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pzp  (R&D Systems)


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    Structured Review

    R&D Systems pzp
    Plasma levels of (A) amyloid precursor <t>protein</t> <t>(APP),</t> (B) cathepsin L, (C) pregnancy zone protein <t>(PZP)</t> and (D) serum amyloid A (SAA1) in healthy controls (HC) (n=16), participants with persistent headache after SARS-CoV-2 vaccine (COvax) (n=31) and participants with persistent headache after COVID-19 ( C19 ) (n=29).
    Pzp, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pzp/pmc12382501-101-6-24?v=R%26D+Systems
    Average 93 stars, based on 3 article reviews
    pzp - by Bioz Stars, 2026-07
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    Images

    1) Product Images from "Altered amyloid plasma profile in patients with disabling headaches after SARS-CoV-2 infection and vaccination"

    Article Title: Altered amyloid plasma profile in patients with disabling headaches after SARS-CoV-2 infection and vaccination

    Journal: BMJ Neurology Open

    doi: 10.1136/bmjno-2024-001013

    Plasma levels of (A) amyloid precursor protein (APP), (B) cathepsin L, (C) pregnancy zone protein (PZP) and (D) serum amyloid A (SAA1) in healthy controls (HC) (n=16), participants with persistent headache after SARS-CoV-2 vaccine (COvax) (n=31) and participants with persistent headache after COVID-19 ( C19 ) (n=29).
    Figure Legend Snippet: Plasma levels of (A) amyloid precursor protein (APP), (B) cathepsin L, (C) pregnancy zone protein (PZP) and (D) serum amyloid A (SAA1) in healthy controls (HC) (n=16), participants with persistent headache after SARS-CoV-2 vaccine (COvax) (n=31) and participants with persistent headache after COVID-19 ( C19 ) (n=29).

    Techniques Used: Clinical Proteomics



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    Plasma levels of (A) amyloid precursor <t>protein</t> <t>(APP),</t> (B) cathepsin L, (C) pregnancy zone protein <t>(PZP)</t> and (D) serum amyloid A (SAA1) in healthy controls (HC) (n=16), participants with persistent headache after SARS-CoV-2 vaccine (COvax) (n=31) and participants with persistent headache after COVID-19 ( C19 ) (n=29).
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    Figure 5. Screening and verification of the differentially expressed gene <t>pzp</t> in DFs and skins based on RNA-seq. (A) DEGs thermograms of 3 independent duplicate samples of the Ctrl, UV, and UV + sEV groups. (B, C) Volcano maps (B) and Venn maps (C) of DEGs. (D) R language analysis of TOP DEGs. (E) RNA-seq analysis of DEGs, including pzp, sall1, fmo2, trh, and tex26. (F) RT-qPCR validation of the DEGs. (G) Western blot detection of the expression of PZP, FMO2, <t>and</t> <t>γ-H2AX.</t> (H) GO functional analysis of pzp. (I) Immunohistochemical detection of PZP expression in skin tissues of nude mice on day 35 of modeling. Scale bar = 20 μm. Data are presented as mean ± SD. n = 3, **P < .01, ***P < .001, ns, no significant difference.
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    Image Search Results


    A Schematic diagram of the subcutaneous tumor formation experiment in C57BL/6c mice; B – D C57BL/6c mice with RM1-tumor received PZP treatment (16 mg/kg, i.p. daily) and anti-PD1 treatment (CAT#BE0146, 200 µg per mouse, BioXCell) or an IgG isotype control (CAT#BE0089, BioXCell) intraperitoneally once every 2 days; C Tumor growth curve, data were presented as mean ± SD (n = 6), ** P ≤ 0.01, *** P ≤ 0.001; D Tumor mass, data were presented as mean ± SD (n = 6), **** P ≤ 0.0001; E – G C57BL/6c mice with RM1-shSting-tumor received PZP treatment (16 mg/kg, i.p. daily) and anti-PD1 treatment (CAT#BE0146, 200 µg per mouse every time, BioXCell) or an IgG isotype control (CAT#BE0089, BioXCell) intraperitoneally once every two days; F Tumor growth curve, data were presented as mean ± SD (n = 6), ns, not significant; G Tumor mass data were presented as mean ± SD (n = 6), ns not significant

    Journal: European Journal of Medical Research

    Article Title: Pirenzepine exhibits anti-prostate cancer activity and enhances checkpoint inhibitor-based immunotherapy by targeting STING

    doi: 10.1186/s40001-025-03520-4

    Figure Lengend Snippet: A Schematic diagram of the subcutaneous tumor formation experiment in C57BL/6c mice; B – D C57BL/6c mice with RM1-tumor received PZP treatment (16 mg/kg, i.p. daily) and anti-PD1 treatment (CAT#BE0146, 200 µg per mouse, BioXCell) or an IgG isotype control (CAT#BE0089, BioXCell) intraperitoneally once every 2 days; C Tumor growth curve, data were presented as mean ± SD (n = 6), ** P ≤ 0.01, *** P ≤ 0.001; D Tumor mass, data were presented as mean ± SD (n = 6), **** P ≤ 0.0001; E – G C57BL/6c mice with RM1-shSting-tumor received PZP treatment (16 mg/kg, i.p. daily) and anti-PD1 treatment (CAT#BE0146, 200 µg per mouse every time, BioXCell) or an IgG isotype control (CAT#BE0089, BioXCell) intraperitoneally once every two days; F Tumor growth curve, data were presented as mean ± SD (n = 6), ns, not significant; G Tumor mass data were presented as mean ± SD (n = 6), ns not significant

    Article Snippet: The PZP (CAT#HY-17037A, MedChemExpress) was dissolved in DMSO.

    Techniques: Control

    FDFT1 knockdown impairs AKT1 phosphorylation via ALDOB to inhibit HCC. A) Bubble diagram of top 15 KEGG results from DEGs between shFDFT1 and shNC groups in Huh7 cells through the DAVID website. B) GSEA results with FDR < 0.25 of high and low FDFT1 expression groups in the TCGA cohort. C) Western blot of total AKT1 and phosphorylated AKT1 (ser473) in FDFT1 knockdown or overexpression HCC cells. n = 3. D) Venn plot of DEGs between shFDFT1 and shNC groups in Huh7 cells and captured proteins interacted with AKT1 through mass spectrometry. E) Co‐IP results show that ALDOB interacts with AKT1 in Huh7 cells. F) Fold change of ALDOB after FDFT1 knockdown in Huh7 cells. n = 3. G) Western blot of ALODB in FDFT1 knockdown or overexpression cells. n = 3. H) Representative images of multiplex fluorescence immunohistochemistry (FDFT1, ALDOB, and DAPI) from HCC tissues with high or low FDFT1 expression. Scale bars, 50 µm. n = 5. I) Western blot results show that ALDOB knockdown using siRNA restores AKT1 phosphorylation in FDFT1 knockdown cells. n = 3. Data are presented as mean ± SD (C, G‐I). Images were quantified by image J (C and G‐I). Data were analyzed by unpaired t‐test (C, G‐H) or one‐way ANOVA (I) with Bonferroni multiple‐comparison correction. KEGG, Kyoto Encyclopedia of genes and genomes; GSEA, gene set enrichment analysis; DEGs, differentially expressed genes; Co‐IP, coimmunoprecipitation; siRNA, small interfering RNA.

    Journal: Advanced Science

    Article Title: Targeting FDFT1 Reduces Cholesterol and Bile Acid Production and Delays Hepatocellular Carcinoma Progression Through the HNF4A/ALDOB/AKT1 Axis

    doi: 10.1002/advs.202411719

    Figure Lengend Snippet: FDFT1 knockdown impairs AKT1 phosphorylation via ALDOB to inhibit HCC. A) Bubble diagram of top 15 KEGG results from DEGs between shFDFT1 and shNC groups in Huh7 cells through the DAVID website. B) GSEA results with FDR < 0.25 of high and low FDFT1 expression groups in the TCGA cohort. C) Western blot of total AKT1 and phosphorylated AKT1 (ser473) in FDFT1 knockdown or overexpression HCC cells. n = 3. D) Venn plot of DEGs between shFDFT1 and shNC groups in Huh7 cells and captured proteins interacted with AKT1 through mass spectrometry. E) Co‐IP results show that ALDOB interacts with AKT1 in Huh7 cells. F) Fold change of ALDOB after FDFT1 knockdown in Huh7 cells. n = 3. G) Western blot of ALODB in FDFT1 knockdown or overexpression cells. n = 3. H) Representative images of multiplex fluorescence immunohistochemistry (FDFT1, ALDOB, and DAPI) from HCC tissues with high or low FDFT1 expression. Scale bars, 50 µm. n = 5. I) Western blot results show that ALDOB knockdown using siRNA restores AKT1 phosphorylation in FDFT1 knockdown cells. n = 3. Data are presented as mean ± SD (C, G‐I). Images were quantified by image J (C and G‐I). Data were analyzed by unpaired t‐test (C, G‐H) or one‐way ANOVA (I) with Bonferroni multiple‐comparison correction. KEGG, Kyoto Encyclopedia of genes and genomes; GSEA, gene set enrichment analysis; DEGs, differentially expressed genes; Co‐IP, coimmunoprecipitation; siRNA, small interfering RNA.

    Article Snippet: For small interfering RNA (siRNA) transfection, siRNAs for ALDOB, PZP , and HNF4A and the negative control were constructed and purchased from RiboBio (China).

    Techniques: Knockdown, Phospho-proteomics, Expressing, Western Blot, Over Expression, Mass Spectrometry, Co-Immunoprecipitation Assay, Multiplex Assay, Fluorescence, Immunohistochemistry, Comparison, Small Interfering RNA

    FDFT1 knockdown causes the reduction of cholesterol and bile acid levels to activate HNF4A. A‐B) Relative cholesterol levels in FDFT1 inhibition cells through shRNA (A) or YM‐53061 (an inhibitor of FDFT1 enzyme activity, B). Cells were treated with YM‐53061 (5 µM) for 24 h. n = 3. C) Total bile acid levels in serum (left) and liver (right) of HCC mice. n = 3. D‐E) The mRNA levels of ALDOB of HCC cells treated with cholesterol (D) or CDCA (E) for 24 h. n = 3. F‐G) Dual‐luciferase reporter assays of HCC cells treated with cholesterol (F) or CDCA (G) for 24 h. n = 3. H‐I) Dual‐luciferase reporter assays of FDFT1 knockdown cells treated with cholesterol (10 µg mL −1 , H) or CDCA (100 µM, I) for 24 h. n = 3. J) Dual‐luciferase reporter assays of FDFT overexpression cells treated with YM‐53061 (5 µM) for 24 h. n = 3. K) Western blot results show AKT1 phosphorylation is recovered in FDFT1 knockdown cells treated with CDCA (100 µM) for 24 h. n = 3. L) Western blot results show AKT1 phosphorylation is rescued in FDFT1 overexpression cells treated with YM‐53061 (5 µM) for 24 h. n = 3. All data are presented as mean ± SD. Images were quantified by image J (K, L). Data were analyzed by unpaired t‐test (A‐C), and one‐way ANOVA with Bonferroni multiple‐comparison correction (D‐L). CHOL, cholesterol; CDCA, chenodeoxycholic acid.

    Journal: Advanced Science

    Article Title: Targeting FDFT1 Reduces Cholesterol and Bile Acid Production and Delays Hepatocellular Carcinoma Progression Through the HNF4A/ALDOB/AKT1 Axis

    doi: 10.1002/advs.202411719

    Figure Lengend Snippet: FDFT1 knockdown causes the reduction of cholesterol and bile acid levels to activate HNF4A. A‐B) Relative cholesterol levels in FDFT1 inhibition cells through shRNA (A) or YM‐53061 (an inhibitor of FDFT1 enzyme activity, B). Cells were treated with YM‐53061 (5 µM) for 24 h. n = 3. C) Total bile acid levels in serum (left) and liver (right) of HCC mice. n = 3. D‐E) The mRNA levels of ALDOB of HCC cells treated with cholesterol (D) or CDCA (E) for 24 h. n = 3. F‐G) Dual‐luciferase reporter assays of HCC cells treated with cholesterol (F) or CDCA (G) for 24 h. n = 3. H‐I) Dual‐luciferase reporter assays of FDFT1 knockdown cells treated with cholesterol (10 µg mL −1 , H) or CDCA (100 µM, I) for 24 h. n = 3. J) Dual‐luciferase reporter assays of FDFT overexpression cells treated with YM‐53061 (5 µM) for 24 h. n = 3. K) Western blot results show AKT1 phosphorylation is recovered in FDFT1 knockdown cells treated with CDCA (100 µM) for 24 h. n = 3. L) Western blot results show AKT1 phosphorylation is rescued in FDFT1 overexpression cells treated with YM‐53061 (5 µM) for 24 h. n = 3. All data are presented as mean ± SD. Images were quantified by image J (K, L). Data were analyzed by unpaired t‐test (A‐C), and one‐way ANOVA with Bonferroni multiple‐comparison correction (D‐L). CHOL, cholesterol; CDCA, chenodeoxycholic acid.

    Article Snippet: For small interfering RNA (siRNA) transfection, siRNAs for ALDOB, PZP , and HNF4A and the negative control were constructed and purchased from RiboBio (China).

    Techniques: Knockdown, Inhibition, shRNA, Activity Assay, Luciferase, Over Expression, Western Blot, Phospho-proteomics, Comparison

    Plasma levels of (A) amyloid precursor protein (APP), (B) cathepsin L, (C) pregnancy zone protein (PZP) and (D) serum amyloid A (SAA1) in healthy controls (HC) (n=16), participants with persistent headache after SARS-CoV-2 vaccine (COvax) (n=31) and participants with persistent headache after COVID-19 ( C19 ) (n=29).

    Journal: BMJ Neurology Open

    Article Title: Altered amyloid plasma profile in patients with disabling headaches after SARS-CoV-2 infection and vaccination

    doi: 10.1136/bmjno-2024-001013

    Figure Lengend Snippet: Plasma levels of (A) amyloid precursor protein (APP), (B) cathepsin L, (C) pregnancy zone protein (PZP) and (D) serum amyloid A (SAA1) in healthy controls (HC) (n=16), participants with persistent headache after SARS-CoV-2 vaccine (COvax) (n=31) and participants with persistent headache after COVID-19 ( C19 ) (n=29).

    Article Snippet: Plasma levels of APP (Cat# DY850), PZP (Cat# DY8280-05), CTSL (Cat# DY952) and SAA1 (Cat# DY3019-05) were measured by ELISA using commercially available antibodies (R&D Systems, Minneapolis, Minnesota, USA) in a 384-format using a combination of a SELMA pipetting robot (Analytik Jena AG, Jena, Germany) and a BioTek dispenser/washer (BioTek Instruments, Winooski, VT).

    Techniques: Clinical Proteomics

    Figure 5. Screening and verification of the differentially expressed gene pzp in DFs and skins based on RNA-seq. (A) DEGs thermograms of 3 independent duplicate samples of the Ctrl, UV, and UV + sEV groups. (B, C) Volcano maps (B) and Venn maps (C) of DEGs. (D) R language analysis of TOP DEGs. (E) RNA-seq analysis of DEGs, including pzp, sall1, fmo2, trh, and tex26. (F) RT-qPCR validation of the DEGs. (G) Western blot detection of the expression of PZP, FMO2, and γ-H2AX. (H) GO functional analysis of pzp. (I) Immunohistochemical detection of PZP expression in skin tissues of nude mice on day 35 of modeling. Scale bar = 20 μm. Data are presented as mean ± SD. n = 3, **P < .01, ***P < .001, ns, no significant difference.

    Journal: Stem cells translational medicine

    Article Title: Mesenchymal stromal cells-derived small extracellular vesicles protect against UV-induced photoaging via regulating pregnancy zone protein.

    doi: 10.1093/stcltm/szae069

    Figure Lengend Snippet: Figure 5. Screening and verification of the differentially expressed gene pzp in DFs and skins based on RNA-seq. (A) DEGs thermograms of 3 independent duplicate samples of the Ctrl, UV, and UV + sEV groups. (B, C) Volcano maps (B) and Venn maps (C) of DEGs. (D) R language analysis of TOP DEGs. (E) RNA-seq analysis of DEGs, including pzp, sall1, fmo2, trh, and tex26. (F) RT-qPCR validation of the DEGs. (G) Western blot detection of the expression of PZP, FMO2, and γ-H2AX. (H) GO functional analysis of pzp. (I) Immunohistochemical detection of PZP expression in skin tissues of nude mice on day 35 of modeling. Scale bar = 20 μm. Data are presented as mean ± SD. n = 3, **P < .01, ***P < .001, ns, no significant difference.

    Article Snippet: The primary antibodies are listed below: β-actin (1:5000, Abclonal), COL1A1 (1:500, Abclonal), MMP-1 (1:500, Abclonal), SIRT3 (1:500, Wanleibio), γ-H2AX (1:500, CST), PZP (1:500, Proteintech), ataxia telangiectasia-mutated protein (ATM, 1:500, Abclonal), p-ATM (1:500, Abclonal), 53BP1 (1:500, Proteintech), MMP-9 (1:500, Wanleibio), FMO2 (1:500, Proteintech), Alix (1:500, CST), CD9 (1:500, CST), CD81 (1:500, Proteintech), CD63 (1:500, Proteintech), TSG101 (1:500, Proteintech), and Calnexin (1:500, CST).

    Techniques: RNA Sequencing, Quantitative RT-PCR, Biomarker Discovery, Western Blot, Expressing, Functional Assay, Immunohistochemical staining

    Figure 6. Validation of PZP and MMP-1 interaction. (A) Known proteins interacting with PZP identified by the STRING database. (B) Predicted protein docking pattern of PZP and MMP-9. (C) Predicted protein docking pattern of PZP and MMP-1. (D) Validation of the interaction between PZP and MMP-1 via co-immunoprecipitation. (E) The co-localization of PZP and MMP-1 in DFs was assessed using immunofluorescence assay. Scale bar = 20 μm. (F) Immunofluorescence co-localization analysis of PZP and MMP-1 in skin tissues of nude mice. Scale bar = 200 μm.

    Journal: Stem cells translational medicine

    Article Title: Mesenchymal stromal cells-derived small extracellular vesicles protect against UV-induced photoaging via regulating pregnancy zone protein.

    doi: 10.1093/stcltm/szae069

    Figure Lengend Snippet: Figure 6. Validation of PZP and MMP-1 interaction. (A) Known proteins interacting with PZP identified by the STRING database. (B) Predicted protein docking pattern of PZP and MMP-9. (C) Predicted protein docking pattern of PZP and MMP-1. (D) Validation of the interaction between PZP and MMP-1 via co-immunoprecipitation. (E) The co-localization of PZP and MMP-1 in DFs was assessed using immunofluorescence assay. Scale bar = 20 μm. (F) Immunofluorescence co-localization analysis of PZP and MMP-1 in skin tissues of nude mice. Scale bar = 200 μm.

    Article Snippet: The primary antibodies are listed below: β-actin (1:5000, Abclonal), COL1A1 (1:500, Abclonal), MMP-1 (1:500, Abclonal), SIRT3 (1:500, Wanleibio), γ-H2AX (1:500, CST), PZP (1:500, Proteintech), ataxia telangiectasia-mutated protein (ATM, 1:500, Abclonal), p-ATM (1:500, Abclonal), 53BP1 (1:500, Proteintech), MMP-9 (1:500, Wanleibio), FMO2 (1:500, Proteintech), Alix (1:500, CST), CD9 (1:500, CST), CD81 (1:500, Proteintech), CD63 (1:500, Proteintech), TSG101 (1:500, Proteintech), and Calnexin (1:500, CST).

    Techniques: Biomarker Discovery, Immunoprecipitation, Immunofluorescence

    Figure 7. PZP ameliorates photoaging by mainly inhibiting MMP-1 expression. After overexpression of the pzp gene (A) SA β-gal staining and its quantization diagram. Scale bar = 100 μm. (B) Detection of the expression of PZP, COL1A1, MMP-1, SIRT3, and ATM signaling pathway-related proteins by Western blot. (C) Fluorescence images of mitotracker staining and SIRT3. Scale bar = 200 μm. (D) Immunofluorescence detection of γ-H2AX expression. Scale bar = 200 μm. After knockdown of the pzp gene (E) SA β-gal staining and its quantization diagram. Scale bar = 100 μm. (F) The levels of COL1A1, MMP-1, and DDR-related proteins were quantified by Western blot. (G) Fluorescence images of mitotracker staining and SIRT3. Scale bar = 200 μm. (H) Analysis of γ-H2AX expression by immunofluorescence. Scale bar = 200 μm. Ctrl + vector: DFs transfected with empty vector,

    Journal: Stem cells translational medicine

    Article Title: Mesenchymal stromal cells-derived small extracellular vesicles protect against UV-induced photoaging via regulating pregnancy zone protein.

    doi: 10.1093/stcltm/szae069

    Figure Lengend Snippet: Figure 7. PZP ameliorates photoaging by mainly inhibiting MMP-1 expression. After overexpression of the pzp gene (A) SA β-gal staining and its quantization diagram. Scale bar = 100 μm. (B) Detection of the expression of PZP, COL1A1, MMP-1, SIRT3, and ATM signaling pathway-related proteins by Western blot. (C) Fluorescence images of mitotracker staining and SIRT3. Scale bar = 200 μm. (D) Immunofluorescence detection of γ-H2AX expression. Scale bar = 200 μm. After knockdown of the pzp gene (E) SA β-gal staining and its quantization diagram. Scale bar = 100 μm. (F) The levels of COL1A1, MMP-1, and DDR-related proteins were quantified by Western blot. (G) Fluorescence images of mitotracker staining and SIRT3. Scale bar = 200 μm. (H) Analysis of γ-H2AX expression by immunofluorescence. Scale bar = 200 μm. Ctrl + vector: DFs transfected with empty vector,

    Article Snippet: The primary antibodies are listed below: β-actin (1:5000, Abclonal), COL1A1 (1:500, Abclonal), MMP-1 (1:500, Abclonal), SIRT3 (1:500, Wanleibio), γ-H2AX (1:500, CST), PZP (1:500, Proteintech), ataxia telangiectasia-mutated protein (ATM, 1:500, Abclonal), p-ATM (1:500, Abclonal), 53BP1 (1:500, Proteintech), MMP-9 (1:500, Wanleibio), FMO2 (1:500, Proteintech), Alix (1:500, CST), CD9 (1:500, CST), CD81 (1:500, Proteintech), CD63 (1:500, Proteintech), TSG101 (1:500, Proteintech), and Calnexin (1:500, CST).

    Techniques: Expressing, Over Expression, Staining, Western Blot, Fluorescence, Immunofluorescence, Knockdown, Plasmid Preparation, Transfection