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t98g  (ATCC)


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    ATCC t98g
    NRP2 mediates the FAK signaling pathway to regulate the malignant progression of GBM cells. (A): NRP2 expression levels in patients from the GSE4290 and GSE68848 data sets. (B): The knockdown effect of sh-NRP2 in U251 and <t>T98G</t> cells was detected by qRT-PCR. (C): WB was used to detect the expressions of pY297-FAK and FAK. (D): The CCK-8 method was used to detect the cell viability of GBM cells in different treatment groups (sh-NC, sh-NRP2, sh-NRP2 + adhesamine). Adhesamine is a FAK activator. (E): The colony formation experiment was used to detect the number of colony formations of GBM cells in different treatment groups; (F): The scratch healing experiment was used to detect the migration ability of GBM cells in different treatment groups; (G): The Transwell experiment was used to detect the invasion ability of GBM cells in different treatment groups; (H): The Annexin V/PI double staining method was used to detect the apoptosis level of cells in different treatment groups. (I): Western blot was used to detect the protein expression of pro-apoptotic indicators clever-caspase3, clever-PARP, BAX and pro-apoptotic indicator BCL2 in different treatment groups. * indicates P < 0.05, **** indicates P < 0.0001.
    T98g, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 2871 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/t98g/product/ATCC
    Average 98 stars, based on 2871 article reviews
    t98g - by Bioz Stars, 2026-05
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    1) Product Images from "The brain imaging feature-related gene NRP2 drives the malignant progression of glioblastoma through the FAK pathway: a Mendelian randomization study"

    Article Title: The brain imaging feature-related gene NRP2 drives the malignant progression of glioblastoma through the FAK pathway: a Mendelian randomization study

    Journal: Translational Oncology

    doi: 10.1016/j.tranon.2026.102732

    NRP2 mediates the FAK signaling pathway to regulate the malignant progression of GBM cells. (A): NRP2 expression levels in patients from the GSE4290 and GSE68848 data sets. (B): The knockdown effect of sh-NRP2 in U251 and T98G cells was detected by qRT-PCR. (C): WB was used to detect the expressions of pY297-FAK and FAK. (D): The CCK-8 method was used to detect the cell viability of GBM cells in different treatment groups (sh-NC, sh-NRP2, sh-NRP2 + adhesamine). Adhesamine is a FAK activator. (E): The colony formation experiment was used to detect the number of colony formations of GBM cells in different treatment groups; (F): The scratch healing experiment was used to detect the migration ability of GBM cells in different treatment groups; (G): The Transwell experiment was used to detect the invasion ability of GBM cells in different treatment groups; (H): The Annexin V/PI double staining method was used to detect the apoptosis level of cells in different treatment groups. (I): Western blot was used to detect the protein expression of pro-apoptotic indicators clever-caspase3, clever-PARP, BAX and pro-apoptotic indicator BCL2 in different treatment groups. * indicates P < 0.05, **** indicates P < 0.0001.
    Figure Legend Snippet: NRP2 mediates the FAK signaling pathway to regulate the malignant progression of GBM cells. (A): NRP2 expression levels in patients from the GSE4290 and GSE68848 data sets. (B): The knockdown effect of sh-NRP2 in U251 and T98G cells was detected by qRT-PCR. (C): WB was used to detect the expressions of pY297-FAK and FAK. (D): The CCK-8 method was used to detect the cell viability of GBM cells in different treatment groups (sh-NC, sh-NRP2, sh-NRP2 + adhesamine). Adhesamine is a FAK activator. (E): The colony formation experiment was used to detect the number of colony formations of GBM cells in different treatment groups; (F): The scratch healing experiment was used to detect the migration ability of GBM cells in different treatment groups; (G): The Transwell experiment was used to detect the invasion ability of GBM cells in different treatment groups; (H): The Annexin V/PI double staining method was used to detect the apoptosis level of cells in different treatment groups. (I): Western blot was used to detect the protein expression of pro-apoptotic indicators clever-caspase3, clever-PARP, BAX and pro-apoptotic indicator BCL2 in different treatment groups. * indicates P < 0.05, **** indicates P < 0.0001.

    Techniques Used: Expressing, Knockdown, Quantitative RT-PCR, CCK-8 Assay, Migration, Double Staining, Western Blot

    NRP2 promotes the malignant progression of GBM by activating FAK. U251 and T98G cell groups: sh-NC, sh-NRP2, sh-NRP2 + oe-FAK. (A): qRT-PCR was used to detect the mRNA level of FAK; (B): WB was used to detect the protein expression of pY397-FAK and FAK; (C): CCK-8 was used to detect cell viability; (D): Scratch test was used to detect the migration ability of cells; (E): Transwell test was used to detect the invasion ability of cells; (F): WB was used to detect the protein expression of apoptotic proteins clever-caspase3, clever-PARP, BAX and anti-apoptotic protein BCL2. * indicates P < 0.05.
    Figure Legend Snippet: NRP2 promotes the malignant progression of GBM by activating FAK. U251 and T98G cell groups: sh-NC, sh-NRP2, sh-NRP2 + oe-FAK. (A): qRT-PCR was used to detect the mRNA level of FAK; (B): WB was used to detect the protein expression of pY397-FAK and FAK; (C): CCK-8 was used to detect cell viability; (D): Scratch test was used to detect the migration ability of cells; (E): Transwell test was used to detect the invasion ability of cells; (F): WB was used to detect the protein expression of apoptotic proteins clever-caspase3, clever-PARP, BAX and anti-apoptotic protein BCL2. * indicates P < 0.05.

    Techniques Used: Quantitative RT-PCR, Expressing, CCK-8 Assay, Migration

    The nude mouse experiment demonstrates that NRP2 mediates the Focal-adhesion pathway to regulate the formation of GBM tumors. (A): Nude mice were subcutaneously injected with sh-NRP2 and sh-NC stably transfected T98G cells. Comparison of tumor size in sh-NRP2 nude mice treated with FAK activator adhesamine. (B): Tumor weights of different treatment groups of nude mice. (C): Tumor volumes of different treatment groups of nude mice. (D): IHC detection of the expression of Ki67, BCL2 and BAX in tumor tissues; (E): WB detection of the expression of pY297-FAK and FAK in tumor tissues.
    Figure Legend Snippet: The nude mouse experiment demonstrates that NRP2 mediates the Focal-adhesion pathway to regulate the formation of GBM tumors. (A): Nude mice were subcutaneously injected with sh-NRP2 and sh-NC stably transfected T98G cells. Comparison of tumor size in sh-NRP2 nude mice treated with FAK activator adhesamine. (B): Tumor weights of different treatment groups of nude mice. (C): Tumor volumes of different treatment groups of nude mice. (D): IHC detection of the expression of Ki67, BCL2 and BAX in tumor tissues; (E): WB detection of the expression of pY297-FAK and FAK in tumor tissues.

    Techniques Used: Injection, Stable Transfection, Transfection, Comparison, Expressing



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    NRP2 mediates the FAK signaling pathway to regulate the malignant progression of GBM cells. (A): NRP2 expression levels in patients from the GSE4290 and GSE68848 data sets. (B): The knockdown effect of sh-NRP2 in U251 and <t>T98G</t> cells was detected by qRT-PCR. (C): WB was used to detect the expressions of pY297-FAK and FAK. (D): The CCK-8 method was used to detect the cell viability of GBM cells in different treatment groups (sh-NC, sh-NRP2, sh-NRP2 + adhesamine). Adhesamine is a FAK activator. (E): The colony formation experiment was used to detect the number of colony formations of GBM cells in different treatment groups; (F): The scratch healing experiment was used to detect the migration ability of GBM cells in different treatment groups; (G): The Transwell experiment was used to detect the invasion ability of GBM cells in different treatment groups; (H): The Annexin V/PI double staining method was used to detect the apoptosis level of cells in different treatment groups. (I): Western blot was used to detect the protein expression of pro-apoptotic indicators clever-caspase3, clever-PARP, BAX and pro-apoptotic indicator BCL2 in different treatment groups. * indicates P < 0.05, **** indicates P < 0.0001.
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    NRP2 mediates the FAK signaling pathway to regulate the malignant progression of GBM cells. (A): NRP2 expression levels in patients from the GSE4290 and GSE68848 data sets. (B): The knockdown effect of sh-NRP2 in U251 and <t>T98G</t> cells was detected by qRT-PCR. (C): WB was used to detect the expressions of pY297-FAK and FAK. (D): The CCK-8 method was used to detect the cell viability of GBM cells in different treatment groups (sh-NC, sh-NRP2, sh-NRP2 + adhesamine). Adhesamine is a FAK activator. (E): The colony formation experiment was used to detect the number of colony formations of GBM cells in different treatment groups; (F): The scratch healing experiment was used to detect the migration ability of GBM cells in different treatment groups; (G): The Transwell experiment was used to detect the invasion ability of GBM cells in different treatment groups; (H): The Annexin V/PI double staining method was used to detect the apoptosis level of cells in different treatment groups. (I): Western blot was used to detect the protein expression of pro-apoptotic indicators clever-caspase3, clever-PARP, BAX and pro-apoptotic indicator BCL2 in different treatment groups. * indicates P < 0.05, **** indicates P < 0.0001.
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    NRP2 mediates the FAK signaling pathway to regulate the malignant progression of GBM cells. (A): NRP2 expression levels in patients from the GSE4290 and GSE68848 data sets. (B): The knockdown effect of sh-NRP2 in U251 and T98G cells was detected by qRT-PCR. (C): WB was used to detect the expressions of pY297-FAK and FAK. (D): The CCK-8 method was used to detect the cell viability of GBM cells in different treatment groups (sh-NC, sh-NRP2, sh-NRP2 + adhesamine). Adhesamine is a FAK activator. (E): The colony formation experiment was used to detect the number of colony formations of GBM cells in different treatment groups; (F): The scratch healing experiment was used to detect the migration ability of GBM cells in different treatment groups; (G): The Transwell experiment was used to detect the invasion ability of GBM cells in different treatment groups; (H): The Annexin V/PI double staining method was used to detect the apoptosis level of cells in different treatment groups. (I): Western blot was used to detect the protein expression of pro-apoptotic indicators clever-caspase3, clever-PARP, BAX and pro-apoptotic indicator BCL2 in different treatment groups. * indicates P < 0.05, **** indicates P < 0.0001.

    Journal: Translational Oncology

    Article Title: The brain imaging feature-related gene NRP2 drives the malignant progression of glioblastoma through the FAK pathway: a Mendelian randomization study

    doi: 10.1016/j.tranon.2026.102732

    Figure Lengend Snippet: NRP2 mediates the FAK signaling pathway to regulate the malignant progression of GBM cells. (A): NRP2 expression levels in patients from the GSE4290 and GSE68848 data sets. (B): The knockdown effect of sh-NRP2 in U251 and T98G cells was detected by qRT-PCR. (C): WB was used to detect the expressions of pY297-FAK and FAK. (D): The CCK-8 method was used to detect the cell viability of GBM cells in different treatment groups (sh-NC, sh-NRP2, sh-NRP2 + adhesamine). Adhesamine is a FAK activator. (E): The colony formation experiment was used to detect the number of colony formations of GBM cells in different treatment groups; (F): The scratch healing experiment was used to detect the migration ability of GBM cells in different treatment groups; (G): The Transwell experiment was used to detect the invasion ability of GBM cells in different treatment groups; (H): The Annexin V/PI double staining method was used to detect the apoptosis level of cells in different treatment groups. (I): Western blot was used to detect the protein expression of pro-apoptotic indicators clever-caspase3, clever-PARP, BAX and pro-apoptotic indicator BCL2 in different treatment groups. * indicates P < 0.05, **** indicates P < 0.0001.

    Article Snippet: The human GBM cell lines U251 and T98G used for functional experiments were purchased from Mingzhou Bio (MINGZHOUBIO, MZ-0186, China) and American Type Culture Collection (ATCC, CRL-1690, USA), respectively.

    Techniques: Expressing, Knockdown, Quantitative RT-PCR, CCK-8 Assay, Migration, Double Staining, Western Blot

    NRP2 promotes the malignant progression of GBM by activating FAK. U251 and T98G cell groups: sh-NC, sh-NRP2, sh-NRP2 + oe-FAK. (A): qRT-PCR was used to detect the mRNA level of FAK; (B): WB was used to detect the protein expression of pY397-FAK and FAK; (C): CCK-8 was used to detect cell viability; (D): Scratch test was used to detect the migration ability of cells; (E): Transwell test was used to detect the invasion ability of cells; (F): WB was used to detect the protein expression of apoptotic proteins clever-caspase3, clever-PARP, BAX and anti-apoptotic protein BCL2. * indicates P < 0.05.

    Journal: Translational Oncology

    Article Title: The brain imaging feature-related gene NRP2 drives the malignant progression of glioblastoma through the FAK pathway: a Mendelian randomization study

    doi: 10.1016/j.tranon.2026.102732

    Figure Lengend Snippet: NRP2 promotes the malignant progression of GBM by activating FAK. U251 and T98G cell groups: sh-NC, sh-NRP2, sh-NRP2 + oe-FAK. (A): qRT-PCR was used to detect the mRNA level of FAK; (B): WB was used to detect the protein expression of pY397-FAK and FAK; (C): CCK-8 was used to detect cell viability; (D): Scratch test was used to detect the migration ability of cells; (E): Transwell test was used to detect the invasion ability of cells; (F): WB was used to detect the protein expression of apoptotic proteins clever-caspase3, clever-PARP, BAX and anti-apoptotic protein BCL2. * indicates P < 0.05.

    Article Snippet: The human GBM cell lines U251 and T98G used for functional experiments were purchased from Mingzhou Bio (MINGZHOUBIO, MZ-0186, China) and American Type Culture Collection (ATCC, CRL-1690, USA), respectively.

    Techniques: Quantitative RT-PCR, Expressing, CCK-8 Assay, Migration

    The nude mouse experiment demonstrates that NRP2 mediates the Focal-adhesion pathway to regulate the formation of GBM tumors. (A): Nude mice were subcutaneously injected with sh-NRP2 and sh-NC stably transfected T98G cells. Comparison of tumor size in sh-NRP2 nude mice treated with FAK activator adhesamine. (B): Tumor weights of different treatment groups of nude mice. (C): Tumor volumes of different treatment groups of nude mice. (D): IHC detection of the expression of Ki67, BCL2 and BAX in tumor tissues; (E): WB detection of the expression of pY297-FAK and FAK in tumor tissues.

    Journal: Translational Oncology

    Article Title: The brain imaging feature-related gene NRP2 drives the malignant progression of glioblastoma through the FAK pathway: a Mendelian randomization study

    doi: 10.1016/j.tranon.2026.102732

    Figure Lengend Snippet: The nude mouse experiment demonstrates that NRP2 mediates the Focal-adhesion pathway to regulate the formation of GBM tumors. (A): Nude mice were subcutaneously injected with sh-NRP2 and sh-NC stably transfected T98G cells. Comparison of tumor size in sh-NRP2 nude mice treated with FAK activator adhesamine. (B): Tumor weights of different treatment groups of nude mice. (C): Tumor volumes of different treatment groups of nude mice. (D): IHC detection of the expression of Ki67, BCL2 and BAX in tumor tissues; (E): WB detection of the expression of pY297-FAK and FAK in tumor tissues.

    Article Snippet: The human GBM cell lines U251 and T98G used for functional experiments were purchased from Mingzhou Bio (MINGZHOUBIO, MZ-0186, China) and American Type Culture Collection (ATCC, CRL-1690, USA), respectively.

    Techniques: Injection, Stable Transfection, Transfection, Comparison, Expressing

    NRP2 mediates the FAK signaling pathway to regulate the malignant progression of GBM cells. (A): NRP2 expression levels in patients from the GSE4290 and GSE68848 data sets. (B): The knockdown effect of sh-NRP2 in U251 and T98G cells was detected by qRT-PCR. (C): WB was used to detect the expressions of pY297-FAK and FAK. (D): The CCK-8 method was used to detect the cell viability of GBM cells in different treatment groups (sh-NC, sh-NRP2, sh-NRP2 + adhesamine). Adhesamine is a FAK activator. (E): The colony formation experiment was used to detect the number of colony formations of GBM cells in different treatment groups; (F): The scratch healing experiment was used to detect the migration ability of GBM cells in different treatment groups; (G): The Transwell experiment was used to detect the invasion ability of GBM cells in different treatment groups; (H): The Annexin V/PI double staining method was used to detect the apoptosis level of cells in different treatment groups. (I): Western blot was used to detect the protein expression of pro-apoptotic indicators clever-caspase3, clever-PARP, BAX and pro-apoptotic indicator BCL2 in different treatment groups. * indicates P < 0.05, **** indicates P < 0.0001.

    Journal: Translational Oncology

    Article Title: The brain imaging feature-related gene NRP2 drives the malignant progression of glioblastoma through the FAK pathway: a Mendelian randomization study

    doi: 10.1016/j.tranon.2026.102732

    Figure Lengend Snippet: NRP2 mediates the FAK signaling pathway to regulate the malignant progression of GBM cells. (A): NRP2 expression levels in patients from the GSE4290 and GSE68848 data sets. (B): The knockdown effect of sh-NRP2 in U251 and T98G cells was detected by qRT-PCR. (C): WB was used to detect the expressions of pY297-FAK and FAK. (D): The CCK-8 method was used to detect the cell viability of GBM cells in different treatment groups (sh-NC, sh-NRP2, sh-NRP2 + adhesamine). Adhesamine is a FAK activator. (E): The colony formation experiment was used to detect the number of colony formations of GBM cells in different treatment groups; (F): The scratch healing experiment was used to detect the migration ability of GBM cells in different treatment groups; (G): The Transwell experiment was used to detect the invasion ability of GBM cells in different treatment groups; (H): The Annexin V/PI double staining method was used to detect the apoptosis level of cells in different treatment groups. (I): Western blot was used to detect the protein expression of pro-apoptotic indicators clever-caspase3, clever-PARP, BAX and pro-apoptotic indicator BCL2 in different treatment groups. * indicates P < 0.05, **** indicates P < 0.0001.

    Article Snippet: T98G cells were cultured in MEM medium containing 10 % FBS (ATCC, 30–2003, USA).

    Techniques: Expressing, Knockdown, Quantitative RT-PCR, CCK-8 Assay, Migration, Double Staining, Western Blot

    NRP2 promotes the malignant progression of GBM by activating FAK. U251 and T98G cell groups: sh-NC, sh-NRP2, sh-NRP2 + oe-FAK. (A): qRT-PCR was used to detect the mRNA level of FAK; (B): WB was used to detect the protein expression of pY397-FAK and FAK; (C): CCK-8 was used to detect cell viability; (D): Scratch test was used to detect the migration ability of cells; (E): Transwell test was used to detect the invasion ability of cells; (F): WB was used to detect the protein expression of apoptotic proteins clever-caspase3, clever-PARP, BAX and anti-apoptotic protein BCL2. * indicates P < 0.05.

    Journal: Translational Oncology

    Article Title: The brain imaging feature-related gene NRP2 drives the malignant progression of glioblastoma through the FAK pathway: a Mendelian randomization study

    doi: 10.1016/j.tranon.2026.102732

    Figure Lengend Snippet: NRP2 promotes the malignant progression of GBM by activating FAK. U251 and T98G cell groups: sh-NC, sh-NRP2, sh-NRP2 + oe-FAK. (A): qRT-PCR was used to detect the mRNA level of FAK; (B): WB was used to detect the protein expression of pY397-FAK and FAK; (C): CCK-8 was used to detect cell viability; (D): Scratch test was used to detect the migration ability of cells; (E): Transwell test was used to detect the invasion ability of cells; (F): WB was used to detect the protein expression of apoptotic proteins clever-caspase3, clever-PARP, BAX and anti-apoptotic protein BCL2. * indicates P < 0.05.

    Article Snippet: T98G cells were cultured in MEM medium containing 10 % FBS (ATCC, 30–2003, USA).

    Techniques: Quantitative RT-PCR, Expressing, CCK-8 Assay, Migration

    The nude mouse experiment demonstrates that NRP2 mediates the Focal-adhesion pathway to regulate the formation of GBM tumors. (A): Nude mice were subcutaneously injected with sh-NRP2 and sh-NC stably transfected T98G cells. Comparison of tumor size in sh-NRP2 nude mice treated with FAK activator adhesamine. (B): Tumor weights of different treatment groups of nude mice. (C): Tumor volumes of different treatment groups of nude mice. (D): IHC detection of the expression of Ki67, BCL2 and BAX in tumor tissues; (E): WB detection of the expression of pY297-FAK and FAK in tumor tissues.

    Journal: Translational Oncology

    Article Title: The brain imaging feature-related gene NRP2 drives the malignant progression of glioblastoma through the FAK pathway: a Mendelian randomization study

    doi: 10.1016/j.tranon.2026.102732

    Figure Lengend Snippet: The nude mouse experiment demonstrates that NRP2 mediates the Focal-adhesion pathway to regulate the formation of GBM tumors. (A): Nude mice were subcutaneously injected with sh-NRP2 and sh-NC stably transfected T98G cells. Comparison of tumor size in sh-NRP2 nude mice treated with FAK activator adhesamine. (B): Tumor weights of different treatment groups of nude mice. (C): Tumor volumes of different treatment groups of nude mice. (D): IHC detection of the expression of Ki67, BCL2 and BAX in tumor tissues; (E): WB detection of the expression of pY297-FAK and FAK in tumor tissues.

    Article Snippet: T98G cells were cultured in MEM medium containing 10 % FBS (ATCC, 30–2003, USA).

    Techniques: Injection, Stable Transfection, Transfection, Comparison, Expressing