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jurkat t cells  (ATCC)


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    ATCC jurkat t cells
    BUD23 knockdown suppresses the proliferative and migration of NSCLC cells. (A) RT-qPCR was used to quantify BUD23 mRNA levels in HBE cells and a panel of NSCLC cell lines. Validation of BUD23 knockdown efficiency in (B) A549 and (C) H1299 cells by RT-qPCR. Assessment of cell viability in (D) A549 and (E) H1299 cells via CCK-8 assay and cell migration in (F) A549 and (G) H1299 cells by wound healing assay (magnification, ×10). CCK-8 assays of (H) A549 and (I) H1299 cells 24 h after BUD23 knockdown with or without subsequent co-culture with <t>Jurkat</t> <t>T</t> cells for 48 h in Transwell chambers. (J) Quantification of apoptosis in A549 and H1299 cells via Annexin V/PI flow cytometry. **P<0.01 and ***P<0.001 vs. HBE, NC, Con or as indicated. NSCLC, non-small cell lung cancer; RT-qPCR, reverse transcription-quantitative PCR; HBE, human bronchial epithelial; CCK-8, Cell Counting Kit-8; NC, negative control; Con, control; Si1/2, small interfering RNA targeting BUD23.
    Jurkat T Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 4349 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/jurkat+cells/pmc13122445-72-43-61?v=ATCC
    Average 99 stars, based on 4349 article reviews
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    Images

    1) Product Images from "BUD23 is associated with malignancy and correlates with immune infiltration in NSCLC"

    Article Title: BUD23 is associated with malignancy and correlates with immune infiltration in NSCLC

    Journal: Oncology Letters

    doi: 10.3892/ol.2026.15608

    BUD23 knockdown suppresses the proliferative and migration of NSCLC cells. (A) RT-qPCR was used to quantify BUD23 mRNA levels in HBE cells and a panel of NSCLC cell lines. Validation of BUD23 knockdown efficiency in (B) A549 and (C) H1299 cells by RT-qPCR. Assessment of cell viability in (D) A549 and (E) H1299 cells via CCK-8 assay and cell migration in (F) A549 and (G) H1299 cells by wound healing assay (magnification, ×10). CCK-8 assays of (H) A549 and (I) H1299 cells 24 h after BUD23 knockdown with or without subsequent co-culture with Jurkat T cells for 48 h in Transwell chambers. (J) Quantification of apoptosis in A549 and H1299 cells via Annexin V/PI flow cytometry. **P<0.01 and ***P<0.001 vs. HBE, NC, Con or as indicated. NSCLC, non-small cell lung cancer; RT-qPCR, reverse transcription-quantitative PCR; HBE, human bronchial epithelial; CCK-8, Cell Counting Kit-8; NC, negative control; Con, control; Si1/2, small interfering RNA targeting BUD23.
    Figure Legend Snippet: BUD23 knockdown suppresses the proliferative and migration of NSCLC cells. (A) RT-qPCR was used to quantify BUD23 mRNA levels in HBE cells and a panel of NSCLC cell lines. Validation of BUD23 knockdown efficiency in (B) A549 and (C) H1299 cells by RT-qPCR. Assessment of cell viability in (D) A549 and (E) H1299 cells via CCK-8 assay and cell migration in (F) A549 and (G) H1299 cells by wound healing assay (magnification, ×10). CCK-8 assays of (H) A549 and (I) H1299 cells 24 h after BUD23 knockdown with or without subsequent co-culture with Jurkat T cells for 48 h in Transwell chambers. (J) Quantification of apoptosis in A549 and H1299 cells via Annexin V/PI flow cytometry. **P<0.01 and ***P<0.001 vs. HBE, NC, Con or as indicated. NSCLC, non-small cell lung cancer; RT-qPCR, reverse transcription-quantitative PCR; HBE, human bronchial epithelial; CCK-8, Cell Counting Kit-8; NC, negative control; Con, control; Si1/2, small interfering RNA targeting BUD23.

    Techniques Used: Knockdown, Migration, Quantitative RT-PCR, Biomarker Discovery, CCK-8 Assay, Wound Healing Assay, Co-Culture Assay, Flow Cytometry, Reverse Transcription, Real-time Polymerase Chain Reaction, Cell Counting, Negative Control, Control, Small Interfering RNA



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    <t>Jurkat</t> T cells were stimulated with anti-CD3/CD28 (5 µg/mL) for 1 h before addition of recombinant <t>human</t> <t>Galectin-10</t> or Galectin-13 (20 µg/mL) for 24 h. Cells were stained with Annexin V and propidium iodide (PI) and analyzed by flow cytometry. Stacked bars decompose the total Annexin V+ population into early-apoptotic (Annexin V+ / PI−, gold) and late-apoptotic / dying (Annexin V+ / PI+, red) fractions. Total Annexin V+ values are annotated above each bar; error bars represent SEM on the total. Total Annexin V+ values were compared across conditions by one-way ANOVA with Dunnett’s multiple-comparison test against the stimulated control. Individual replicate values are shown as overlaid points (n = 3 per condition). Human Galectin-10 produced ∼84% total Annexin V+ positivity, the great majority of which had progressed to the late-apoptotic / dying state by 24 h compared with stimulated alone (p<0.001). Galectin-13 produced a more modest increase. This assay was selected because the porcine LGALS13-annotated proteomic signal is interpreted as a CLC/Galectin-10-like orthologous axis; it supports prioritization of that axis but does not prove porcine protein identity or causality in the perfused spleen.
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    Image Search Results


    BUD23 knockdown suppresses the proliferative and migration of NSCLC cells. (A) RT-qPCR was used to quantify BUD23 mRNA levels in HBE cells and a panel of NSCLC cell lines. Validation of BUD23 knockdown efficiency in (B) A549 and (C) H1299 cells by RT-qPCR. Assessment of cell viability in (D) A549 and (E) H1299 cells via CCK-8 assay and cell migration in (F) A549 and (G) H1299 cells by wound healing assay (magnification, ×10). CCK-8 assays of (H) A549 and (I) H1299 cells 24 h after BUD23 knockdown with or without subsequent co-culture with Jurkat T cells for 48 h in Transwell chambers. (J) Quantification of apoptosis in A549 and H1299 cells via Annexin V/PI flow cytometry. **P<0.01 and ***P<0.001 vs. HBE, NC, Con or as indicated. NSCLC, non-small cell lung cancer; RT-qPCR, reverse transcription-quantitative PCR; HBE, human bronchial epithelial; CCK-8, Cell Counting Kit-8; NC, negative control; Con, control; Si1/2, small interfering RNA targeting BUD23.

    Journal: Oncology Letters

    Article Title: BUD23 is associated with malignancy and correlates with immune infiltration in NSCLC

    doi: 10.3892/ol.2026.15608

    Figure Lengend Snippet: BUD23 knockdown suppresses the proliferative and migration of NSCLC cells. (A) RT-qPCR was used to quantify BUD23 mRNA levels in HBE cells and a panel of NSCLC cell lines. Validation of BUD23 knockdown efficiency in (B) A549 and (C) H1299 cells by RT-qPCR. Assessment of cell viability in (D) A549 and (E) H1299 cells via CCK-8 assay and cell migration in (F) A549 and (G) H1299 cells by wound healing assay (magnification, ×10). CCK-8 assays of (H) A549 and (I) H1299 cells 24 h after BUD23 knockdown with or without subsequent co-culture with Jurkat T cells for 48 h in Transwell chambers. (J) Quantification of apoptosis in A549 and H1299 cells via Annexin V/PI flow cytometry. **P<0.01 and ***P<0.001 vs. HBE, NC, Con or as indicated. NSCLC, non-small cell lung cancer; RT-qPCR, reverse transcription-quantitative PCR; HBE, human bronchial epithelial; CCK-8, Cell Counting Kit-8; NC, negative control; Con, control; Si1/2, small interfering RNA targeting BUD23.

    Article Snippet: The HBE [full name: HBE4-E6/E7 (Human Bronchial Epithelial Cells; cat. no. CRL-2078)] cell line, A549 lung adenocarcinoma cell line (cat. no. CCL-185), H1299 lung large cell carcinoma cell line (cat. no. CRL-5803), H460 lung large cell carcinoma cell line (cat. no. HTB-177) and Jurkat T cells (cat. no. TIB-152; a childhood T acute lymphoblastic leukemia T-cell line), were purchased from the American Type Culture Collection.

    Techniques: Knockdown, Migration, Quantitative RT-PCR, Biomarker Discovery, CCK-8 Assay, Wound Healing Assay, Co-Culture Assay, Flow Cytometry, Reverse Transcription, Real-time Polymerase Chain Reaction, Cell Counting, Negative Control, Control, Small Interfering RNA

    Jurkat T cells were stimulated with anti-CD3/CD28 (5 µg/mL) for 1 h before addition of recombinant human Galectin-10 or Galectin-13 (20 µg/mL) for 24 h. Cells were stained with Annexin V and propidium iodide (PI) and analyzed by flow cytometry. Stacked bars decompose the total Annexin V+ population into early-apoptotic (Annexin V+ / PI−, gold) and late-apoptotic / dying (Annexin V+ / PI+, red) fractions. Total Annexin V+ values are annotated above each bar; error bars represent SEM on the total. Total Annexin V+ values were compared across conditions by one-way ANOVA with Dunnett’s multiple-comparison test against the stimulated control. Individual replicate values are shown as overlaid points (n = 3 per condition). Human Galectin-10 produced ∼84% total Annexin V+ positivity, the great majority of which had progressed to the late-apoptotic / dying state by 24 h compared with stimulated alone (p<0.001). Galectin-13 produced a more modest increase. This assay was selected because the porcine LGALS13-annotated proteomic signal is interpreted as a CLC/Galectin-10-like orthologous axis; it supports prioritization of that axis but does not prove porcine protein identity or causality in the perfused spleen.

    Journal: bioRxiv

    Article Title: Acellular normothermic spleen perfusion resolves transcriptional and non-transcriptional mechanisms of steroid immunosuppression

    doi: 10.64898/2026.05.16.725632

    Figure Lengend Snippet: Jurkat T cells were stimulated with anti-CD3/CD28 (5 µg/mL) for 1 h before addition of recombinant human Galectin-10 or Galectin-13 (20 µg/mL) for 24 h. Cells were stained with Annexin V and propidium iodide (PI) and analyzed by flow cytometry. Stacked bars decompose the total Annexin V+ population into early-apoptotic (Annexin V+ / PI−, gold) and late-apoptotic / dying (Annexin V+ / PI+, red) fractions. Total Annexin V+ values are annotated above each bar; error bars represent SEM on the total. Total Annexin V+ values were compared across conditions by one-way ANOVA with Dunnett’s multiple-comparison test against the stimulated control. Individual replicate values are shown as overlaid points (n = 3 per condition). Human Galectin-10 produced ∼84% total Annexin V+ positivity, the great majority of which had progressed to the late-apoptotic / dying state by 24 h compared with stimulated alone (p<0.001). Galectin-13 produced a more modest increase. This assay was selected because the porcine LGALS13-annotated proteomic signal is interpreted as a CLC/Galectin-10-like orthologous axis; it supports prioritization of that axis but does not prove porcine protein identity or causality in the perfused spleen.

    Article Snippet: In activated Jurkat cells, human Galectin-10 produced marked Annexin V and Annexin V/PI positivity at 24 h.

    Techniques: Recombinant, Staining, Flow Cytometry, Comparison, Control, Produced