution-guided protein design of IscB for persistent epigenome editing in vivo.
    Article Snippet: The membrane was then washed an additional 3× as above and imaged on a BioRad Chemidoc imager. .. Serum PCSK9 levels were measured by ELISA using the Mouse Proprotein Convertase 9/PCSK9 Quantikine ELISA Kit (R&D Systems) using a 200-fold dilution as per the manufacturer’s instructions. .. Total cholesterol levels were measured using an Amplex Red Cholesterol Assay Kit (Thermo Fisher Scientific) following the manufacturer’s instructions.

    Article Title: New Loss-of-Function Mutations in PCSK9 Reduce Plasma LDL Cholesterol
    Article Snippet: Blood was collected from the posterior orbital cavity, and serum TC and TG levels were measured using the Total Cholesterol Assay Kit and Triglyceride Assay Kit (Beijing Kehua Biotechnology Co, Ltd). .. Serum PCSK9 levels were determined using a PCSK9 quantikine ELISA kit (R&D Systems; DPC900) as described recently.14,15 Livers were collected for real-time quantitative polymerase chain reaction and immunoblotting. .. The anti-c-Myc affinity gel (E6654), cycloheximide (C7698), antiFLAG (DYKDDDDK) M2 affinity gel (A2220), phenylmethanesulfonyl fluoride (P7626), protease inhibitor cocktail (P8340), and sodium mevalonate (M4667) were from Sigma Aldrich.

    Bio-Plex Pro Assay:

    Article Title: Identification of a Variant in APOB Gene as a Major Cause of Hypobetalipoproteinemia in Lebanese Families
    Article Snippet: .. We measured plasma and serum PCSK9 levels using a commercial ELISA kit (Human Proprotein Convertase 9/PCSK9 Duoset catalogue no. DY3888; R&D Systems, Minneapolis, MN, USA) and the Bio-Plex Pro assay technology (Luminex Corporation, Austin, TX, USA) as previously described [ ]. ..

    other:

    Article Title: An in-depth analysis shows a hidden atherogenic lipoprotein profile in non-diabetic chronic kidney disease patients.
    Article Snippet: Background: Chronic kidney disease (CKD) is an independent risk factor for atherosclerotic disease.. We hypothesized that CKD promotes a proatherogenic lipid profile modifying lipoprotein composition and particle number.. Methods: Cross-sectional study in 395 non-diabetic individuals (209 CKD patients and 186 controls) without statin therapy.

    Real-time Polymerase Chain Reaction:

    Article Title: New Loss-of-Function Mutations in PCSK9 Reduce Plasma LDL Cholesterol
    Article Snippet: Blood was collected from the posterior orbital cavity, and serum TC and TG levels were measured using the Total Cholesterol Assay Kit and Triglyceride Assay Kit (Beijing Kehua Biotechnology Co, Ltd). .. Serum PCSK9 levels were determined using a PCSK9 quantikine ELISA kit (R&D Systems; DPC900) as described recently.14,15 Livers were collected for real-time quantitative polymerase chain reaction and immunoblotting. .. The anti-c-Myc affinity gel (E6654), cycloheximide (C7698), antiFLAG (DYKDDDDK) M2 affinity gel (A2220), phenylmethanesulfonyl fluoride (P7626), protease inhibitor cocktail (P8340), and sodium mevalonate (M4667) were from Sigma Aldrich.

    Western Blot:

    Article Title: New Loss-of-Function Mutations in PCSK9 Reduce Plasma LDL Cholesterol
    Article Snippet: Blood was collected from the posterior orbital cavity, and serum TC and TG levels were measured using the Total Cholesterol Assay Kit and Triglyceride Assay Kit (Beijing Kehua Biotechnology Co, Ltd). .. Serum PCSK9 levels were determined using a PCSK9 quantikine ELISA kit (R&D Systems; DPC900) as described recently.14,15 Livers were collected for real-time quantitative polymerase chain reaction and immunoblotting. .. The anti-c-Myc affinity gel (E6654), cycloheximide (C7698), antiFLAG (DYKDDDDK) M2 affinity gel (A2220), phenylmethanesulfonyl fluoride (P7626), protease inhibitor cocktail (P8340), and sodium mevalonate (M4667) were from Sigma Aldrich.



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    qPCR-measured inhibitory rate of modified PC sequence on target <t>PCSK9</t> mRNA in Hep3B cells The modification patterns involved in studying the preferences of residues at certain positions are shown (A). The inhibitory rates of modified siRNAs on target PCSK9 mRNA were measured in Hep3B cells (B). siRNAs were transfected into Hep3B cells at a concentration of 50 pM, and the PCSK9 mRNA levels in cells after 48 h of transfection were measured by qPCR as described. The inhibitory rate of the PC without GalNAc is shown as a black bar on the left. Means ± SD are shown. Differences were analyzed using one-way ANOVA. Multiple comparisons were conducted between the PC group and other groups using GraphPad Prism, and p values were adjusted using Dunnett’s method. siRNAs with significantly higher inhibition efficacies are labeled on the graph. ∗ p < 0.05, ∗∗ p < 0.01.
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    R&D Systems serum pcsk9 levels
    qPCR-measured inhibitory rate of modified PC sequence on target <t>PCSK9</t> mRNA in Hep3B cells The modification patterns involved in studying the preferences of residues at certain positions are shown (A). The inhibitory rates of modified siRNAs on target PCSK9 mRNA were measured in Hep3B cells (B). siRNAs were transfected into Hep3B cells at a concentration of 50 pM, and the PCSK9 mRNA levels in cells after 48 h of transfection were measured by qPCR as described. The inhibitory rate of the PC without GalNAc is shown as a black bar on the left. Means ± SD are shown. Differences were analyzed using one-way ANOVA. Multiple comparisons were conducted between the PC group and other groups using GraphPad Prism, and p values were adjusted using Dunnett’s method. siRNAs with significantly higher inhibition efficacies are labeled on the graph. ∗ p < 0.05, ∗∗ p < 0.01.
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    Figure 1. Western blot analysis of <t>PCSK9</t> and LDLR expression in PC cell lines and overview and validation of PCSK9 knockdown in CWR-R1ca cells. (A) PCSK9 and LDLR expression levels in diverse PC cell lines (left panel). Densitometric analysis of PCSK9 and LDLR expression levels (right panel). (B) Overview of methodology and validation of the knockdown efficacy of PCSK9 in CWR-R1ca cell transfection using shRNA-plasmid specific to PCSK9. Western blotting showed a 75% PCSK9 reduction in transfected CWR-R1ca-KD cells compared to the wild-type cells. *** p < 0.01 for statistical significance. Scanning densitometry was obtained for all blots, carried out in duplicate, and the integrated optical density of each band was normalized with the corresponding density found for β-actin in the same blot. Results are shown in the bar graphs to their respective Western blot images. Vertical bars in the graph indicate the normalized integrated optical density of bands visualized in each lane.
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    qPCR-measured inhibitory rate of modified PC sequence on target PCSK9 mRNA in Hep3B cells The modification patterns involved in studying the preferences of residues at certain positions are shown (A). The inhibitory rates of modified siRNAs on target PCSK9 mRNA were measured in Hep3B cells (B). siRNAs were transfected into Hep3B cells at a concentration of 50 pM, and the PCSK9 mRNA levels in cells after 48 h of transfection were measured by qPCR as described. The inhibitory rate of the PC without GalNAc is shown as a black bar on the left. Means ± SD are shown. Differences were analyzed using one-way ANOVA. Multiple comparisons were conducted between the PC group and other groups using GraphPad Prism, and p values were adjusted using Dunnett’s method. siRNAs with significantly higher inhibition efficacies are labeled on the graph. ∗ p < 0.05, ∗∗ p < 0.01.

    Journal: Molecular Therapy. Methods & Clinical Development

    Article Title: Design and systematic evaluation of novel chemical modification patterns enable the identification of a potent siRNA targeting PCSK9

    doi: 10.1016/j.omtm.2025.101609

    Figure Lengend Snippet: qPCR-measured inhibitory rate of modified PC sequence on target PCSK9 mRNA in Hep3B cells The modification patterns involved in studying the preferences of residues at certain positions are shown (A). The inhibitory rates of modified siRNAs on target PCSK9 mRNA were measured in Hep3B cells (B). siRNAs were transfected into Hep3B cells at a concentration of 50 pM, and the PCSK9 mRNA levels in cells after 48 h of transfection were measured by qPCR as described. The inhibitory rate of the PC without GalNAc is shown as a black bar on the left. Means ± SD are shown. Differences were analyzed using one-way ANOVA. Multiple comparisons were conducted between the PC group and other groups using GraphPad Prism, and p values were adjusted using Dunnett’s method. siRNAs with significantly higher inhibition efficacies are labeled on the graph. ∗ p < 0.05, ∗∗ p < 0.01.

    Article Snippet: Serum PCSK9 levels were determined using ELISA (Proteintech, KE00181).

    Techniques: Modification, Sequencing, Transfection, Concentration Assay, Inhibition, Labeling

    Inhibition efficiency of YK1597-DV29PG5 on PCSK9, LDL-C, and TC in cynomolgus monkeys Inhibitory rates of YK1597-DV29PG5 at different doses (3, 6, and 10 mg/kg s.c.) on target protein LDL-C and TC in cynomolgus monkeys ( n = 6) were measured with ELISA after introduction for a period of 84 days, with group means ± SD shown. Expression of the target protein PCSK9 was measured over a period of 84 days (A), and the relevant percentages of PCSK9 protein expression during that period are shown (B). LDL-C levels are shown in (C and D), while the levels of TC are shown in (E and F).

    Journal: Molecular Therapy. Methods & Clinical Development

    Article Title: Design and systematic evaluation of novel chemical modification patterns enable the identification of a potent siRNA targeting PCSK9

    doi: 10.1016/j.omtm.2025.101609

    Figure Lengend Snippet: Inhibition efficiency of YK1597-DV29PG5 on PCSK9, LDL-C, and TC in cynomolgus monkeys Inhibitory rates of YK1597-DV29PG5 at different doses (3, 6, and 10 mg/kg s.c.) on target protein LDL-C and TC in cynomolgus monkeys ( n = 6) were measured with ELISA after introduction for a period of 84 days, with group means ± SD shown. Expression of the target protein PCSK9 was measured over a period of 84 days (A), and the relevant percentages of PCSK9 protein expression during that period are shown (B). LDL-C levels are shown in (C and D), while the levels of TC are shown in (E and F).

    Article Snippet: Serum PCSK9 levels were determined using ELISA (Proteintech, KE00181).

    Techniques: Inhibition, Enzyme-linked Immunosorbent Assay, Expressing

    Inhibition of PCSK9 mRNA by the newly designed siRNAs with ESC pattern modification Six siRNAs were transfected into Hep3B cells at 50 pM using Lipofectamine RNAiMAX to determine their effects on the inhibition of PCSK9 . The sequence of the PC was selected and modified with the ESC pattern and used as the PC. Cells were incubated in a 37°C, 5% CO 2 incubator for 48 h before harvesting. The levels of PCSK9 expression were then measured using qPCR. Means ± SD are shown. One-way ANOVA and multiple comparisons were carried out between the PC-ESC group and other groups using GraphPad Prism, and p values were adjusted using Dunnett’s method. siRNAs with significantly higher inhibition efficacy are labeled on the graph. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

    Journal: Molecular Therapy. Methods & Clinical Development

    Article Title: Design and systematic evaluation of novel chemical modification patterns enable the identification of a potent siRNA targeting PCSK9

    doi: 10.1016/j.omtm.2025.101609

    Figure Lengend Snippet: Inhibition of PCSK9 mRNA by the newly designed siRNAs with ESC pattern modification Six siRNAs were transfected into Hep3B cells at 50 pM using Lipofectamine RNAiMAX to determine their effects on the inhibition of PCSK9 . The sequence of the PC was selected and modified with the ESC pattern and used as the PC. Cells were incubated in a 37°C, 5% CO 2 incubator for 48 h before harvesting. The levels of PCSK9 expression were then measured using qPCR. Means ± SD are shown. One-way ANOVA and multiple comparisons were carried out between the PC-ESC group and other groups using GraphPad Prism, and p values were adjusted using Dunnett’s method. siRNAs with significantly higher inhibition efficacy are labeled on the graph. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001.

    Article Snippet: Serum PCSK9 levels were determined using ELISA (Proteintech, KE00181).

    Techniques: Inhibition, Modification, Transfection, Sequencing, Incubation, Expressing, Labeling

    qPCR-measured inhibitory rate of siRNAs with new modification patterns on PCSK9 mRNA in Hep3B cells and the inhibition of modified siRNAs on serum PCSK9 and LDL-C in transgenic mice (A) The inhibitory rates of modified siRNAs on target PCSK9 mRNA were measured in Hep3B cells. siRNAs were transfected into Hep3B cells at a concentration of 50 pM using Lipofectamine RNAiMAX. Cells were then incubated in a 37°C, 5% CO 2 incubator for 48 h before harvesting, and the PCSK9 mRNA levels in cells after transfection were measured by qPCR as introduced. The inhibitory rate of PC without GalNAc is shown as a black bar on the left. Group means ± SD are shown. One-way ANOVA and multiple comparisons were conducted between the PC group and other groups using GraphPad Prism. For sequences based on YK1588 and YK1598, multiple comparisons were also performed between ESC groups and other modification groups. p values were adjusted using Dunnett’s method. siRNAs with significantly higher inhibition efficacy are labeled on the graph. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (B–D) In vivo inhibition efficiency of newly designed siRNAs with our modification patterns (dose: 6 mg/kg) was measured using hPCSK9 transgenic mice (B6-hPCSK9, n = 5). Group means ± SD are shown. Target protein expression level and LDL-C level were measured using ELISA and a clinical chemistry analyzer, respectively, as described. The inhibitory rate of the PC is shown to compare the inhibition efficiencies of newly designed siRNAs. The serum hPCSK9 inhibitory rates of modified siRNAs based on basic sequences 1596, 1597, and 1599 are shown in (B–D), respectively.

    Journal: Molecular Therapy. Methods & Clinical Development

    Article Title: Design and systematic evaluation of novel chemical modification patterns enable the identification of a potent siRNA targeting PCSK9

    doi: 10.1016/j.omtm.2025.101609

    Figure Lengend Snippet: qPCR-measured inhibitory rate of siRNAs with new modification patterns on PCSK9 mRNA in Hep3B cells and the inhibition of modified siRNAs on serum PCSK9 and LDL-C in transgenic mice (A) The inhibitory rates of modified siRNAs on target PCSK9 mRNA were measured in Hep3B cells. siRNAs were transfected into Hep3B cells at a concentration of 50 pM using Lipofectamine RNAiMAX. Cells were then incubated in a 37°C, 5% CO 2 incubator for 48 h before harvesting, and the PCSK9 mRNA levels in cells after transfection were measured by qPCR as introduced. The inhibitory rate of PC without GalNAc is shown as a black bar on the left. Group means ± SD are shown. One-way ANOVA and multiple comparisons were conducted between the PC group and other groups using GraphPad Prism. For sequences based on YK1588 and YK1598, multiple comparisons were also performed between ESC groups and other modification groups. p values were adjusted using Dunnett’s method. siRNAs with significantly higher inhibition efficacy are labeled on the graph. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001. (B–D) In vivo inhibition efficiency of newly designed siRNAs with our modification patterns (dose: 6 mg/kg) was measured using hPCSK9 transgenic mice (B6-hPCSK9, n = 5). Group means ± SD are shown. Target protein expression level and LDL-C level were measured using ELISA and a clinical chemistry analyzer, respectively, as described. The inhibitory rate of the PC is shown to compare the inhibition efficiencies of newly designed siRNAs. The serum hPCSK9 inhibitory rates of modified siRNAs based on basic sequences 1596, 1597, and 1599 are shown in (B–D), respectively.

    Article Snippet: Serum PCSK9 levels were determined using ELISA (Proteintech, KE00181).

    Techniques: Modification, Inhibition, Transgenic Assay, Transfection, Concentration Assay, Incubation, Labeling, In Vivo, Expressing, Enzyme-linked Immunosorbent Assay

    Inhibition of modified siRNAs on PCSK9 in transgenic mice and cynomolgus monkeys (A) In vivo inhibition efficiencies of YK1597-DV27G and YK1597-DV29G (light blue and purple triangles, respectively) were measured together with siRNAs possessing the same sequences but with a 5′-VP at the 5′-end of AS strands (YK1597-DV27PG and YK1597-DV29PG shown as dark blue squares and green triangles, respectively). Group means ± SD are shown. (B) Efficacy evaluation at a dose of 2 mg/kg using hPCSK9 transgenic mice (B6-hPCSK9, n = 6). Group means ± SD are shown, and the inhibition of inclisiran is shown as the control (red dots). The expression level of the target protein PCSK9 was measured by ELISA as introduced, and the serum hPCSK9 inhibitory rate is shown (A). The inhibition of PCSK9 mRNA in the liver of transgenic mice was measured at the end of the experiment (day 35) using qPCR. Differences in serum PCSK9 between PC and other groups were analyzed using two-way ANOVA, and differences in liver mRNA levels between PC and other groups were analyzed using one-way ANOVA. Multiple comparisons were then performed between the PC group and other groups. Groups with significantly higher inhibition efficacies are labeled on the graph. p values were corrected using Dunnett’s method. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (C) Serum PCSK9 and LDL-C inhibitory rates of YK1597-DV27PG and YK1597-DV29PG (dark blue and green triangles, respectively) were also measured in cynomolgus monkeys dosed at 6 mg/mL (male, n = 2). Group means ± SD are shown.

    Journal: Molecular Therapy. Methods & Clinical Development

    Article Title: Design and systematic evaluation of novel chemical modification patterns enable the identification of a potent siRNA targeting PCSK9

    doi: 10.1016/j.omtm.2025.101609

    Figure Lengend Snippet: Inhibition of modified siRNAs on PCSK9 in transgenic mice and cynomolgus monkeys (A) In vivo inhibition efficiencies of YK1597-DV27G and YK1597-DV29G (light blue and purple triangles, respectively) were measured together with siRNAs possessing the same sequences but with a 5′-VP at the 5′-end of AS strands (YK1597-DV27PG and YK1597-DV29PG shown as dark blue squares and green triangles, respectively). Group means ± SD are shown. (B) Efficacy evaluation at a dose of 2 mg/kg using hPCSK9 transgenic mice (B6-hPCSK9, n = 6). Group means ± SD are shown, and the inhibition of inclisiran is shown as the control (red dots). The expression level of the target protein PCSK9 was measured by ELISA as introduced, and the serum hPCSK9 inhibitory rate is shown (A). The inhibition of PCSK9 mRNA in the liver of transgenic mice was measured at the end of the experiment (day 35) using qPCR. Differences in serum PCSK9 between PC and other groups were analyzed using two-way ANOVA, and differences in liver mRNA levels between PC and other groups were analyzed using one-way ANOVA. Multiple comparisons were then performed between the PC group and other groups. Groups with significantly higher inhibition efficacies are labeled on the graph. p values were corrected using Dunnett’s method. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (C) Serum PCSK9 and LDL-C inhibitory rates of YK1597-DV27PG and YK1597-DV29PG (dark blue and green triangles, respectively) were also measured in cynomolgus monkeys dosed at 6 mg/mL (male, n = 2). Group means ± SD are shown.

    Article Snippet: Serum PCSK9 levels were determined using ELISA (Proteintech, KE00181).

    Techniques: Inhibition, Modification, Transgenic Assay, In Vivo, Control, Expressing, Enzyme-linked Immunosorbent Assay, Labeling

    Demographic, clinical, and laboratory data of participants

    Journal: Archives of Rheumatology

    Article Title: Proprotein convertase subtilisin/kexin 9 (PCSK9) in patients with diffuse systemic sclerosis: A marker of disease activity and severe disease manifestations with potential therapeutic implementations

    doi: 10.46497/ArchRheumatol.2023.9638

    Figure Lengend Snippet: Demographic, clinical, and laboratory data of participants

    Article Snippet: Serum PCSK9 levels were measured by enzyme-linked immunosorbent assay (ELISA) (CUSABIO kit, Catalog Number: CSB-EL017647HU, Houston, USA).

    Techniques: Modification, Standard Deviation, Sedimentation

    Correlation of study parameters with  PCSK9

    Journal: Archives of Rheumatology

    Article Title: Proprotein convertase subtilisin/kexin 9 (PCSK9) in patients with diffuse systemic sclerosis: A marker of disease activity and severe disease manifestations with potential therapeutic implementations

    doi: 10.46497/ArchRheumatol.2023.9638

    Figure Lengend Snippet: Correlation of study parameters with PCSK9

    Article Snippet: Serum PCSK9 levels were measured by enzyme-linked immunosorbent assay (ELISA) (CUSABIO kit, Catalog Number: CSB-EL017647HU, Houston, USA).

    Techniques: Modification, Sedimentation

    Figure 1. Western blot analysis of PCSK9 and LDLR expression in PC cell lines and overview and validation of PCSK9 knockdown in CWR-R1ca cells. (A) PCSK9 and LDLR expression levels in diverse PC cell lines (left panel). Densitometric analysis of PCSK9 and LDLR expression levels (right panel). (B) Overview of methodology and validation of the knockdown efficacy of PCSK9 in CWR-R1ca cell transfection using shRNA-plasmid specific to PCSK9. Western blotting showed a 75% PCSK9 reduction in transfected CWR-R1ca-KD cells compared to the wild-type cells. *** p < 0.01 for statistical significance. Scanning densitometry was obtained for all blots, carried out in duplicate, and the integrated optical density of each band was normalized with the corresponding density found for β-actin in the same blot. Results are shown in the bar graphs to their respective Western blot images. Vertical bars in the graph indicate the normalized integrated optical density of bands visualized in each lane.

    Journal: Marine drugs

    Article Title: Pseurotin A Validation as a Metastatic Castration-Resistant Prostate Cancer Recurrence-Suppressing Lead via PCSK9-LDLR Axis Modulation.

    doi: 10.3390/md21040215

    Figure Lengend Snippet: Figure 1. Western blot analysis of PCSK9 and LDLR expression in PC cell lines and overview and validation of PCSK9 knockdown in CWR-R1ca cells. (A) PCSK9 and LDLR expression levels in diverse PC cell lines (left panel). Densitometric analysis of PCSK9 and LDLR expression levels (right panel). (B) Overview of methodology and validation of the knockdown efficacy of PCSK9 in CWR-R1ca cell transfection using shRNA-plasmid specific to PCSK9. Western blotting showed a 75% PCSK9 reduction in transfected CWR-R1ca-KD cells compared to the wild-type cells. *** p < 0.01 for statistical significance. Scanning densitometry was obtained for all blots, carried out in duplicate, and the integrated optical density of each band was normalized with the corresponding density found for β-actin in the same blot. Results are shown in the bar graphs to their respective Western blot images. Vertical bars in the graph indicate the normalized integrated optical density of bands visualized in each lane.

    Article Snippet: Mice serum PCSK9 levels were measured using a Rockland ELISA kit (Rockland Immunochemicals, Inc.

    Techniques: Western Blot, Expressing, Biomarker Discovery, Knockdown, Transfection, shRNA, Plasmid Preparation

    Figure 2. Effects of PS and PCSK9 knockdown on the proliferation, migration, and colony formation of CWR-R1ca cells. (A) Comparison of different PS treatments on the proliferation of wild and PCSK9- KD CWR-R1ca cells over 72 h culture period. (B) Long-term (10-day) anti-proliferative effects of PS on wild-type CWR-R1ca cells. Vertical bars indicate mean cell count ±SEM (n = 6) in MTT/proliferation assay for each treatment group over the same culture period. (C) Comparison of the migratory ability of wild and PCSK9-KD CWR-R1ca cells in wound-healing scratch assay. (D) Comparison of the antimigratory effect of PS treatments against the wild-type versus PCSK9-KD CWR-R1ca cells over 24 h. (E) Comparison of the wild-type versus PCSK9-KD CWR-R1ca cells’ colony formation ability. (F) Comparison of PS treatments’ anti-clonogenicity activity in wild-type versus PCSK9-KD CWR-R1ca cells over 12 days. Vertical bars indicate the percentage of cell migration and colony formation of wild-type and CWR-R1ca-KD cells at the experiment end calculated relative to the vehicle-treated controls (n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 for statistical significance compared to VCs.

    Journal: Marine drugs

    Article Title: Pseurotin A Validation as a Metastatic Castration-Resistant Prostate Cancer Recurrence-Suppressing Lead via PCSK9-LDLR Axis Modulation.

    doi: 10.3390/md21040215

    Figure Lengend Snippet: Figure 2. Effects of PS and PCSK9 knockdown on the proliferation, migration, and colony formation of CWR-R1ca cells. (A) Comparison of different PS treatments on the proliferation of wild and PCSK9- KD CWR-R1ca cells over 72 h culture period. (B) Long-term (10-day) anti-proliferative effects of PS on wild-type CWR-R1ca cells. Vertical bars indicate mean cell count ±SEM (n = 6) in MTT/proliferation assay for each treatment group over the same culture period. (C) Comparison of the migratory ability of wild and PCSK9-KD CWR-R1ca cells in wound-healing scratch assay. (D) Comparison of the antimigratory effect of PS treatments against the wild-type versus PCSK9-KD CWR-R1ca cells over 24 h. (E) Comparison of the wild-type versus PCSK9-KD CWR-R1ca cells’ colony formation ability. (F) Comparison of PS treatments’ anti-clonogenicity activity in wild-type versus PCSK9-KD CWR-R1ca cells over 12 days. Vertical bars indicate the percentage of cell migration and colony formation of wild-type and CWR-R1ca-KD cells at the experiment end calculated relative to the vehicle-treated controls (n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001 for statistical significance compared to VCs.

    Article Snippet: Mice serum PCSK9 levels were measured using a Rockland ELISA kit (Rockland Immunochemicals, Inc.

    Techniques: Knockdown, Migration, Comparison, Cell Counting, Proliferation Assay, Wound Healing Assay, Activity Assay

    Figure 3. Expression of PCSK9 in PC tissue cores. PCSK9 expression was evaluated by immuno- histochemistry in tissue microarray slide comprising 64 cases/192 PC tissue cores and 6 normal prostate cases/18 tissue cores. The protein expression was evaluated in tissues collected from PC patients at Gleason score 5 (A), GS = 7 (B), and GS = 8 (C) in addition to normal prostate tissues (D). Magnification is 400×.

    Journal: Marine drugs

    Article Title: Pseurotin A Validation as a Metastatic Castration-Resistant Prostate Cancer Recurrence-Suppressing Lead via PCSK9-LDLR Axis Modulation.

    doi: 10.3390/md21040215

    Figure Lengend Snippet: Figure 3. Expression of PCSK9 in PC tissue cores. PCSK9 expression was evaluated by immuno- histochemistry in tissue microarray slide comprising 64 cases/192 PC tissue cores and 6 normal prostate cases/18 tissue cores. The protein expression was evaluated in tissues collected from PC patients at Gleason score 5 (A), GS = 7 (B), and GS = 8 (C) in addition to normal prostate tissues (D). Magnification is 400×.

    Article Snippet: Mice serum PCSK9 levels were measured using a Rockland ELISA kit (Rockland Immunochemicals, Inc.

    Techniques: Expressing, Immunohistochemistry, Microarray

    Figure 8. Systemic effects of HFD versus regular diet on mice serum cholesterol, LDL-C, PCSK9, and PSA levels. (A) Comparison of the HFD’s effect versus regular diet on mice mean serum total cholesterol levels. (B) Comparison of the HFD’s effect versus regular diet on mice serum LDL-C levels. (C) Comparison of the HFD’s effect versus regular diet on mice serum PCSK9 levels. (D) Comparison of the HFD’s effect versus regular diet on mice serum PSA levels. (E) Comparative of Western blotting analysis of HFD’s effect versus regular diet on the PCSK9 expression levels in CWR-R1ca cell tumors. (F) Western blot densitometric analysis of PCSK9 expression levels. Error bars represent the SEM for each experimental group. Each point is the mean of triplicate. **** p < 0.0001 for statistical significance compared to regular diet group. “ns” consider statistically not significant p > 0.5.

    Journal: Marine drugs

    Article Title: Pseurotin A Validation as a Metastatic Castration-Resistant Prostate Cancer Recurrence-Suppressing Lead via PCSK9-LDLR Axis Modulation.

    doi: 10.3390/md21040215

    Figure Lengend Snippet: Figure 8. Systemic effects of HFD versus regular diet on mice serum cholesterol, LDL-C, PCSK9, and PSA levels. (A) Comparison of the HFD’s effect versus regular diet on mice mean serum total cholesterol levels. (B) Comparison of the HFD’s effect versus regular diet on mice serum LDL-C levels. (C) Comparison of the HFD’s effect versus regular diet on mice serum PCSK9 levels. (D) Comparison of the HFD’s effect versus regular diet on mice serum PSA levels. (E) Comparative of Western blotting analysis of HFD’s effect versus regular diet on the PCSK9 expression levels in CWR-R1ca cell tumors. (F) Western blot densitometric analysis of PCSK9 expression levels. Error bars represent the SEM for each experimental group. Each point is the mean of triplicate. **** p < 0.0001 for statistical significance compared to regular diet group. “ns” consider statistically not significant p > 0.5.

    Article Snippet: Mice serum PCSK9 levels were measured using a Rockland ELISA kit (Rockland Immunochemicals, Inc.

    Techniques: Comparison, Western Blot, Expressing