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ATCC murine cell lines el4

POU2AF1 promotes T-ALL development via transcriptional activation of SLC7A11. ( A ) Western blot analysis of SLC7A11 protein levels in the <t>EL4</t> cell lines. ( B ) The protein level of SLC7A11 was determined in WT and KO T-ALL cells by Western blotting ( n = 3). ( C ) POU2AF1 and SLC7A11 levels were measured in bone marrow cells from transplanted WT, Bcat1 -KO, Pou2af1 -overexpressing WT or Bcat1 -KO mice by Western blotting. ( D ) Luciferase reporter assay evaluating the transcriptional activation of Slc7a11 by Pou2af1 -WT and Pou2af1 -K5R ( n = 3). ( E ) ChIP assay showing the binding of Pou2af1 -WT and Pou2af1 -K5R to the Slc7a11 promoter region ( n = 3). ( F – G ) Representative flow cytometric analysis of GFP + mCherry + leukemia cells (The markers for the indication of leukemia cells were GFP + and mCherry + , which were the tags for the MSCV- Notch1 -IRES-GFP plasmid and MSCV-mCherry overexpression plasmid) in peripheral blood from recipient mice 3 weeks after transplantation with WT and KO T-ALL cells overexpressing Slc7a11 . ( H – I ) Representative images and quantification of the liver, spleen and thymus morphology in recipient mice ( n = 3). ( J ) Survival analysis of recipient mice ( n = 5). The data are presented as the means ± SDs. One-way ANOVA with Tukey’s multiple comparison test ( G ), log-rank test ( J ) and two-way ANOVA with Sidak’s multiple comparison test ( D , I ) were used for comparisons of statistical significance (*, P < 0.05; **, P < 0.01; and ***, P < 0.001)

Murine Cell Lines El4, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1932 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "BCAA catabolism mediates POU2AF1 propionylation to enhance T-ALL development"

Article Title: BCAA catabolism mediates POU2AF1 propionylation to enhance T-ALL development

Journal: Cellular Oncology

doi: 10.1007/s13402-026-01201-w

POU2AF1 promotes T-ALL development via transcriptional activation of SLC7A11. ( A ) Western blot analysis of SLC7A11 protein levels in the EL4 cell lines. ( B ) The protein level of SLC7A11 was determined in WT and KO T-ALL cells by Western blotting ( n = 3). ( C ) POU2AF1 and SLC7A11 levels were measured in bone marrow cells from transplanted WT, Bcat1 -KO, Pou2af1 -overexpressing WT or Bcat1 -KO mice by Western blotting. ( D ) Luciferase reporter assay evaluating the transcriptional activation of Slc7a11 by Pou2af1 -WT and Pou2af1 -K5R ( n = 3). ( E ) ChIP assay showing the binding of Pou2af1 -WT and Pou2af1 -K5R to the Slc7a11 promoter region ( n = 3). ( F – G ) Representative flow cytometric analysis of GFP + mCherry + leukemia cells (The markers for the indication of leukemia cells were GFP + and mCherry + , which were the tags for the MSCV- Notch1 -IRES-GFP plasmid and MSCV-mCherry overexpression plasmid) in peripheral blood from recipient mice 3 weeks after transplantation with WT and KO T-ALL cells overexpressing Slc7a11 . ( H – I ) Representative images and quantification of the liver, spleen and thymus morphology in recipient mice ( n = 3). ( J ) Survival analysis of recipient mice ( n = 5). The data are presented as the means ± SDs. One-way ANOVA with Tukey’s multiple comparison test ( G ), log-rank test ( J ) and two-way ANOVA with Sidak’s multiple comparison test ( D , I ) were used for comparisons of statistical significance (*, P < 0.05; **, P < 0.01; and ***, P < 0.001)

Figure Legend Snippet: POU2AF1 promotes T-ALL development via transcriptional activation of SLC7A11. ( A ) Western blot analysis of SLC7A11 protein levels in the EL4 cell lines. ( B ) The protein level of SLC7A11 was determined in WT and KO T-ALL cells by Western blotting ( n = 3). ( C ) POU2AF1 and SLC7A11 levels were measured in bone marrow cells from transplanted WT, Bcat1 -KO, Pou2af1 -overexpressing WT or Bcat1 -KO mice by Western blotting. ( D ) Luciferase reporter assay evaluating the transcriptional activation of Slc7a11 by Pou2af1 -WT and Pou2af1 -K5R ( n = 3). ( E ) ChIP assay showing the binding of Pou2af1 -WT and Pou2af1 -K5R to the Slc7a11 promoter region ( n = 3). ( F – G ) Representative flow cytometric analysis of GFP + mCherry + leukemia cells (The markers for the indication of leukemia cells were GFP + and mCherry + , which were the tags for the MSCV- Notch1 -IRES-GFP plasmid and MSCV-mCherry overexpression plasmid) in peripheral blood from recipient mice 3 weeks after transplantation with WT and KO T-ALL cells overexpressing Slc7a11 . ( H – I ) Representative images and quantification of the liver, spleen and thymus morphology in recipient mice ( n = 3). ( J ) Survival analysis of recipient mice ( n = 5). The data are presented as the means ± SDs. One-way ANOVA with Tukey’s multiple comparison test ( G ), log-rank test ( J ) and two-way ANOVA with Sidak’s multiple comparison test ( D , I ) were used for comparisons of statistical significance (*, P < 0.05; **, P < 0.01; and ***, P < 0.001)

Techniques Used: Activation Assay, Western Blot, Luciferase, Reporter Assay, Binding Assay, Plasmid Preparation, Over Expression, Transplantation Assay, Comparison

Targeting BCAT1 metabolism significantly impaired T-ALL progression. ( A – D ) Analysis of the proliferation of EL4 ( A ), L1210 ( B ), Jurkat ( C ), and MOLT-4 ( D ) cells treated in vitro with 10 mM gabapentin (n=4). ( E ) Representative flow cytometric analysis of peripheral blood at 3 weeks post-transplantation from T-ALL model mice following treatment with IgG, anti-PD-1 antibody, low-BCAA, or combined low-BCAA + anti-PD-1 antibody. ( F ) Quantification of the peripheral blood data shown in Panel E (n=5). ( G ) Overall survival analysis of treated mice (n=5). ( H ) Schematic model illustrating how BCAT1-driven branched-chain amino acid metabolism promotes T-ALL progression via Kpr-mediated activation of POU2AF1. The data are presented as the means ± SDs. One-way ANOVA with Tukey’s multiple comparison test ( F ), log-rank test ( G ), and two-way ANOVA with Sidak’s multiple comparison test (A–D) were used for comparisons of statistical significance (*, P <0.05; **, P <0.01; and ***, P <0.001)

Figure Legend Snippet: Targeting BCAT1 metabolism significantly impaired T-ALL progression. ( A – D ) Analysis of the proliferation of EL4 ( A ), L1210 ( B ), Jurkat ( C ), and MOLT-4 ( D ) cells treated in vitro with 10 mM gabapentin (n=4). ( E ) Representative flow cytometric analysis of peripheral blood at 3 weeks post-transplantation from T-ALL model mice following treatment with IgG, anti-PD-1 antibody, low-BCAA, or combined low-BCAA + anti-PD-1 antibody. ( F ) Quantification of the peripheral blood data shown in Panel E (n=5). ( G ) Overall survival analysis of treated mice (n=5). ( H ) Schematic model illustrating how BCAT1-driven branched-chain amino acid metabolism promotes T-ALL progression via Kpr-mediated activation of POU2AF1. The data are presented as the means ± SDs. One-way ANOVA with Tukey’s multiple comparison test ( F ), log-rank test ( G ), and two-way ANOVA with Sidak’s multiple comparison test (A–D) were used for comparisons of statistical significance (*, P <0.05; **, P <0.01; and ***, P <0.001)

Techniques Used: In Vitro, Transplantation Assay, Activation Assay, Comparison

Irradiation:

Article Title: In vitro stimulation of human tonsillar subepithelial B cells: requirement for interaction with activated T cells
Article Snippet: The purified CD4+ T cells were stimulated with PHA (Dako, Glostrup, Denmark) and subsequently expanded with 100 U/ml rIL-2 (Glaxo, Geneva, Switzerland). .. SE B cells (1 × 105 cells/well) were stimulated in 96-well culture plates by adding equal numbers of irradiated (5.000 rad) murine EL4 cells and 10 ng/ml PMA (Sigma, St Louis, MO), or irradiated (3.000 rad) human CD4+ T cell blasts stimulated with 10 ? g/ml anti-CD3 mAb (OK-T3 from ATCC; Rockville, MD). ..

Cell Characterization:

Article Title: Investigation of the Immunomodulatory effect of Berberis vulgaris on core-pulsed dendritic cell vaccine
Article Snippet: Cytoplasmic contents of cytokines protein expression of INF-γ was screened according to the instructions of Mouse INF-γ ELISA kit (Komabiotech, Korea). .. In a 96-well rounded-bottomed plate, splenocytes of non-treated mice were co-cultured with murine EL4 cells (ATCC® TIB39 TM) with a final cell count of 0.5 × 10 6 cell/well at E: T ratios of 1:25, 1:12.5, 1:6.2, 1:3.1 and 1:1.6. ..

Article Title: Investigation of the Immunomodulatory effect of Berberis vulgaris on core-pulsed dendritic cell vaccine.
Article Snippet: Cytoplasmic contents of cytokines protein expression of INF-γ was screened according to the instructions of Mouse INF-γ ELISA kit (Komabiotech, Korea). .. Determination of the optimum effector cells: target cells ratio (E:T) In a 96-well rounded-bottomed plate, splenocytes of non-treated mice were co-cultured with murine EL4 cells (ATCC® TIB39 TM) with a final cell count of 0.5 × 106 cell/ well at E: T ratios of 1:25, 1:12.5, 1:6.2, 1:3.1 and 1:1.6. ..

Isolation:

Article Title: Absence of XMRV in Peripheral Blood Mononuclear Cells of ARV-Treatment Naïve HIV-1 Infected and HIV-1/HCV Coinfected Individuals and Blood Donors
Article Snippet: .. DNA isolated from a vial of preserved murine EL4 cells (ATCC no. TIB-39), kindly provided by Dr. Qizhi C. Yao, was used as a positive control. ..

Article Title: Characterisation of independent DNA and multiple Zn-binding domains at the N terminus of human DNA-(cytosine-5) methyltransferase: modulating the property of a DNA-binding domain by contiguous Zn-binding motifs.
Article Snippet: We report here a detailed mapping and characterisation of a DNA-binding Chemical Carcinogenesis domain at the N terminus of human DNA-(cytosine-5) methyltransferase.. Laboratory, Institute of A small region, B1 (codon 202 to 369), was first identified by its Znand Molecular and Cell Biology gross DNA-binding properties.. Further fine-mapping using deletion and National University of point mutation analysis shows that the DNAand Zn-binding domains Singapore, 10 Kent Ridge involve separate peptide motifs, KRRKTTPKEPTEKK (codons 202 to 215) Cresent, Singapore 0511 for a bipartite DNA-binding oligopeptide (DB1) and CX2CX13HX2 Republic of Singapore D(X)23EX2EX13CX3H (codons 232 to 297) for possibly two contiguous Zn-binding domains (AZn), which can function independently.

Positive Control:

Cloning:

Polymerase Chain Reaction:

Image Search Results

Journal: Cellular Oncology

Article Title: BCAA catabolism mediates POU2AF1 propionylation to enhance T-ALL development

doi: 10.1007/s13402-026-01201-w

Figure Lengend Snippet: POU2AF1 promotes T-ALL development via transcriptional activation of SLC7A11. ( A ) Western blot analysis of SLC7A11 protein levels in the EL4 cell lines. ( B ) The protein level of SLC7A11 was determined in WT and KO T-ALL cells by Western blotting ( n = 3). ( C ) POU2AF1 and SLC7A11 levels were measured in bone marrow cells from transplanted WT, Bcat1 -KO, Pou2af1 -overexpressing WT or Bcat1 -KO mice by Western blotting. ( D ) Luciferase reporter assay evaluating the transcriptional activation of Slc7a11 by Pou2af1 -WT and Pou2af1 -K5R ( n = 3). ( E ) ChIP assay showing the binding of Pou2af1 -WT and Pou2af1 -K5R to the Slc7a11 promoter region ( n = 3). ( F – G ) Representative flow cytometric analysis of GFP + mCherry + leukemia cells (The markers for the indication of leukemia cells were GFP + and mCherry + , which were the tags for the MSCV- Notch1 -IRES-GFP plasmid and MSCV-mCherry overexpression plasmid) in peripheral blood from recipient mice 3 weeks after transplantation with WT and KO T-ALL cells overexpressing Slc7a11 . ( H – I ) Representative images and quantification of the liver, spleen and thymus morphology in recipient mice ( n = 3). ( J ) Survival analysis of recipient mice ( n = 5). The data are presented as the means ± SDs. One-way ANOVA with Tukey’s multiple comparison test ( G ), log-rank test ( J ) and two-way ANOVA with Sidak’s multiple comparison test ( D , I ) were used for comparisons of statistical significance (*, P < 0.05; **, P < 0.01; and ***, P < 0.001)

Article Snippet: These viral particles were subsequently used to infect NOTCH-GFP+ bone marrow leukemia cells, human cell lines Jurkat and MOLT-4 (ATCC), murine cell lines EL4 and L1210 (ATCC), as well as primary T-ALL patient samples, followed by assessment of in vitro cell proliferation.

Techniques: Activation Assay, Western Blot, Luciferase, Reporter Assay, Binding Assay, Plasmid Preparation, Over Expression, Transplantation Assay, Comparison

Journal: Cellular Oncology

Article Title: BCAA catabolism mediates POU2AF1 propionylation to enhance T-ALL development

doi: 10.1007/s13402-026-01201-w

Figure Lengend Snippet: Targeting BCAT1 metabolism significantly impaired T-ALL progression. ( A – D ) Analysis of the proliferation of EL4 ( A ), L1210 ( B ), Jurkat ( C ), and MOLT-4 ( D ) cells treated in vitro with 10 mM gabapentin (n=4). ( E ) Representative flow cytometric analysis of peripheral blood at 3 weeks post-transplantation from T-ALL model mice following treatment with IgG, anti-PD-1 antibody, low-BCAA, or combined low-BCAA + anti-PD-1 antibody. ( F ) Quantification of the peripheral blood data shown in Panel E (n=5). ( G ) Overall survival analysis of treated mice (n=5). ( H ) Schematic model illustrating how BCAT1-driven branched-chain amino acid metabolism promotes T-ALL progression via Kpr-mediated activation of POU2AF1. The data are presented as the means ± SDs. One-way ANOVA with Tukey’s multiple comparison test ( F ), log-rank test ( G ), and two-way ANOVA with Sidak’s multiple comparison test (A–D) were used for comparisons of statistical significance (*, P <0.05; **, P <0.01; and ***, P <0.001)

Techniques: In Vitro, Transplantation Assay, Activation Assay, Comparison

Identification of Val-ILs affecting T lymphoma growth (A) Transmission electron microscopy imaging showing a representative image of Val-ILs. Magnifications, ×94K (left) and ×310K (right); scale bars: 100 nm (left) and 50 nm (right). (B) Representative quantification and size of Val-ILs measured by NTA. (C) C57BL/6 mice were s.c. injected with 10 6 EL4 cells, into the side of the body. When tumors reached 50 mm 3 , mice were treated with Val-ILs i.v. injected on days 6 and 9 (10 12 NPs). A screening of 31 NPs loaded with different antibodies identified nine NPs that exhibited a strong tumor volume reduction by day 12 (pink bars). (D) Mice were treated with Val-ILs (10 12 NPs) on days 6, 9, and 12. The efficacy of the nine individual Val-ILs, as well as the combined Val-ILs targeting the nine identified antigens (Val-ILs-Combo), was evaluated on day 12 (left panel) and over time (right panel), n = 4 mice per group, two independent experiments performed. (E) Mice were i.v. injected with trackable NPs labeled with the PKH67 green fluorescent dye, n = 4 mice. The proportion and the number of PKH67 + NPs detected by FC in different tissues, after 18 h. PKH67 + NPs were detected in the spleen, the lymph nodes, and the bone marrow, whereas undetected (ud) in the blood, the thymus, the kidney, and the tumor. UV, unilamellar vesicle. (F) Mice were i.v. injected with Val-ILs labeled with PKH67. Cells were extracted 18 h later from various tissues and analyzed by FC, n = 5 mice per group. Data showing that trackable NPs bound to immunosuppressive cells in the spleen and the TDLNs. MFI, mean fluorescence intensity. Data are shown as means ± SD, p values are compared to Val-ILs-IgG or between the different groups and are calculated using one-way ANOVA with Tukey’s multiple comparisons test. See also .

Journal: Cell Reports Medicine

Article Title: Valrubicin-loaded immunoliposomes targeting antigens on immunosuppressive cells to circumvent resistance to cancer immunotherapy

doi: 10.1016/j.xcrm.2026.102632

Figure Lengend Snippet: Identification of Val-ILs affecting T lymphoma growth (A) Transmission electron microscopy imaging showing a representative image of Val-ILs. Magnifications, ×94K (left) and ×310K (right); scale bars: 100 nm (left) and 50 nm (right). (B) Representative quantification and size of Val-ILs measured by NTA. (C) C57BL/6 mice were s.c. injected with 10 6 EL4 cells, into the side of the body. When tumors reached 50 mm 3 , mice were treated with Val-ILs i.v. injected on days 6 and 9 (10 12 NPs). A screening of 31 NPs loaded with different antibodies identified nine NPs that exhibited a strong tumor volume reduction by day 12 (pink bars). (D) Mice were treated with Val-ILs (10 12 NPs) on days 6, 9, and 12. The efficacy of the nine individual Val-ILs, as well as the combined Val-ILs targeting the nine identified antigens (Val-ILs-Combo), was evaluated on day 12 (left panel) and over time (right panel), n = 4 mice per group, two independent experiments performed. (E) Mice were i.v. injected with trackable NPs labeled with the PKH67 green fluorescent dye, n = 4 mice. The proportion and the number of PKH67 + NPs detected by FC in different tissues, after 18 h. PKH67 + NPs were detected in the spleen, the lymph nodes, and the bone marrow, whereas undetected (ud) in the blood, the thymus, the kidney, and the tumor. UV, unilamellar vesicle. (F) Mice were i.v. injected with Val-ILs labeled with PKH67. Cells were extracted 18 h later from various tissues and analyzed by FC, n = 5 mice per group. Data showing that trackable NPs bound to immunosuppressive cells in the spleen and the TDLNs. MFI, mean fluorescence intensity. Data are shown as means ± SD, p values are compared to Val-ILs-IgG or between the different groups and are calculated using one-way ANOVA with Tukey’s multiple comparisons test. See also .

Article Snippet: In this study, we utilized the murine T lymphoma EL4 cells (ATCC, TIB-39, C57BL/6 strain), the murine B lymphoma A20 cells (ATCC, TIB-208, BALB/c strain), the murine breast cancer 4T1 cells (ATCC, CRL-2539, BALB/c strain) and the murine Lewis lung carcinoma LLC1 (LL/2) cells (ATCC, CRL-1642, C57BL/6 strain).

Techniques: Transmission Assay, Electron Microscopy, Imaging, Injection, Labeling, Fluorescence

Val-ILs affect immunosuppressive cells and T lymphoma growth C57BL/6 mice were s.c. injected with 10 6 EL4 cells into the body side. When tumors reached 50 mm 3 , mice were i.v. injected with Val-ILs (10 12 NPs) on days 6 and 9. Analyses were performed on day 12 (excepted for L). (A) UMAP data frame and heatmap following FC showing expression levels of the different populations of immune cells in the TME of T lymphoma-bearing mice. Mean normalized data of n = 7 untreated mice. (B) UMAP data frame and heatmap following FC showing expression levels of the nine antigens targeted by Val-ILs-Combo among immune cells detected in the TME, mean normalized data of n = 7 untreated mice. (C) Treatment with NPs reduced the tumor volumes measured in vivo. Image of tumors isolated ex vivo. (D) NPs affected the repartition of immune cells in the TME. (E) NPs reduced the number of immunosuppressive cells in the TME. (F) NPs affected the repartition of immune cells in the spleen. (G) NPs reduced the number of immunosuppressive cells in the spleen. (H) MFI measured by FC on TAMs in the TME and macrophages in the spleen, to identify M1-like and M2-like phenotypes. (I) FC on tDCs in the TME and DCs in the spleen, to identify the percentage of activated MHC II + DCs. (J) FC on T-Ly in the TDLNs showing an increase in these populations. (K) Val-ILs-Combo affected the amount of Th17 and Tregs in the TDLNs. (L) Tumor growth volumes measured in vivo , following i.v. injection of Val-ILs-Combo and/or αPD-1 (200 μg), n = 8 mice per group. (M) FC plots and heatmaps showing the expression levels of the nine antigens targeted by Val-ILs-Combo on immunosuppressive cells, in the TME; mean normalized data of n = 5 mice. (N) Histogram showing the number of antigens targeted by the NPs and found repressed ( p < 0.05) on various immune cell populations. The number of mice used per group is indicated on the figure; data are shown as means ± SD, p values are compared to Val-ILs-IgG and are calculated using two-tailed unpaired Student’s t test. See also .

Journal: Cell Reports Medicine

Article Title: Valrubicin-loaded immunoliposomes targeting antigens on immunosuppressive cells to circumvent resistance to cancer immunotherapy

doi: 10.1016/j.xcrm.2026.102632

Figure Lengend Snippet: Val-ILs affect immunosuppressive cells and T lymphoma growth C57BL/6 mice were s.c. injected with 10 6 EL4 cells into the body side. When tumors reached 50 mm 3 , mice were i.v. injected with Val-ILs (10 12 NPs) on days 6 and 9. Analyses were performed on day 12 (excepted for L). (A) UMAP data frame and heatmap following FC showing expression levels of the different populations of immune cells in the TME of T lymphoma-bearing mice. Mean normalized data of n = 7 untreated mice. (B) UMAP data frame and heatmap following FC showing expression levels of the nine antigens targeted by Val-ILs-Combo among immune cells detected in the TME, mean normalized data of n = 7 untreated mice. (C) Treatment with NPs reduced the tumor volumes measured in vivo. Image of tumors isolated ex vivo. (D) NPs affected the repartition of immune cells in the TME. (E) NPs reduced the number of immunosuppressive cells in the TME. (F) NPs affected the repartition of immune cells in the spleen. (G) NPs reduced the number of immunosuppressive cells in the spleen. (H) MFI measured by FC on TAMs in the TME and macrophages in the spleen, to identify M1-like and M2-like phenotypes. (I) FC on tDCs in the TME and DCs in the spleen, to identify the percentage of activated MHC II + DCs. (J) FC on T-Ly in the TDLNs showing an increase in these populations. (K) Val-ILs-Combo affected the amount of Th17 and Tregs in the TDLNs. (L) Tumor growth volumes measured in vivo , following i.v. injection of Val-ILs-Combo and/or αPD-1 (200 μg), n = 8 mice per group. (M) FC plots and heatmaps showing the expression levels of the nine antigens targeted by Val-ILs-Combo on immunosuppressive cells, in the TME; mean normalized data of n = 5 mice. (N) Histogram showing the number of antigens targeted by the NPs and found repressed ( p < 0.05) on various immune cell populations. The number of mice used per group is indicated on the figure; data are shown as means ± SD, p values are compared to Val-ILs-IgG and are calculated using two-tailed unpaired Student’s t test. See also .

Techniques: Injection, Expressing, In Vivo, Isolation, Ex Vivo, Two Tailed Test

MiR‐19a‐3p enhances CD4 + T cell‐mediated suppression of HBx‐expressing tumour in vivo. (A) Schematic diagram of tumour cell transplantation and agomir injection. (B) MiR‐19a‐3p significantly abrogated the higher tumour growth rate caused by HBx. Tumour growth curves of the indicated groups were measured every 2 days ( n = 6 for each group). (C) Tumour weights were measured at day 19. (D) Flow cytometry analysis to detect the subpopulations of CD4 + T cells in tumour tissues collected from a subcutaneous injection model of EL4 mice. In all experiments, cells were first gated on the CD45 + population and then on the CD4 + population. (E) The CD4 + T cell percentage was increased under miR‐19a‐3p treatment, as shown by IHC analysis. Scale bar = 100 µm. (F, G) The levels of IFN‐γ (F) and Granzyme B (G) in the tumour tissues were measured by ELISA. (H) Schematic diagram of humanized SUDHL‐4 xenograft model with adoptive transfer of human CD4⁺ T cells and agomir injection. (I) Tumour growth curves of indicated groups measured every 2 days ( n = 6 for each group). (J) Tumour weights of indicated groups were measured at day 23. (K) IHC analysis of CD4⁺ T cell infiltration in SUDHL‐4 tumour tissues. Scale bar = 100 µm. (L, M) ELISA quantification of IFN‐γ (L) and Granzyme B (M) in SUDHL‐4 tumour tissues. The data represent the mean ± SD of six independent experiments. For panels B‐G, *HBx+agomir‐NC vs. Ctrl+agomir‐NC; #HBx+agomir‐19a‐3p vs. HBx+agomir‐NC. For panels I‐M, *HBx+agomir‐NC+CD4 vs. Ctrl+agomir‐NC+CD4; #HBx+agomir‐19a‐3p+CD4 vs. HBx+agomir‐NC+CD4. * p < .05, ** p < .01, ***/ ### p < .001.

Journal: Clinical and Translational Medicine

Article Title: HBx hijacks the miR‐19a‐3p/BAMBI/TGF‐β1 axis to impair the anti‐tumour activity of CD4 + T cells in diffuse large B‐cell lymphoma

doi: 10.1002/ctm2.70578

Figure Lengend Snippet: MiR‐19a‐3p enhances CD4 + T cell‐mediated suppression of HBx‐expressing tumour in vivo. (A) Schematic diagram of tumour cell transplantation and agomir injection. (B) MiR‐19a‐3p significantly abrogated the higher tumour growth rate caused by HBx. Tumour growth curves of the indicated groups were measured every 2 days ( n = 6 for each group). (C) Tumour weights were measured at day 19. (D) Flow cytometry analysis to detect the subpopulations of CD4 + T cells in tumour tissues collected from a subcutaneous injection model of EL4 mice. In all experiments, cells were first gated on the CD45 + population and then on the CD4 + population. (E) The CD4 + T cell percentage was increased under miR‐19a‐3p treatment, as shown by IHC analysis. Scale bar = 100 µm. (F, G) The levels of IFN‐γ (F) and Granzyme B (G) in the tumour tissues were measured by ELISA. (H) Schematic diagram of humanized SUDHL‐4 xenograft model with adoptive transfer of human CD4⁺ T cells and agomir injection. (I) Tumour growth curves of indicated groups measured every 2 days ( n = 6 for each group). (J) Tumour weights of indicated groups were measured at day 23. (K) IHC analysis of CD4⁺ T cell infiltration in SUDHL‐4 tumour tissues. Scale bar = 100 µm. (L, M) ELISA quantification of IFN‐γ (L) and Granzyme B (M) in SUDHL‐4 tumour tissues. The data represent the mean ± SD of six independent experiments. For panels B‐G, *HBx+agomir‐NC vs. Ctrl+agomir‐NC; #HBx+agomir‐19a‐3p vs. HBx+agomir‐NC. For panels I‐M, *HBx+agomir‐NC+CD4 vs. Ctrl+agomir‐NC+CD4; #HBx+agomir‐19a‐3p+CD4 vs. HBx+agomir‐NC+CD4. * p < .05, ** p < .01, ***/ ### p < .001.

Article Snippet: Human SUDHL‐4 and HEK293T cells (ATCC, USA) and murine EL4 B‐lymphoma cells (Shanghai Fuheng Biotechnology) were authenticated by STR profiling and routinely screened for mycoplasma.

Techniques: Expressing, In Vivo, Transplantation Assay, Injection, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Adoptive Transfer Assay

$The DLBCL‐derived TGF‐β1 translates HBx/miR‐19a‐3p/BAMBI signalling into CD4 + T cell exclusion and immune escape. (A) Ligand (L) and receptor (R) counts in significant DLBCL‐CD4 + T cell interactions ( GSE182434 ). (B, C) The expression level of TGF‐β1 were measured by ELISA. (D) IHC analysis of TGF‐β1 in the EL4 tumour tissues. Scale bar = 100 µm. (E) Schematic diagram of tumour cell transplantation and antibody injection. (F) Tumour growth curves of EL4 tumours in mice. (G) Tumour weights were measured at day 19. (H) CD4 + T cell infiltration in tumour tissues determined by IHC. Scale bar = 100 µm. (I, J) The levels of IFN‐γ (I) and Granzyme B (J) in the tumour tissues were measured by ELISA. (K, L) High expression level of BAMBI (K) or TGFB1 (L) correlated with reduced CD4 + T cells enrichment ( GSE125966 ). (M) Patients with poor response to R‐CHOP treatment exhibited higher expression of BAMBI and TGFB1 ( GSE23501 ). (N) Compared with patients with favourable outcomes (durable remission ≥4 years), those with poor prognosis (primary refractory or relapsed disease) showed significantly higher expression of BAMBI and TGFB1 ( GSE178965 ). The data represent mean ± SD of at least three independent experiments. ** p < .01, ***/ ### p < .001.$

Journal: Clinical and Translational Medicine

Article Title: HBx hijacks the miR‐19a‐3p/BAMBI/TGF‐β1 axis to impair the anti‐tumour activity of CD4 + T cells in diffuse large B‐cell lymphoma

doi: 10.1002/ctm2.70578

Figure Lengend Snippet: The DLBCL‐derived TGF‐β1 translates HBx/miR‐19a‐3p/BAMBI signalling into CD4 + T cell exclusion and immune escape. (A) Ligand (L) and receptor (R) counts in significant DLBCL‐CD4 + T cell interactions ( GSE182434 ). (B, C) The expression level of TGF‐β1 were measured by ELISA. (D) IHC analysis of TGF‐β1 in the EL4 tumour tissues. Scale bar = 100 µm. (E) Schematic diagram of tumour cell transplantation and antibody injection. (F) Tumour growth curves of EL4 tumours in mice. (G) Tumour weights were measured at day 19. (H) CD4 + T cell infiltration in tumour tissues determined by IHC. Scale bar = 100 µm. (I, J) The levels of IFN‐γ (I) and Granzyme B (J) in the tumour tissues were measured by ELISA. (K, L) High expression level of BAMBI (K) or TGFB1 (L) correlated with reduced CD4 + T cells enrichment ( GSE125966 ). (M) Patients with poor response to R‐CHOP treatment exhibited higher expression of BAMBI and TGFB1 ( GSE23501 ). (N) Compared with patients with favourable outcomes (durable remission ≥4 years), those with poor prognosis (primary refractory or relapsed disease) showed significantly higher expression of BAMBI and TGFB1 ( GSE178965 ). The data represent mean ± SD of at least three independent experiments. ** p < .01, ***/ ### p < .001.

Techniques: Derivative Assay, Expressing, Enzyme-linked Immunosorbent Assay, Transplantation Assay, Injection

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murine cell lines el4 (ATCC)

Structured Review

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1) Product Images from "BCAA catabolism mediates POU2AF1 propionylation to enhance T-ALL development"

Related Articles

Irradiation:

Cell Characterization:

Isolation:

Positive Control:

Cloning:

Polymerase Chain Reaction:

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