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innotest b-amyloid(1-42) (Fujirebio Inc)

Name: innotest b-amyloid(1-42)
Brand: Fujirebio Inc
Rating: 96 (740 reviews)

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Fujirebio Inc innotest b-amyloid(1-42)
Innotest B Amyloid(1 42), supplied by Fujirebio Inc, used in various techniques. Bioz Stars score: 96/100, based on 740 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 96 stars, based on 740 article reviews

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The nEL mRNA vaccine synergizes with NK cells to promote the eradication of EBV + NPC in humanized mice (A) Scheme of the animal experiment. Human PBMC-engrafted NOG mice were implanted subcutaneously with CNE2-EBV cells. One week after tumor inoculation, mice were treated with mRNA vaccine and NK cells (Vac+NK), NK cells alone (NK), or liposomes and PBS (Control) every 3 to 4 days ( n = 6 per group). Blood and tumor samples were collected for analysis at the end of the experiment. (B) Tumor growth curves of each group (ordinary two-way ANOVA with Tukey’s multiple comparisons test, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). (C) Photograph of harvested tumor tissues from each group. The cross symbol indicates eradicated tumors by the combined therapy. (D) Average tumor weight of each group (ordinary one-way ANOVA with Tukey’s multiple comparisons test, ∗ p < 0.05, ∗∗∗∗ p < 0.0001). (E) HE staining and (F) IHC staining of <t>EBNA1</t> in tumor sections from each group. Scale bars: 500 μm (top), 100 μm (bottom, enlarged boxed regions). (G) Body weight and food intake changes of PBMC-humanized mice in the control, NK, and Vac+NK groups at different time points ( n = 6 per group). A group of non-humanized NOG mice was additionally recorded for reference. (H) Tumor growth curves of each group from humanized mice reconstituted with PBMC source from donor #3 (ordinary two-way ANOVA with Tukey’s multiple comparisons test, ∗∗ p < 0.01, ∗∗∗∗ p < 0.0001). All data represented as means ± SEM.

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Journal: Molecular Therapy Oncology

Article Title: Epstein-Barr virus mRNA vaccine synergizes with NK cells to enhance nasopharyngeal carcinoma eradication in humanized mice

doi: 10.1016/j.omton.2025.200986

Figure Lengend Snippet: The nEL mRNA vaccine synergizes with NK cells to promote the eradication of EBV + NPC in humanized mice (A) Scheme of the animal experiment. Human PBMC-engrafted NOG mice were implanted subcutaneously with CNE2-EBV cells. One week after tumor inoculation, mice were treated with mRNA vaccine and NK cells (Vac+NK), NK cells alone (NK), or liposomes and PBS (Control) every 3 to 4 days ( n = 6 per group). Blood and tumor samples were collected for analysis at the end of the experiment. (B) Tumor growth curves of each group (ordinary two-way ANOVA with Tukey’s multiple comparisons test, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001). (C) Photograph of harvested tumor tissues from each group. The cross symbol indicates eradicated tumors by the combined therapy. (D) Average tumor weight of each group (ordinary one-way ANOVA with Tukey’s multiple comparisons test, ∗ p < 0.05, ∗∗∗∗ p < 0.0001). (E) HE staining and (F) IHC staining of EBNA1 in tumor sections from each group. Scale bars: 500 μm (top), 100 μm (bottom, enlarged boxed regions). (G) Body weight and food intake changes of PBMC-humanized mice in the control, NK, and Vac+NK groups at different time points ( n = 6 per group). A group of non-humanized NOG mice was additionally recorded for reference. (H) Tumor growth curves of each group from humanized mice reconstituted with PBMC source from donor #3 (ordinary two-way ANOVA with Tukey’s multiple comparisons test, ∗∗ p < 0.01, ∗∗∗∗ p < 0.0001). All data represented as means ± SEM.

Article Snippet: For immunostaining, antigen retrieval was performed and then blocked with 10% goat serum (Solarbio, SL038) for 1 h, followed by incubation with primary antibodies against CD56 (1:200, Affinity, DF7832), granzyme B (1:200, Affinity, AF0175), perforin (1:200, Affinity, DF6004), CD4 (1:100, Abcam, DF16080), CD8 (1:100, Abcam, ab17147), IFN-γ (1:100, Affinity, DF6045), and EBNA1 (1:100, Santa Cruz, 81581) at 4°C for overnight.

Techniques: Liposomes, Control, Staining, Immunohistochemistry

Journal: PLOS Pathogens

Article Title: STAT3, MYC, and EBNA1 cooperate through a ZC3H18 transcriptional network to regulate survival and proliferation of EBV-positive lymphomas

doi: 10.1371/journal.ppat.1013166

Figure Lengend Snippet: (A-D) HH514-16 BL cells were seeded at 2 × 10 5 /ml. After 24 hours, cells were exposed to varying concentrations of LLL12B (STAT3 inhibitor; A), APTO-253 (MYC inhibitor; B), and VK-1727 (EBNA1 inhibitor; C) for 48 hours. Cells were then collected and analyzed by immunoblotting.

Article Snippet: The following antibodies were used for immunostaining: rabbit anti-STAT3 antibody (4904S, Cell Signaling Technology), mouse anti-EBNA1 antibody (sc-81581, Santa Cruz Biotechnology), rabbit anti-MYC antibody (A190-105A, Bethyl Laboratories), mouse anti-β-actin antibody (clone AC-15) (A1978, Sigma-Aldrich), rabbit anti-phospho-IκBα (Ser32) antibody (2859S, Cell Signaling Technology), rabbit anti-IκBα antibody (9242S, Cell Signaling Technology), rabbit anti-p65 antibody (8242S, Cell Signaling Technology), rabbit anti-p50 antibody (13586, Cell Signaling Technology), rabbit anti-ZC3H18 antibody (A304-682A, Bethyl Laboratories), rabbit anti-Caspase 3 antibody (GTX110543, GeneTex), mouse anti-Cyclin A antibody (sc-53228, Santa Cruz Biotechnology), rabbit anti-Cyclin B antibody (4138S, Cell Signaling Technology), rabbit anti-Cyclin E antibody (A301-566, Bethyl Laboratories), mouse anti-ZEBRA antibody (sc-53904, Santa Cruz Biotechnology), rabbit anti-PCNA antibody (A300-276, Bethyl Laboratories), HRP-conjugated goat anti-mouse IgG (626520, Thermo Fisher Scientific), and HRP-conjugated goat anti-rabbit IgG (31460, Thermo Fisher Scientific).

Techniques: Western Blot

(A-F) One million HH514-16 BL cells were transfected with two siRNAs targeting each STAT3 (A, D), c-MYC (B, E), or BKRF1 (EBNA1; C, F) versus control siRNA. After 24 hours, cells were collected for immunoblotting with indicated antibodies (A-C) or subjected to RT-qPCR to analyze ZC3H18 , STAT3 , c-MYC , and EBNA1 transcript levels (D-F). (G) One million EBV - BJAB cells were transfected with two siRNAs targeting STAT3 versus control siRNA. After 24 hours, cells were collected for RT-qPCR to analyze STAT3 , c-MYC and ZC3H18 transcript levels. (H) One million cells were seeded at 5 × 10 5 /ml and harvested 24 hours later. The abundance of STAT3 and c-MYC transcripts was analyzed by RT-qPCR in EBV - BJAB, EBV - Akata BL, and EBV + Akata BL cells. (I) STAT3, MYC and EBNA1 plasmids were transfected into EBV - BJAB, EBV - Akata BL, and EBV + Akata BL cells. After 48 hours, cells were collected for RT-qPCR to assess the abundance of ZC3H18 , STAT3 , c-MYC and EBNA1 transcripts. Error bars, SEM of 3 technical replicates; *, p < 0.05; **, p < 0.01; ***, p < 0.001 (versus control); NS, not significant; experiments were performed two to four times.

Journal: PLOS Pathogens

Article Title: STAT3, MYC, and EBNA1 cooperate through a ZC3H18 transcriptional network to regulate survival and proliferation of EBV-positive lymphomas

doi: 10.1371/journal.ppat.1013166

Figure Lengend Snippet: (A-F) One million HH514-16 BL cells were transfected with two siRNAs targeting each STAT3 (A, D), c-MYC (B, E), or BKRF1 (EBNA1; C, F) versus control siRNA. After 24 hours, cells were collected for immunoblotting with indicated antibodies (A-C) or subjected to RT-qPCR to analyze ZC3H18 , STAT3 , c-MYC , and EBNA1 transcript levels (D-F). (G) One million EBV - BJAB cells were transfected with two siRNAs targeting STAT3 versus control siRNA. After 24 hours, cells were collected for RT-qPCR to analyze STAT3 , c-MYC and ZC3H18 transcript levels. (H) One million cells were seeded at 5 × 10 5 /ml and harvested 24 hours later. The abundance of STAT3 and c-MYC transcripts was analyzed by RT-qPCR in EBV - BJAB, EBV - Akata BL, and EBV + Akata BL cells. (I) STAT3, MYC and EBNA1 plasmids were transfected into EBV - BJAB, EBV - Akata BL, and EBV + Akata BL cells. After 48 hours, cells were collected for RT-qPCR to assess the abundance of ZC3H18 , STAT3 , c-MYC and EBNA1 transcripts. Error bars, SEM of 3 technical replicates; *, p < 0.05; **, p < 0.01; ***, p < 0.001 (versus control); NS, not significant; experiments were performed two to four times.

Techniques: Transfection, Control, Western Blot, Quantitative RT-PCR

(A-I) One million LCL were seeded at 5 × 10 5 /ml. After 24 hours, cells were transfected with control siRNA or two siRNAs targeting each STAT3 (A, B) or BKRF1 (EBNA1; C, D). After another 24 hours, cells were collected for immunoblotting with indicated antibodies (A, C) or RT-qPCR (B, D) to measure c-MYC transcript levels. (E, H) Four million LCL were subjected to ChIP with indicated antibodies or control IgG followed by qPCR with primers targeting the c-MYC (E), STAT3 (H), and EBNA1 (H) promoters. Data were normalized to IgG; error bars represent SEM of technical replicates. The experiment was performed twice. (F, G) One million LCL were transduced with lenti-shControl (shCtrl) or lenti-shZC3H18 (shZC3H18#1, #2) for 7 days and then analyzed by RT-qPCR to quantify STAT3 , c-MYC , EBNA1 , and BZLF1 transcripts (F) or immunoblotting to confirm depletion of ZC3H18 (G). (I) Four million LCL were subjected to ChIP using indicated antibodies or control IgG. Precipitated DNA was subjected to qPCR analysis with primers targeting promoter regions of EBNA1 promoters Cp, Wp, or Qp. Data were normalized to input. Error bars, SEM of 3 technical replicates; *, p < 0.05; **, p < 0.01; ***, p < 0.001 (versus control); NS, not significant; experiments were performed twice.

Journal: PLOS Pathogens

Article Title: STAT3, MYC, and EBNA1 cooperate through a ZC3H18 transcriptional network to regulate survival and proliferation of EBV-positive lymphomas

doi: 10.1371/journal.ppat.1013166

Figure Lengend Snippet: (A-I) One million LCL were seeded at 5 × 10 5 /ml. After 24 hours, cells were transfected with control siRNA or two siRNAs targeting each STAT3 (A, B) or BKRF1 (EBNA1; C, D). After another 24 hours, cells were collected for immunoblotting with indicated antibodies (A, C) or RT-qPCR (B, D) to measure c-MYC transcript levels. (E, H) Four million LCL were subjected to ChIP with indicated antibodies or control IgG followed by qPCR with primers targeting the c-MYC (E), STAT3 (H), and EBNA1 (H) promoters. Data were normalized to IgG; error bars represent SEM of technical replicates. The experiment was performed twice. (F, G) One million LCL were transduced with lenti-shControl (shCtrl) or lenti-shZC3H18 (shZC3H18#1, #2) for 7 days and then analyzed by RT-qPCR to quantify STAT3 , c-MYC , EBNA1 , and BZLF1 transcripts (F) or immunoblotting to confirm depletion of ZC3H18 (G). (I) Four million LCL were subjected to ChIP using indicated antibodies or control IgG. Precipitated DNA was subjected to qPCR analysis with primers targeting promoter regions of EBNA1 promoters Cp, Wp, or Qp. Data were normalized to input. Error bars, SEM of 3 technical replicates; *, p < 0.05; **, p < 0.01; ***, p < 0.001 (versus control); NS, not significant; experiments were performed twice.

Techniques: Transfection, Control, Western Blot, Quantitative RT-PCR, Transduction

(A-C) HH514-16 BL cells were seeded at 5 × 10 5 /ml. After 24 hours, 4 million cells were subjected to ChIP using indicated antibodies or control IgG. Precipitated DNA was subjected to qPCR analysis with primers targeting indicated promoters (A), EBNA1 promoters Cp, Wp, or Qp (B), or gene body regions of c-MYC or ZC3H18 (C). Data were normalized to input. Error bars, SEM of 3 technical replicates; *, p < 0.05; **, p < 0.01; ***, p < 0.001 (versus control); NS, not significant; experiments were performed twice.

Journal: PLOS Pathogens

Article Title: STAT3, MYC, and EBNA1 cooperate through a ZC3H18 transcriptional network to regulate survival and proliferation of EBV-positive lymphomas

doi: 10.1371/journal.ppat.1013166

Figure Lengend Snippet: (A-C) HH514-16 BL cells were seeded at 5 × 10 5 /ml. After 24 hours, 4 million cells were subjected to ChIP using indicated antibodies or control IgG. Precipitated DNA was subjected to qPCR analysis with primers targeting indicated promoters (A), EBNA1 promoters Cp, Wp, or Qp (B), or gene body regions of c-MYC or ZC3H18 (C). Data were normalized to input. Error bars, SEM of 3 technical replicates; *, p < 0.05; **, p < 0.01; ***, p < 0.001 (versus control); NS, not significant; experiments were performed twice.

Techniques: Control

STAT3, in EBV-infected B cells, localizes to the nucleus to regulate the expression of multiple genes, including MYC and BKRF1 (EBNA1), which in turn promote the expression of the transcription factor ZC3H18. ZC3H18 transcriptionally regulates STAT3, c-MYC, and EBNA1 while also contributing to NF-κB components even in the absence of LMP1, thereby contributing to cell survival and proliferation.

Journal: PLOS Pathogens

Article Title: STAT3, MYC, and EBNA1 cooperate through a ZC3H18 transcriptional network to regulate survival and proliferation of EBV-positive lymphomas

doi: 10.1371/journal.ppat.1013166

Figure Lengend Snippet: STAT3, in EBV-infected B cells, localizes to the nucleus to regulate the expression of multiple genes, including MYC and BKRF1 (EBNA1), which in turn promote the expression of the transcription factor ZC3H18. ZC3H18 transcriptionally regulates STAT3, c-MYC, and EBNA1 while also contributing to NF-κB components even in the absence of LMP1, thereby contributing to cell survival and proliferation.

Techniques: Infection, Expressing