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recombinant human light tnfsf14 protein  (R&D Systems)


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    Structured Review

    R&D Systems recombinant human light tnfsf14 protein
    Recombinant Human Light Tnfsf14 Protein, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant human light tnfsf14 protein/product/R&D Systems
    Average 94 stars, based on 22 article reviews
    recombinant human light tnfsf14 protein - by Bioz Stars, 2026-05
    94/100 stars

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    A. The abundance of total IHL isolated from WT and Il-17a -/- mice is quantified (N = 4-6 per group). B. Total number of IHL isolated from WT and Il-17a -/- mice reared on control or DDC diet is normalized to liver weight (N = 4-6 per group). C. The proportion of CD45 + cells in the IHL as determined by flow cytometry (N = 4-6 per group). D. (Left panel) CD4 + T cells abundance in gated CD45 + immune cells, and (Right panel ) the proportion of <t>LIGHT</t> + cells in the CD4 + T cell fraction (N = 3 per group). E. (Left panel) NK T cell abundance in gated CD45 + immune cells, and (Right panel ) proportion of LIGHT + cells in the NK T cell fraction (N = 4-6 per group). F. LIGHT positivity in CD4 + T cell subsets, Th1, Th2, Th17, and T-reg, was determined by flow cytometry (N = 3 per group). G. WT primary mouse splenocytes when stimulated with PMA/ionomycin or vehicle display (left panel) a similar proportion of CD3 + CD4 + T cells, (middle panel) an increased abundance of IFNγ + CD 4 + T cells and (right panel) an increased proportion of LIGHT + CD4 + T cells (N = 3 per group). H. The expression of pro-fibrogenic genes ACTA2, COL1A1, PDGFRA and CTGF is elevated in primary human hepatic stellate cells when stimulated with <t>recombinant</t> LIGHT (N = 3 per group). * - p < 0.05, ** - p < 0.01, *** - p < 0.005, **** - p < 0.001.
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    A. The abundance of total IHL isolated from WT and Il-17a -/- mice is quantified (N = 4-6 per group). B. Total number of IHL isolated from WT and Il-17a -/- mice reared on control or DDC diet is normalized to liver weight (N = 4-6 per group). C. The proportion of CD45 + cells in the IHL as determined by flow cytometry (N = 4-6 per group). D. (Left panel) CD4 + T cells abundance in gated CD45 + immune cells, and (Right panel ) the proportion of <t>LIGHT</t> + cells in the CD4 + T cell fraction (N = 3 per group). E. (Left panel) NK T cell abundance in gated CD45 + immune cells, and (Right panel ) proportion of LIGHT + cells in the NK T cell fraction (N = 4-6 per group). F. LIGHT positivity in CD4 + T cell subsets, Th1, Th2, Th17, and T-reg, was determined by flow cytometry (N = 3 per group). G. WT primary mouse splenocytes when stimulated with PMA/ionomycin or vehicle display (left panel) a similar proportion of CD3 + CD4 + T cells, (middle panel) an increased abundance of IFNγ + CD 4 + T cells and (right panel) an increased proportion of LIGHT + CD4 + T cells (N = 3 per group). H. The expression of pro-fibrogenic genes ACTA2, COL1A1, PDGFRA and CTGF is elevated in primary human hepatic stellate cells when stimulated with <t>recombinant</t> LIGHT (N = 3 per group). * - p < 0.05, ** - p < 0.01, *** - p < 0.005, **** - p < 0.001.
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    LOP enhances the inhibitory effects of 5-FU on HCT8R cells through autophagy activation. (A) Western blot analysis of changes in <t>LC3</t> and Beclin protein expression in HCT8R cells treated with LOP and 5-FU. (B) Confocal microscopy images, showing the generation of autophagic vesicles in HCT8R cells transfected with the EGFP-LC3 plasmid, and treated with LOP and 5-FU. (C) Western blot analysis of Beclin protein expression in HCT8R cells treated with or without 3-MA. (D) Statistical analysis of changes in Beclin expression in HCT8R cells treated with or without 3-MA. (E) Transwell assays were performed, assessing the migratory capability of HCT8R cells treated with LOP, 5-FU, with or without 3-MA. *P<0.05, **P<0.01 (n=3). 3-MA, 3-methyladenine; 5-FU, 5-fluorouracil; DMSO, dimethyl sulfoxide; LC3, microtubule-associated protein 1 light chain 3; LOP, loperamide; ns, not significant.
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    A. The abundance of total IHL isolated from WT and Il-17a -/- mice is quantified (N = 4-6 per group). B. Total number of IHL isolated from WT and Il-17a -/- mice reared on control or DDC diet is normalized to liver weight (N = 4-6 per group). C. The proportion of CD45 + cells in the IHL as determined by flow cytometry (N = 4-6 per group). D. (Left panel) CD4 + T cells abundance in gated CD45 + immune cells, and (Right panel ) the proportion of LIGHT + cells in the CD4 + T cell fraction (N = 3 per group). E. (Left panel) NK T cell abundance in gated CD45 + immune cells, and (Right panel ) proportion of LIGHT + cells in the NK T cell fraction (N = 4-6 per group). F. LIGHT positivity in CD4 + T cell subsets, Th1, Th2, Th17, and T-reg, was determined by flow cytometry (N = 3 per group). G. WT primary mouse splenocytes when stimulated with PMA/ionomycin or vehicle display (left panel) a similar proportion of CD3 + CD4 + T cells, (middle panel) an increased abundance of IFNγ + CD 4 + T cells and (right panel) an increased proportion of LIGHT + CD4 + T cells (N = 3 per group). H. The expression of pro-fibrogenic genes ACTA2, COL1A1, PDGFRA and CTGF is elevated in primary human hepatic stellate cells when stimulated with recombinant LIGHT (N = 3 per group). * - p < 0.05, ** - p < 0.01, *** - p < 0.005, **** - p < 0.001.

    Journal: PLOS One

    Article Title: Genetic ablation of interleukin-17A augments fibrosis in a mouse model of cholestatic liver injury

    doi: 10.1371/journal.pone.0342251

    Figure Lengend Snippet: A. The abundance of total IHL isolated from WT and Il-17a -/- mice is quantified (N = 4-6 per group). B. Total number of IHL isolated from WT and Il-17a -/- mice reared on control or DDC diet is normalized to liver weight (N = 4-6 per group). C. The proportion of CD45 + cells in the IHL as determined by flow cytometry (N = 4-6 per group). D. (Left panel) CD4 + T cells abundance in gated CD45 + immune cells, and (Right panel ) the proportion of LIGHT + cells in the CD4 + T cell fraction (N = 3 per group). E. (Left panel) NK T cell abundance in gated CD45 + immune cells, and (Right panel ) proportion of LIGHT + cells in the NK T cell fraction (N = 4-6 per group). F. LIGHT positivity in CD4 + T cell subsets, Th1, Th2, Th17, and T-reg, was determined by flow cytometry (N = 3 per group). G. WT primary mouse splenocytes when stimulated with PMA/ionomycin or vehicle display (left panel) a similar proportion of CD3 + CD4 + T cells, (middle panel) an increased abundance of IFNγ + CD 4 + T cells and (right panel) an increased proportion of LIGHT + CD4 + T cells (N = 3 per group). H. The expression of pro-fibrogenic genes ACTA2, COL1A1, PDGFRA and CTGF is elevated in primary human hepatic stellate cells when stimulated with recombinant LIGHT (N = 3 per group). * - p < 0.05, ** - p < 0.01, *** - p < 0.005, **** - p < 0.001.

    Article Snippet: Cells were rested for 4 hours and stimulated with medium containing vehicle or recombinant human LIGHT (664-LI, R&D systems, Minneapolis, MN) for 72 hours refreshing the medium at 48 hours.

    Techniques: Isolation, Control, Flow Cytometry, Expressing, Recombinant

    LOP enhances the inhibitory effects of 5-FU on HCT8R cells through autophagy activation. (A) Western blot analysis of changes in LC3 and Beclin protein expression in HCT8R cells treated with LOP and 5-FU. (B) Confocal microscopy images, showing the generation of autophagic vesicles in HCT8R cells transfected with the EGFP-LC3 plasmid, and treated with LOP and 5-FU. (C) Western blot analysis of Beclin protein expression in HCT8R cells treated with or without 3-MA. (D) Statistical analysis of changes in Beclin expression in HCT8R cells treated with or without 3-MA. (E) Transwell assays were performed, assessing the migratory capability of HCT8R cells treated with LOP, 5-FU, with or without 3-MA. *P<0.05, **P<0.01 (n=3). 3-MA, 3-methyladenine; 5-FU, 5-fluorouracil; DMSO, dimethyl sulfoxide; LC3, microtubule-associated protein 1 light chain 3; LOP, loperamide; ns, not significant.

    Journal: Oncology Reports

    Article Title: Loperamide reverses 5-FU resistance in colorectal cancer by activating autophagy

    doi: 10.3892/or.2025.8966

    Figure Lengend Snippet: LOP enhances the inhibitory effects of 5-FU on HCT8R cells through autophagy activation. (A) Western blot analysis of changes in LC3 and Beclin protein expression in HCT8R cells treated with LOP and 5-FU. (B) Confocal microscopy images, showing the generation of autophagic vesicles in HCT8R cells transfected with the EGFP-LC3 plasmid, and treated with LOP and 5-FU. (C) Western blot analysis of Beclin protein expression in HCT8R cells treated with or without 3-MA. (D) Statistical analysis of changes in Beclin expression in HCT8R cells treated with or without 3-MA. (E) Transwell assays were performed, assessing the migratory capability of HCT8R cells treated with LOP, 5-FU, with or without 3-MA. *P<0.05, **P<0.01 (n=3). 3-MA, 3-methyladenine; 5-FU, 5-fluorouracil; DMSO, dimethyl sulfoxide; LC3, microtubule-associated protein 1 light chain 3; LOP, loperamide; ns, not significant.

    Article Snippet: Transfection was subsequently performed using Lipo8000 TM reagent (Beyotime Institute of Biotechnology) in combination with 2 μg pEGFP (cat. no. 165830; Addgene, Inc.) or pEGFP-microtubule-associated protein 1 light chain 3 (LC3) plasmid (cat. no. 24920; Addgene, Inc.) and Opti-MEM TM serum-free medium (Gibco; Thermo Fisher Scientific Inc.).

    Techniques: Activation Assay, Western Blot, Expressing, Confocal Microscopy, Transfection, Plasmid Preparation