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recombinant mouse pcsk9 protein (R&D Systems)

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R&D Systems recombinant mouse pcsk9 protein
Recombinant Mouse Pcsk9 Protein, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/recombinant+mouse+pcsk9+protein/Recombinant+Mouse+Proprotein+Convertase+9%2FPCSK9+Protein%2C+CF/us12577546-826-15-19
Average 94 stars, based on 4 article reviews

recombinant mouse pcsk9 protein - by Bioz Stars, 2026-09

94/100 stars

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Article Title: Programmable DNA base editing by Nme2Cas9-deaminase fusion proteins
Article Snippet: Serum cholesterol level was measured using the InfinityTM colorimetric endpoint assay (Thermo-Scientific) following the manufacturer's protocol and as previously described (Ibraheim et al., 2018). .. For the anti-PCSK9 Western blot, 40 μg of protein from tissue or 2 ng of Recombinant Mouse PCSK9 Protein (R&D Systems, 9258-SE-020) were loaded onto a MiniPROTEAN® TGXTM Precast Gel (Bio-Rad). .. The separated bands were transferred onto a PVDF membrane and blocked with 5% Blocking-Grade Blocker solution (Bio-Rad) for 2 hours at room temperature.

Article Title: A compact, high-accuracy Cas9 with a dinucleotide PAM for in vivo genome editing
Article Snippet: Serum cholesterol level was measured using the Infinity TM colorimetric endpoint assay (Thermo-Scientific) following the manufacturer’s protocol and as previously described ( Ibraheim et al., 2018 ). .. For the anti-PCSK9 Western blot, 40 μg of protein from tissue or 2 ng of Recombinant Mouse PCSK9 Protein (R&D Systems, 9258-SE-020) were loaded onto a MiniPROTEAN® TGX TM Precast Gel (Bio-Rad). .. The separated bands were transferred onto a PVDF membrane and blocked with 5% Blocking-Grade Blocker solution (Bio-Rad) for 2 hours at room temperature.

Recombinant:

Article Title: Rosa26-LSL-dCas9-VPR: a versatile mouse model for tissue specific and simultaneous activation of multiple genes for drug discovery
Article Snippet: The following primary antibodies were used: LDLR (1:50, PAB8804, Abnova), SERPINA1A (1:20, MAB7690, R&D Systems), PCSK9 (1:10, AF3985, R&D Systems) and β-actin (1:20, NB600-501, Novus Biologicals). .. Specificity of PCSK9 detection was confirmed using recombinant mouse PCSK9 protein (9258-SE-022, R&D Systems). .. Compass software version 6.0.0 (Protein Simple) was used to analyze the data.

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Fig. 1 Therapeutic efficacy of cVLP-PCSK9 and cVLP-HER2 vaccines as standalone or combined approach. A Experimental design; B Kaplan–Meier tumor free survival plot, n = 6; *p < 0.05; ***p < 0.01; long-rank test; C Tumor growth curves, each point represents the mean (and SEM) of all mice in each group, n = 6; D Single mice growth curves of each treated group

Journal: Journal of translational medicine

Article Title: Targeting PCSK9, through an innovative cVLP-based vaccine, enhanced the therapeutic activity of a cVLP-HER2 vaccine in a preclinical model of HER2-positive mammary carcinoma.

doi: 10.1186/s12967-025-06126-w

Figure Lengend Snippet: Fig. 1 Therapeutic efficacy of cVLP-PCSK9 and cVLP-HER2 vaccines as standalone or combined approach. A Experimental design; B Kaplan–Meier tumor free survival plot, n = 6; *p < 0.05; ***p < 0.01; long-rank test; C Tumor growth curves, each point represents the mean (and SEM) of all mice in each group, n = 6; D Single mice growth curves of each treated group

Article Snippet: PCSK9 protein level in mouse sera was evaluated by Mouse Proprotein Convertase 9/PCSK9 Quantikine ELISA Kit (R&D Systems, Minneapolis, MN, USA) according to the manufacturer’s protocol.

Techniques: Drug discovery, Vaccines

Fig. 3 Anti-PCSK9 responses induced by cVLP-PCSK9 vaccine. A Mean (and SEM) of anti-PCSK9 antibody titers measured by ELISA represented as logarithm of Optical Density (OD) value multiplied by dilution factor of the serum sample, n = 6. Vehicle vs. cVLP-PCSK9, at least p < 0.01, from day 56; Vehicle vs. cVLP-HER2 + cVLP-PCSK9, p < 0.05, from day 98; cVLP-HER2 vs. cVLP-PCSK9, at least p < 0.05, from day 56; cVLP-PCSK9 vs. cVLP-HER2 + cVLP-PCSK9, at least p < 0.05, from day 98; cVLP-HER2 vs. cVLP-HER2 + cVLP-PCSK9, p < 0.05, day 98. All statistics were carried out by Welch t-test. B Percentage of the increase of anti-PCSK9 total antibodies after the last vaccination. Histogram reports mean (and SEM) of each group. *p < 0.05 vs Vehicle, + p < 0.05 vs cVLP-HER2, #p < 0.05 at least vs cVLP-HER2 + cVLP-PCSK9 by Welch’s t-test; C PCSK9 protein levels in mouse serum (µg/mL), each point represents the mean (and SEM) for each experimental group, n = 5–6. D Percentage of the increase of anti-PCSK9 protein inhibition after the last vaccination. Histogram reports mean (and SEM) of each group. + p < 0.05 vs cVLP-HER2, #p < 0.05 at least vs cVLP-HER2 + cVLP-PCSK9 by Welch’s t-test

Journal: Journal of translational medicine

Article Title: Targeting PCSK9, through an innovative cVLP-based vaccine, enhanced the therapeutic activity of a cVLP-HER2 vaccine in a preclinical model of HER2-positive mammary carcinoma.

doi: 10.1186/s12967-025-06126-w

Figure Lengend Snippet: Fig. 3 Anti-PCSK9 responses induced by cVLP-PCSK9 vaccine. A Mean (and SEM) of anti-PCSK9 antibody titers measured by ELISA represented as logarithm of Optical Density (OD) value multiplied by dilution factor of the serum sample, n = 6. Vehicle vs. cVLP-PCSK9, at least p < 0.01, from day 56; Vehicle vs. cVLP-HER2 + cVLP-PCSK9, p < 0.05, from day 98; cVLP-HER2 vs. cVLP-PCSK9, at least p < 0.05, from day 56; cVLP-PCSK9 vs. cVLP-HER2 + cVLP-PCSK9, at least p < 0.05, from day 98; cVLP-HER2 vs. cVLP-HER2 + cVLP-PCSK9, p < 0.05, day 98. All statistics were carried out by Welch t-test. B Percentage of the increase of anti-PCSK9 total antibodies after the last vaccination. Histogram reports mean (and SEM) of each group. *p < 0.05 vs Vehicle, + p < 0.05 vs cVLP-HER2, #p < 0.05 at least vs cVLP-HER2 + cVLP-PCSK9 by Welch’s t-test; C PCSK9 protein levels in mouse serum (µg/mL), each point represents the mean (and SEM) for each experimental group, n = 5–6. D Percentage of the increase of anti-PCSK9 protein inhibition after the last vaccination. Histogram reports mean (and SEM) of each group. + p < 0.05 vs cVLP-HER2, #p < 0.05 at least vs cVLP-HER2 + cVLP-PCSK9 by Welch’s t-test

Techniques: Enzyme-linked Immunosorbent Assay, Inhibition

Fig. 4 Inhibition of human breast cancer cell 3D agar colony growth by antibodies elicited by vaccinations. Upper panel, colony inhibition assay on BT-474 (HER2 + + + , trastuzumab sensitive) and BT-474 C5 (HER2 + + + , trastuzumab resistant), n = 2. Each bar represents the mean (and SEM) number of colonies larger than 90 µm as counted in two independent cultures with the aid of a micrometer. *p < 0.05 vs untreated, °p < 0.05 vs cVLP-PCSK9, + p < 0.05 vs cVLP-HER2, by t student’s test, unpaired. Lower panel, representative pictures of live agar colonies were acquired with an inverted microscope (dark-field, 25X)

Journal: Journal of translational medicine

Article Title: Targeting PCSK9, through an innovative cVLP-based vaccine, enhanced the therapeutic activity of a cVLP-HER2 vaccine in a preclinical model of HER2-positive mammary carcinoma.

doi: 10.1186/s12967-025-06126-w

Figure Lengend Snippet: Fig. 4 Inhibition of human breast cancer cell 3D agar colony growth by antibodies elicited by vaccinations. Upper panel, colony inhibition assay on BT-474 (HER2 + + + , trastuzumab sensitive) and BT-474 C5 (HER2 + + + , trastuzumab resistant), n = 2. Each bar represents the mean (and SEM) number of colonies larger than 90 µm as counted in two independent cultures with the aid of a micrometer. *p < 0.05 vs untreated, °p < 0.05 vs cVLP-PCSK9, + p < 0.05 vs cVLP-HER2, by t student’s test, unpaired. Lower panel, representative pictures of live agar colonies were acquired with an inverted microscope (dark-field, 25X)

Techniques: Inhibition, Inverted Microscopy

a Venn diagram of genes upregulated in 15376T compared with Lin28b-KO 15376T and 14837T as determined by RNA-sequencing (RNA-seq). b , c The levels of Wnt5a in 15376T, Lin28b-KO 15376T, and 14837T were measured by real-‍time qPCR ( b ) and western blotting ( c ). Representative of n = 3 independent experiments ( c ). d , e The levels of WNT5A in PANC-1, LIN28B-KO PANC-1, and Mia Paca-2 were measured by real-‍time qPCR ( d ) and western blotting ( e ). Representative of n = 3 independent experiments ( e ). f Wnt5a levels in the supernatants of 15376T, Lin28b-KO 15376T, and 14837T were examined by ELISA. g WNT5A levels in the supernatants of PANC-1, LIN28B-KO PANC-1 and Mia Paca-2 were examined by ELISA. h , i 14837CAFs ( h ) or 15376CAFs ( i ) ‍were cultured with 15376T-CM or Wnt5a-KO 15376T-CM for 6 days. Then, Lin28b levels were measured by western blotting. Lin28b levels in 15376T were included as a positive control. Representative of n = 3 independent experiments. j – l hCAFs were cultured with PANC-1-CM ( j ), WNT5A-KO PANC-1-CM ( j ), PANC03.27-CM ( k ), WNT5A-KO PANC03.27-CM ( k ), hPDAC1 # -CM ( l ), and WNT5A-KO hPDAC1 # -CM ( l ) for 6 days. Then, the levels of LIN28B were measured by western blotting. LIN28B levels in PANC-1 ( j ), PANC03.27 ( k ), and hPDAC1 # ( l ) were included as a positive control. Representative of n = 3 independent experiments. m Wnt5a levels in the supernatants of low (30–40%) and high (80–90%) density inoculated 15376T were examined by ELISA. n – q 14837CAFs ( n , o ) or 15376CAFs ( p , q ) were ‍treated with 100 ng/ml or 200 ng/ml recombinant-Wnt5a(r-mWnt5a) for 6 days. Cells were collected for Western blotting at indicated time points. Lin28b levels in 15376T were included as a positive control. Representative of n = 3 independent experiments ( n – q ). r , s 14837CAFs ( r ) or 15376CAFs ( s ) were cultured with 14837T-‍CM or 15376T-‍CM in the presence or absence of 1 μg/ml Wnt5a neutralizing antibody (anti-Wnt5a) for 6 days. Then, cells were collected for Western blotting. Lin28b levels in 15376T were included as a positive control. Representative of n = 3 independent experiments ( r , s ). t Orthotopic PDAC tumors generated with 15376T or Wnt5a-KO 15376T were analyzed by Wnt5a, Lin28b and α-SMA immunofluorescence staining (n = 6 mice). Representative images are shown. Scale bar: 30 μm. Three biologically independent experiments were performed ( b , d , f , g , m ). Data are shown as mean ± s.d. P -values were determined by one-way ANOVA with Tukey’s multiple comparison test ( b , d , f , g ) or two-tailed unpaired Student’s t-tests ( m ).

Journal: Nature Communications

Article Title: The Lin28b/Wnt5a axis drives pancreas cancer through crosstalk between cancer associated fibroblasts and tumor epithelium

doi: 10.1038/s41467-023-42508-8

Figure Lengend Snippet: a Venn diagram of genes upregulated in 15376T compared with Lin28b-KO 15376T and 14837T as determined by RNA-sequencing (RNA-seq). b , c The levels of Wnt5a in 15376T, Lin28b-KO 15376T, and 14837T were measured by real-‍time qPCR ( b ) and western blotting ( c ). Representative of n = 3 independent experiments ( c ). d , e The levels of WNT5A in PANC-1, LIN28B-KO PANC-1, and Mia Paca-2 were measured by real-‍time qPCR ( d ) and western blotting ( e ). Representative of n = 3 independent experiments ( e ). f Wnt5a levels in the supernatants of 15376T, Lin28b-KO 15376T, and 14837T were examined by ELISA. g WNT5A levels in the supernatants of PANC-1, LIN28B-KO PANC-1 and Mia Paca-2 were examined by ELISA. h , i 14837CAFs ( h ) or 15376CAFs ( i ) ‍were cultured with 15376T-CM or Wnt5a-KO 15376T-CM for 6 days. Then, Lin28b levels were measured by western blotting. Lin28b levels in 15376T were included as a positive control. Representative of n = 3 independent experiments. j – l hCAFs were cultured with PANC-1-CM ( j ), WNT5A-KO PANC-1-CM ( j ), PANC03.27-CM ( k ), WNT5A-KO PANC03.27-CM ( k ), hPDAC1 # -CM ( l ), and WNT5A-KO hPDAC1 # -CM ( l ) for 6 days. Then, the levels of LIN28B were measured by western blotting. LIN28B levels in PANC-1 ( j ), PANC03.27 ( k ), and hPDAC1 # ( l ) were included as a positive control. Representative of n = 3 independent experiments. m Wnt5a levels in the supernatants of low (30–40%) and high (80–90%) density inoculated 15376T were examined by ELISA. n – q 14837CAFs ( n , o ) or 15376CAFs ( p , q ) were ‍treated with 100 ng/ml or 200 ng/ml recombinant-Wnt5a(r-mWnt5a) for 6 days. Cells were collected for Western blotting at indicated time points. Lin28b levels in 15376T were included as a positive control. Representative of n = 3 independent experiments ( n – q ). r , s 14837CAFs ( r ) or 15376CAFs ( s ) were cultured with 14837T-‍CM or 15376T-‍CM in the presence or absence of 1 μg/ml Wnt5a neutralizing antibody (anti-Wnt5a) for 6 days. Then, cells were collected for Western blotting. Lin28b levels in 15376T were included as a positive control. Representative of n = 3 independent experiments ( r , s ). t Orthotopic PDAC tumors generated with 15376T or Wnt5a-KO 15376T were analyzed by Wnt5a, Lin28b and α-SMA immunofluorescence staining (n = 6 mice). Representative images are shown. Scale bar: 30 μm. Three biologically independent experiments were performed ( b , d , f , g , m ). Data are shown as mean ± s.d. P -values were determined by one-way ANOVA with Tukey’s multiple comparison test ( b , d , f , g ) or two-tailed unpaired Student’s t-tests ( m ).

Article Snippet: Recombinant protein of Pcsk9 (#50251-M08H) and PGRN (#50396-M08H) was purchased from SinoBiological.

Techniques: RNA Sequencing Assay, Western Blot, Enzyme-linked Immunosorbent Assay, Cell Culture, Positive Control, Recombinant, Generated, Immunofluorescence, Staining, Comparison, Two Tailed Test

$Before the experiment started, CAFs were cultured with 15376T-‍CM for 6 days to induce Lin28b expression. CM for CAFs culture was replaced daily. a The ability of CAFs-CM to increase PDAC proliferation was abolished after boiling at 100 °C for 15 min as well as after three consecutive freeze (−80 °C, 10 min)-thaw (60 °C, 10 min) cycles. b The factor secreted by CAFs that increases PDAC proliferation was retained in the >3-kDa fraction of CAFs-CM. c CAFs were cultured with 15376T-‍CM for 6 days and then they were cultured with FBS-free 15376T-CM for 24 h. Then, CM from 15376CAFs or Lin28b-KO 15376CAFs were harvested for quantitative secretomics analysis. A heat map shows cytokines which are downregulated in Lin28b-KO 15376CAFs-CM. d , e CRISPR/Cas9-resistent flag-Lin28b-WT(r) and flag-Lin28b-MU(r) were overexpressed in Lin28b-KO CAFs. Western blotting was then performed to determine Lin28b protein levels ( d ). let-‍7 (let-7a, let-7b, let-7c, let-7d, let-7e, let-7f, let-7g, let-7i, mir-98) levels were measured by real-time qPCR ( e ). Representative of n = 3 independent experiments ( d ). f – j The levels of Clu ( f ), Cxcl5 ( g ), FN ( h ), PGRN ( i ), and Pcsk9 ( j ) in the supernatants of indicated cells were examined by ELISA. k 15376T were ‍treated with 100 ng/ml recombinant PGRN (r-mPGRN) or 100 ng/ml recombinant Pcsk9 (r-‍mPcsk9) under low glucose (2 mM) for 2 days. The cells were counted to calculate the cell proliferation. l 15376T were co-cultured with 15376CAFs in transwell chambers, and treated with or without 1 μg/ml neutralizing antibody (anti-Pcsk9 or anti-PGRN) under low glucose (2 mM) for 2 days. The cells were counted to calculate the cell proliferation. m , n Western blotting was used to detect the knocking-out efficiency of Pcsk9 in 15376CAFs ( m ). Representative of n = 2 independent experiments. 15376T were co-cultured with 15376CAFs or Pcsk9-KO 15376CAFs in transwell chambers for 2 days. The cells were counted to calculate the cell proliferation ( n ). o – s 15376T was orthotopically co-injected with 15376CAFs or Pcsk9-KO 15376CAFs into C57BL/6 J mice and the tumors were harvested after 1 week ( n = 6 mice). IHC was performed with Pcsk9 and α-SMA antibodies ( o ) and Pcsk9 IHC scores in CAFs were plotted ( n = 10 views per group) ( p ). The pancreas was weighed ( q ) and analyzed by Ki-67 and CK19 IHC staining ( r ). The proportion of ki67-positive ( s ) cell was shown ( n = 10 views per group). Scale bar: 30 μM. ( t ) 15376T were orthotopically injected into C57BL/6 J mice. About 200 μg anti-Pcsk9 monoclonal antibodies (alirocumab) were intraperitoneally injected on days 3, 5, 8, and 11. After 2 weeks, the pancreas was weighed ( n = 6 mice). Three biologically independent experiments were performed ( e , f – j , t ). Four biologically independent experiments were performed ( a , b , k , l ). Data are shown as mean ± s.d. P -values were determined by one-way ANOVA with Tukey’s multiple comparison test ( a , b , e – l , n ) or two-tailed unpaired Student’s t-tests ( p , q , s , t ).$

Journal: Nature Communications

Article Title: The Lin28b/Wnt5a axis drives pancreas cancer through crosstalk between cancer associated fibroblasts and tumor epithelium

doi: 10.1038/s41467-023-42508-8

Figure Lengend Snippet: Before the experiment started, CAFs were cultured with 15376T-‍CM for 6 days to induce Lin28b expression. CM for CAFs culture was replaced daily. a The ability of CAFs-CM to increase PDAC proliferation was abolished after boiling at 100 °C for 15 min as well as after three consecutive freeze (−80 °C, 10 min)-thaw (60 °C, 10 min) cycles. b The factor secreted by CAFs that increases PDAC proliferation was retained in the >3-kDa fraction of CAFs-CM. c CAFs were cultured with 15376T-‍CM for 6 days and then they were cultured with FBS-free 15376T-CM for 24 h. Then, CM from 15376CAFs or Lin28b-KO 15376CAFs were harvested for quantitative secretomics analysis. A heat map shows cytokines which are downregulated in Lin28b-KO 15376CAFs-CM. d , e CRISPR/Cas9-resistent flag-Lin28b-WT(r) and flag-Lin28b-MU(r) were overexpressed in Lin28b-KO CAFs. Western blotting was then performed to determine Lin28b protein levels ( d ). let-‍7 (let-7a, let-7b, let-7c, let-7d, let-7e, let-7f, let-7g, let-7i, mir-98) levels were measured by real-time qPCR ( e ). Representative of n = 3 independent experiments ( d ). f – j The levels of Clu ( f ), Cxcl5 ( g ), FN ( h ), PGRN ( i ), and Pcsk9 ( j ) in the supernatants of indicated cells were examined by ELISA. k 15376T were ‍treated with 100 ng/ml recombinant PGRN (r-mPGRN) or 100 ng/ml recombinant Pcsk9 (r-‍mPcsk9) under low glucose (2 mM) for 2 days. The cells were counted to calculate the cell proliferation. l 15376T were co-cultured with 15376CAFs in transwell chambers, and treated with or without 1 μg/ml neutralizing antibody (anti-Pcsk9 or anti-PGRN) under low glucose (2 mM) for 2 days. The cells were counted to calculate the cell proliferation. m , n Western blotting was used to detect the knocking-out efficiency of Pcsk9 in 15376CAFs ( m ). Representative of n = 2 independent experiments. 15376T were co-cultured with 15376CAFs or Pcsk9-KO 15376CAFs in transwell chambers for 2 days. The cells were counted to calculate the cell proliferation ( n ). o – s 15376T was orthotopically co-injected with 15376CAFs or Pcsk9-KO 15376CAFs into C57BL/6 J mice and the tumors were harvested after 1 week ( n = 6 mice). IHC was performed with Pcsk9 and α-SMA antibodies ( o ) and Pcsk9 IHC scores in CAFs were plotted ( n = 10 views per group) ( p ). The pancreas was weighed ( q ) and analyzed by Ki-67 and CK19 IHC staining ( r ). The proportion of ki67-positive ( s ) cell was shown ( n = 10 views per group). Scale bar: 30 μM. ( t ) 15376T were orthotopically injected into C57BL/6 J mice. About 200 μg anti-Pcsk9 monoclonal antibodies (alirocumab) were intraperitoneally injected on days 3, 5, 8, and 11. After 2 weeks, the pancreas was weighed ( n = 6 mice). Three biologically independent experiments were performed ( e , f – j , t ). Four biologically independent experiments were performed ( a , b , k , l ). Data are shown as mean ± s.d. P -values were determined by one-way ANOVA with Tukey’s multiple comparison test ( a , b , e – l , n ) or two-tailed unpaired Student’s t-tests ( p , q , s , t ).

Article Snippet: Recombinant protein of Pcsk9 (#50251-M08H) and PGRN (#50396-M08H) was purchased from SinoBiological.

Techniques: Cell Culture, Expressing, CRISPR, Western Blot, Enzyme-linked Immunosorbent Assay, Recombinant, Injection, Immunohistochemistry, Comparison, Two Tailed Test

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