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hpv 16 e7 fragment  (Addgene inc)


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    Addgene inc hpv 16 e7 fragment
    A. Table of patient samples used in snRNA-seq, with the status of a few gene alterations listed. B. Sample MRIs from one patient showing T1 contrast-enhanced and T2 weighted images. On the left is the preoperative study demonstrating location of contrast enhancing zone (yellow arrow) containing the presumed solid tumor and the broader, T2-hyperintense signal (red arrow) that containing the presumed infiltrating tumor. The middle image shows the pre-operative regions selected for biopsy and the right image shows the intraoperative neuronavigation biopsy acquisition. C. The workflow from sample biopsy, processing, snRNA-sequencing, and data analysis. D. Bar plots of cell type proportions in the infiltrating and solid tumor regions. Each bar represents the mean proportion of the selected cell type in the region and the positive and negative standard deviation are represented by the bracket. Each dot represents the cell type proportion of a single sample. E. Representative images of expanded Nf1- knockout OPCs (GFP + PDGFRα + ) generated by transduction of MSCV carrying Nf1 guide RNA/Cas9. WT OPCs (GFP - PDGFRα + ) were excluded from the expanded Nf1 -null OPC clones, suggesting OPC competition. Scale bar: 50 μm. F. Representative images of expanded Rb -inactivated OPCs (GFP + PDGFRα + ) upon transduction of MSCV <t>carrying</t> <t>HPV-16</t> E7 protein that inactivates Rb function. Expanded GFP + Rb -inactivated OPCs (orange arrow) intermixed with WT OPCs (GFP - PDGFRα + , white arrow-head), suggesting the lack of OPC competition. Scale bar: 50 μm G. Representative images showing the expansion of OPCs with EGFR mutation ( EGFRvIII ). The expanded clone of EGFRvIII -expressing OPCs excluded WT OPCs (GFP - PDGFRα + ), suggesting OPC competition. Scale bar: 50 μm. H. Summary of the sufficiency and insufficiency in driving OPC competition of all examined gliomagenic mutations in this study.
    Hpv 16 E7 Fragment, supplied by Addgene inc, 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/result/hpv 16 e7 fragment/product/Addgene inc
    Average 93 stars, based on 3 article reviews
    hpv 16 e7 fragment - by Bioz Stars, 2026-06
    93/100 stars

    Images

    1) Product Images from "Critical role of cell competition in gliomagenesis"

    Article Title: Critical role of cell competition in gliomagenesis

    Journal: bioRxiv

    doi: 10.64898/2026.01.15.699808

    A. Table of patient samples used in snRNA-seq, with the status of a few gene alterations listed. B. Sample MRIs from one patient showing T1 contrast-enhanced and T2 weighted images. On the left is the preoperative study demonstrating location of contrast enhancing zone (yellow arrow) containing the presumed solid tumor and the broader, T2-hyperintense signal (red arrow) that containing the presumed infiltrating tumor. The middle image shows the pre-operative regions selected for biopsy and the right image shows the intraoperative neuronavigation biopsy acquisition. C. The workflow from sample biopsy, processing, snRNA-sequencing, and data analysis. D. Bar plots of cell type proportions in the infiltrating and solid tumor regions. Each bar represents the mean proportion of the selected cell type in the region and the positive and negative standard deviation are represented by the bracket. Each dot represents the cell type proportion of a single sample. E. Representative images of expanded Nf1- knockout OPCs (GFP + PDGFRα + ) generated by transduction of MSCV carrying Nf1 guide RNA/Cas9. WT OPCs (GFP - PDGFRα + ) were excluded from the expanded Nf1 -null OPC clones, suggesting OPC competition. Scale bar: 50 μm. F. Representative images of expanded Rb -inactivated OPCs (GFP + PDGFRα + ) upon transduction of MSCV carrying HPV-16 E7 protein that inactivates Rb function. Expanded GFP + Rb -inactivated OPCs (orange arrow) intermixed with WT OPCs (GFP - PDGFRα + , white arrow-head), suggesting the lack of OPC competition. Scale bar: 50 μm G. Representative images showing the expansion of OPCs with EGFR mutation ( EGFRvIII ). The expanded clone of EGFRvIII -expressing OPCs excluded WT OPCs (GFP - PDGFRα + ), suggesting OPC competition. Scale bar: 50 μm. H. Summary of the sufficiency and insufficiency in driving OPC competition of all examined gliomagenic mutations in this study.
    Figure Legend Snippet: A. Table of patient samples used in snRNA-seq, with the status of a few gene alterations listed. B. Sample MRIs from one patient showing T1 contrast-enhanced and T2 weighted images. On the left is the preoperative study demonstrating location of contrast enhancing zone (yellow arrow) containing the presumed solid tumor and the broader, T2-hyperintense signal (red arrow) that containing the presumed infiltrating tumor. The middle image shows the pre-operative regions selected for biopsy and the right image shows the intraoperative neuronavigation biopsy acquisition. C. The workflow from sample biopsy, processing, snRNA-sequencing, and data analysis. D. Bar plots of cell type proportions in the infiltrating and solid tumor regions. Each bar represents the mean proportion of the selected cell type in the region and the positive and negative standard deviation are represented by the bracket. Each dot represents the cell type proportion of a single sample. E. Representative images of expanded Nf1- knockout OPCs (GFP + PDGFRα + ) generated by transduction of MSCV carrying Nf1 guide RNA/Cas9. WT OPCs (GFP - PDGFRα + ) were excluded from the expanded Nf1 -null OPC clones, suggesting OPC competition. Scale bar: 50 μm. F. Representative images of expanded Rb -inactivated OPCs (GFP + PDGFRα + ) upon transduction of MSCV carrying HPV-16 E7 protein that inactivates Rb function. Expanded GFP + Rb -inactivated OPCs (orange arrow) intermixed with WT OPCs (GFP - PDGFRα + , white arrow-head), suggesting the lack of OPC competition. Scale bar: 50 μm G. Representative images showing the expansion of OPCs with EGFR mutation ( EGFRvIII ). The expanded clone of EGFRvIII -expressing OPCs excluded WT OPCs (GFP - PDGFRα + ), suggesting OPC competition. Scale bar: 50 μm. H. Summary of the sufficiency and insufficiency in driving OPC competition of all examined gliomagenic mutations in this study.

    Techniques Used: Sequencing, Standard Deviation, Knock-Out, Generated, Transduction, Clone Assay, Mutagenesis, Expressing



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    A. Table of patient samples used in snRNA-seq, with the status of a few gene alterations listed. B. Sample MRIs from one patient showing T1 contrast-enhanced and T2 weighted images. On the left is the preoperative study demonstrating location of contrast enhancing zone (yellow arrow) containing the presumed solid tumor and the broader, T2-hyperintense signal (red arrow) that containing the presumed infiltrating tumor. The middle image shows the pre-operative regions selected for biopsy and the right image shows the intraoperative neuronavigation biopsy acquisition. C. The workflow from sample biopsy, processing, snRNA-sequencing, and data analysis. D. Bar plots of cell type proportions in the infiltrating and solid tumor regions. Each bar represents the mean proportion of the selected cell type in the region and the positive and negative standard deviation are represented by the bracket. Each dot represents the cell type proportion of a single sample. E. Representative images of expanded Nf1- knockout OPCs (GFP + PDGFRα + ) generated by transduction of MSCV carrying Nf1 guide RNA/Cas9. WT OPCs (GFP - PDGFRα + ) were excluded from the expanded Nf1 -null OPC clones, suggesting OPC competition. Scale bar: 50 μm. F. Representative images of expanded Rb -inactivated OPCs (GFP + PDGFRα + ) upon transduction of MSCV <t>carrying</t> <t>HPV-16</t> E7 protein that inactivates Rb function. Expanded GFP + Rb -inactivated OPCs (orange arrow) intermixed with WT OPCs (GFP - PDGFRα + , white arrow-head), suggesting the lack of OPC competition. Scale bar: 50 μm G. Representative images showing the expansion of OPCs with EGFR mutation ( EGFRvIII ). The expanded clone of EGFRvIII -expressing OPCs excluded WT OPCs (GFP - PDGFRα + ), suggesting OPC competition. Scale bar: 50 μm. H. Summary of the sufficiency and insufficiency in driving OPC competition of all examined gliomagenic mutations in this study.
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    A. Table of patient samples used in snRNA-seq, with the status of a few gene alterations listed. B. Sample MRIs from one patient showing T1 contrast-enhanced and T2 weighted images. On the left is the preoperative study demonstrating location of contrast enhancing zone (yellow arrow) containing the presumed solid tumor and the broader, T2-hyperintense signal (red arrow) that containing the presumed infiltrating tumor. The middle image shows the pre-operative regions selected for biopsy and the right image shows the intraoperative neuronavigation biopsy acquisition. C. The workflow from sample biopsy, processing, snRNA-sequencing, and data analysis. D. Bar plots of cell type proportions in the infiltrating and solid tumor regions. Each bar represents the mean proportion of the selected cell type in the region and the positive and negative standard deviation are represented by the bracket. Each dot represents the cell type proportion of a single sample. E. Representative images of expanded Nf1- knockout OPCs (GFP + PDGFRα + ) generated by transduction of MSCV carrying Nf1 guide RNA/Cas9. WT OPCs (GFP - PDGFRα + ) were excluded from the expanded Nf1 -null OPC clones, suggesting OPC competition. Scale bar: 50 μm. F. Representative images of expanded Rb -inactivated OPCs (GFP + PDGFRα + ) upon transduction of MSCV <t>carrying</t> <t>HPV-16</t> E7 protein that inactivates Rb function. Expanded GFP + Rb -inactivated OPCs (orange arrow) intermixed with WT OPCs (GFP - PDGFRα + , white arrow-head), suggesting the lack of OPC competition. Scale bar: 50 μm G. Representative images showing the expansion of OPCs with EGFR mutation ( EGFRvIII ). The expanded clone of EGFRvIII -expressing OPCs excluded WT OPCs (GFP - PDGFRα + ), suggesting OPC competition. Scale bar: 50 μm. H. Summary of the sufficiency and insufficiency in driving OPC competition of all examined gliomagenic mutations in this study.
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    A. Table of patient samples used in snRNA-seq, with the status of a few gene alterations listed. B. Sample MRIs from one patient showing T1 contrast-enhanced and T2 weighted images. On the left is the preoperative study demonstrating location of contrast enhancing zone (yellow arrow) containing the presumed solid tumor and the broader, T2-hyperintense signal (red arrow) that containing the presumed infiltrating tumor. The middle image shows the pre-operative regions selected for biopsy and the right image shows the intraoperative neuronavigation biopsy acquisition. C. The workflow from sample biopsy, processing, snRNA-sequencing, and data analysis. D. Bar plots of cell type proportions in the infiltrating and solid tumor regions. Each bar represents the mean proportion of the selected cell type in the region and the positive and negative standard deviation are represented by the bracket. Each dot represents the cell type proportion of a single sample. E. Representative images of expanded Nf1- knockout OPCs (GFP + PDGFRα + ) generated by transduction of MSCV carrying Nf1 guide RNA/Cas9. WT OPCs (GFP - PDGFRα + ) were excluded from the expanded Nf1 -null OPC clones, suggesting OPC competition. Scale bar: 50 μm. F. Representative images of expanded Rb -inactivated OPCs (GFP + PDGFRα + ) upon transduction of MSCV <t>carrying</t> <t>HPV-16</t> E7 protein that inactivates Rb function. Expanded GFP + Rb -inactivated OPCs (orange arrow) intermixed with WT OPCs (GFP - PDGFRα + , white arrow-head), suggesting the lack of OPC competition. Scale bar: 50 μm G. Representative images showing the expansion of OPCs with EGFR mutation ( EGFRvIII ). The expanded clone of EGFRvIII -expressing OPCs excluded WT OPCs (GFP - PDGFRα + ), suggesting OPC competition. Scale bar: 50 μm. H. Summary of the sufficiency and insufficiency in driving OPC competition of all examined gliomagenic mutations in this study.
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    Image Search Results


    A. Table of patient samples used in snRNA-seq, with the status of a few gene alterations listed. B. Sample MRIs from one patient showing T1 contrast-enhanced and T2 weighted images. On the left is the preoperative study demonstrating location of contrast enhancing zone (yellow arrow) containing the presumed solid tumor and the broader, T2-hyperintense signal (red arrow) that containing the presumed infiltrating tumor. The middle image shows the pre-operative regions selected for biopsy and the right image shows the intraoperative neuronavigation biopsy acquisition. C. The workflow from sample biopsy, processing, snRNA-sequencing, and data analysis. D. Bar plots of cell type proportions in the infiltrating and solid tumor regions. Each bar represents the mean proportion of the selected cell type in the region and the positive and negative standard deviation are represented by the bracket. Each dot represents the cell type proportion of a single sample. E. Representative images of expanded Nf1- knockout OPCs (GFP + PDGFRα + ) generated by transduction of MSCV carrying Nf1 guide RNA/Cas9. WT OPCs (GFP - PDGFRα + ) were excluded from the expanded Nf1 -null OPC clones, suggesting OPC competition. Scale bar: 50 μm. F. Representative images of expanded Rb -inactivated OPCs (GFP + PDGFRα + ) upon transduction of MSCV carrying HPV-16 E7 protein that inactivates Rb function. Expanded GFP + Rb -inactivated OPCs (orange arrow) intermixed with WT OPCs (GFP - PDGFRα + , white arrow-head), suggesting the lack of OPC competition. Scale bar: 50 μm G. Representative images showing the expansion of OPCs with EGFR mutation ( EGFRvIII ). The expanded clone of EGFRvIII -expressing OPCs excluded WT OPCs (GFP - PDGFRα + ), suggesting OPC competition. Scale bar: 50 μm. H. Summary of the sufficiency and insufficiency in driving OPC competition of all examined gliomagenic mutations in this study.

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    Article Title: Critical role of cell competition in gliomagenesis

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    Figure Lengend Snippet: A. Table of patient samples used in snRNA-seq, with the status of a few gene alterations listed. B. Sample MRIs from one patient showing T1 contrast-enhanced and T2 weighted images. On the left is the preoperative study demonstrating location of contrast enhancing zone (yellow arrow) containing the presumed solid tumor and the broader, T2-hyperintense signal (red arrow) that containing the presumed infiltrating tumor. The middle image shows the pre-operative regions selected for biopsy and the right image shows the intraoperative neuronavigation biopsy acquisition. C. The workflow from sample biopsy, processing, snRNA-sequencing, and data analysis. D. Bar plots of cell type proportions in the infiltrating and solid tumor regions. Each bar represents the mean proportion of the selected cell type in the region and the positive and negative standard deviation are represented by the bracket. Each dot represents the cell type proportion of a single sample. E. Representative images of expanded Nf1- knockout OPCs (GFP + PDGFRα + ) generated by transduction of MSCV carrying Nf1 guide RNA/Cas9. WT OPCs (GFP - PDGFRα + ) were excluded from the expanded Nf1 -null OPC clones, suggesting OPC competition. Scale bar: 50 μm. F. Representative images of expanded Rb -inactivated OPCs (GFP + PDGFRα + ) upon transduction of MSCV carrying HPV-16 E7 protein that inactivates Rb function. Expanded GFP + Rb -inactivated OPCs (orange arrow) intermixed with WT OPCs (GFP - PDGFRα + , white arrow-head), suggesting the lack of OPC competition. Scale bar: 50 μm G. Representative images showing the expansion of OPCs with EGFR mutation ( EGFRvIII ). The expanded clone of EGFRvIII -expressing OPCs excluded WT OPCs (GFP - PDGFRα + ), suggesting OPC competition. Scale bar: 50 μm. H. Summary of the sufficiency and insufficiency in driving OPC competition of all examined gliomagenic mutations in this study.

    Article Snippet: To inactivate Rb function, the HPV-16 E7 fragment was amplified from plasmid p1324 HPV-16 E7 (Addgene#8643) and cloned to replace Cas9 in MSCV vector, maintaining the in-frame fusion with T2A-EGFP for accurate reporting.

    Techniques: Sequencing, Standard Deviation, Knock-Out, Generated, Transduction, Clone Assay, Mutagenesis, Expressing