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R&D Systems recombinant human ccl5

FADD in hepatoma cells directs intratumoral CD8 + T-cell infiltration via the <t>CCL5–CCR5</t> chemotaxis pathway. A, Schematic of the in vivo T-cell migration assay. B, Tumor weights and relative FADD mRNA levels in HepG2-vector and HepG2- FADD tumors 14 days after inoculation ( n = 8). C, Representative IHC images of CD8 in HepG2-vector and HepG2- FADD tumors and quantification thereof ( n = 10). Scale bar, 100 μm. D, Tumor weights and relative FADD mRNA levels in Huh7-sh Ctrl and Huh7-sh FADD tumors 14 days after inoculation ( n = 8). E, Representative IHC images of CD8 in Huh7-sh Ctrl and Huh7-sh FADD tumors and quantification thereof ( n = 10). Scale bar, 100 μm. F, Venn diagram of 521 immune-related genes from and cytokines/chemokines from ImmPort identified 36 overlapping cytokines and chemokines. G, mRNA levels of the 36 cytokines and chemokines in HepG2-vector, HepG2-FADD, Huh7-sh Ctrl , and Huh7-sh FADD cells, as well as tumors generated in A . H, Schematic of NSG-HuPBL humanized mouse model ( n = 8–10). I and J, Representative coimmunofluorescence images of CD8 and CCR5 in HepG2-vector and HepG2- FADD ( I ) and Huh7-sh Ctrl and Huh7-sh FADD tumors ( J ). Hoechst marks cell nuclei. Quantification of CCR5 + CD8 + cell proportions in the indicated groups is also provided. Scale bar, 100 μm. Data are presented as the mean ± SD for at least two (mouse models) or three (Western blotting) independent experiments and analyzed with the paired ( B–E , I and J ) or unpaired ( G ) two-tailed Student t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Recombinant Human Ccl5, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 48 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/recombinant+human+ccl5/Recombinant+Human+CCL5%2FRANTES+Protein/pmc12434399-109-19-25
Average 93 stars, based on 48 article reviews

recombinant human ccl5 - by Bioz Stars, 2026-10

93/100 stars

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1) Product Images from "FADD Activation in Hepatocellular Carcinoma Potentiates CD8 + T-cell Responses and Sensitizes to Immune Checkpoint Inhibitors"

Article Title: FADD Activation in Hepatocellular Carcinoma Potentiates CD8 + T-cell Responses and Sensitizes to Immune Checkpoint Inhibitors

Journal: Cancer Research

doi: 10.1158/0008-5472.CAN-24-3854

FADD in hepatoma cells directs intratumoral CD8 + T-cell infiltration via the CCL5–CCR5 chemotaxis pathway. A, Schematic of the in vivo T-cell migration assay. B, Tumor weights and relative FADD mRNA levels in HepG2-vector and HepG2- FADD tumors 14 days after inoculation ( n = 8). C, Representative IHC images of CD8 in HepG2-vector and HepG2- FADD tumors and quantification thereof ( n = 10). Scale bar, 100 μm. D, Tumor weights and relative FADD mRNA levels in Huh7-sh Ctrl and Huh7-sh FADD tumors 14 days after inoculation ( n = 8). E, Representative IHC images of CD8 in Huh7-sh Ctrl and Huh7-sh FADD tumors and quantification thereof ( n = 10). Scale bar, 100 μm. F, Venn diagram of 521 immune-related genes from and cytokines/chemokines from ImmPort identified 36 overlapping cytokines and chemokines. G, mRNA levels of the 36 cytokines and chemokines in HepG2-vector, HepG2-FADD, Huh7-sh Ctrl , and Huh7-sh FADD cells, as well as tumors generated in A . H, Schematic of NSG-HuPBL humanized mouse model ( n = 8–10). I and J, Representative coimmunofluorescence images of CD8 and CCR5 in HepG2-vector and HepG2- FADD ( I ) and Huh7-sh Ctrl and Huh7-sh FADD tumors ( J ). Hoechst marks cell nuclei. Quantification of CCR5 + CD8 + cell proportions in the indicated groups is also provided. Scale bar, 100 μm. Data are presented as the mean ± SD for at least two (mouse models) or three (Western blotting) independent experiments and analyzed with the paired ( B–E , I and J ) or unpaired ( G ) two-tailed Student t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Figure Legend Snippet: FADD in hepatoma cells directs intratumoral CD8 + T-cell infiltration via the CCL5–CCR5 chemotaxis pathway. A, Schematic of the in vivo T-cell migration assay. B, Tumor weights and relative FADD mRNA levels in HepG2-vector and HepG2- FADD tumors 14 days after inoculation ( n = 8). C, Representative IHC images of CD8 in HepG2-vector and HepG2- FADD tumors and quantification thereof ( n = 10). Scale bar, 100 μm. D, Tumor weights and relative FADD mRNA levels in Huh7-sh Ctrl and Huh7-sh FADD tumors 14 days after inoculation ( n = 8). E, Representative IHC images of CD8 in Huh7-sh Ctrl and Huh7-sh FADD tumors and quantification thereof ( n = 10). Scale bar, 100 μm. F, Venn diagram of 521 immune-related genes from and cytokines/chemokines from ImmPort identified 36 overlapping cytokines and chemokines. G, mRNA levels of the 36 cytokines and chemokines in HepG2-vector, HepG2-FADD, Huh7-sh Ctrl , and Huh7-sh FADD cells, as well as tumors generated in A . H, Schematic of NSG-HuPBL humanized mouse model ( n = 8–10). I and J, Representative coimmunofluorescence images of CD8 and CCR5 in HepG2-vector and HepG2- FADD ( I ) and Huh7-sh Ctrl and Huh7-sh FADD tumors ( J ). Hoechst marks cell nuclei. Quantification of CCR5 + CD8 + cell proportions in the indicated groups is also provided. Scale bar, 100 μm. Data are presented as the mean ± SD for at least two (mouse models) or three (Western blotting) independent experiments and analyzed with the paired ( B–E , I and J ) or unpaired ( G ) two-tailed Student t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Techniques Used: Chemotaxis Assay, In Vivo, Cell Migration Assay, Plasmid Preparation, Generated, Western Blot, Two Tailed Test

FADD upregulates CCL5 by activating NF-κB transcription in HCC cells. A, Western blotting analysis of p-FADD Ser194 , FADD, p-IκBα Ser32 , IκBα, NF-κB-p50, p-NF-κB-p65 Ser536 , and NF-κB-p65. B, Relative CCL5 mRNA levels in the indicated groups. C, Relative mRNA levels of FADD and CCL5 in HepG2-vector and HepG2-FADD cells treated with siNC, siNF-κB-p50, or siNF-κB-p65. D, ChIP-qPCR analysis of NF-κB-p65 in the CCL5 promoter of HepG2-vector, HepG2- FADD , and HepG2- FADD -S194A stable cells. The CCL5 promoter region for TF binding is also shown. Data are presented as the mean ± SD for at least three (Western blot and qPCR) or two (ChIP-qPCR) independent experiments and analyzed with the unpaired, two-tailed Student t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Figure Legend Snippet: FADD upregulates CCL5 by activating NF-κB transcription in HCC cells. A, Western blotting analysis of p-FADD Ser194 , FADD, p-IκBα Ser32 , IκBα, NF-κB-p50, p-NF-κB-p65 Ser536 , and NF-κB-p65. B, Relative CCL5 mRNA levels in the indicated groups. C, Relative mRNA levels of FADD and CCL5 in HepG2-vector and HepG2-FADD cells treated with siNC, siNF-κB-p50, or siNF-κB-p65. D, ChIP-qPCR analysis of NF-κB-p65 in the CCL5 promoter of HepG2-vector, HepG2- FADD , and HepG2- FADD -S194A stable cells. The CCL5 promoter region for TF binding is also shown. Data are presented as the mean ± SD for at least three (Western blot and qPCR) or two (ChIP-qPCR) independent experiments and analyzed with the unpaired, two-tailed Student t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Techniques Used: Western Blot, Plasmid Preparation, ChIP-qPCR, Binding Assay, Two Tailed Test

$Phosphorylated FADD promotes NF-κB transcriptional activity via formation of a nuclear p-FADD/SAM68/NF-κB complex in HCC cells. A, Representative co-immunofluorescence images of p-FADD Ser194 (red), FADD (green), and nuclei (DAPI, blue) in HepG2- FADD and HepG2-FADD-S194 stable cell lines. Scale bar, 100 μm. B, Western blotting analysis of p-FADD Ser194 and FADD in the cytoplasmic (Cyto) and nuclear (Nuc) fractions. C, Coomassie brilliant blue staining for co-IP of nuclear proteins pulled down with anti-FADD antibody in HepG2-vector, HepG2-FADD, and HepG2-FADD-S194A stable cell lines. D, Venn diagram of 547 proteins identified through MS analysis in samples from C . E, Correlations of the 110 unique HepG2- FADD nuclear proteins with FADD expression, positive regulation of IκB kinase/NF-κB signaling pathway signatures, and positive regulation of NF-κB TF activity in samples from the TCGA-LIHC dataset. F, Protein–protein interaction network analysis of SAM68 with eight nodes. An average node degree of 4.25 with a median (0.4) level of confidence is required as the minimum required interaction score. G, Co-IP of nuclear FADD and SAM68 in HepG2-vector, HepG2-FADD, and HepG2-FADD-S194A stable cell lines, followed by Western blotting analysis of p-FADD Ser194 , FADD, SAM68, NF-κB-p50, p-NF-κB-p65 Ser536 , and NF-κB-p65. Lamin B serves as the loading control for nuclear lysate input, and IgG is the control for the IP assay. L, ladder. H, Western blotting analysis of SAM68, p-FADD Ser194 , FADD, p-IκBα Ser32 , IκBα, NF-κB-p50, p-NF-κB-p65 Ser536 , and NF-κB-p65. I, Relative mRNA levels of FADD and CCL5 in HepG2-vector and HepG2- FADD cells treated with siNC or siSAM68 (#1 and #2). J, Co-IP of nuclear FADD and SAM68 from HepG2-vector, HepG2- FADD , and HepG2-FADD treated with siSAM68 (#2), followed by Western blotting analysis of p-FADD Ser194 , FADD, SAM68, NF-κB-p50, p-NF-κB-p65 Ser536 , and NF-κB-p65. Histone H3 served as the nuclear lysate input loading control, and IgG is the IP assay control. K, Relative induction of NF-κB luciferase in HepG2-vector and HepG2- FADD cells treated with siNC or siSAM68 (#2). Data are presented as the mean ± SD for at least three independent experiments (coimmunofluorescence, Western blotting, and co-IP) and analyzed with the unpaired, two-tailed Student t test. Two-tailed Pearson correlation was used to compute the correlation between variables. *, P < 0.05; **, P < 0.01; ***, P < 0.001.$
Figure Legend Snippet: Phosphorylated FADD promotes NF-κB transcriptional activity via formation of a nuclear p-FADD/SAM68/NF-κB complex in HCC cells. A, Representative co-immunofluorescence images of p-FADD Ser194 (red), FADD (green), and nuclei (DAPI, blue) in HepG2- FADD and HepG2-FADD-S194 stable cell lines. Scale bar, 100 μm. B, Western blotting analysis of p-FADD Ser194 and FADD in the cytoplasmic (Cyto) and nuclear (Nuc) fractions. C, Coomassie brilliant blue staining for co-IP of nuclear proteins pulled down with anti-FADD antibody in HepG2-vector, HepG2-FADD, and HepG2-FADD-S194A stable cell lines. D, Venn diagram of 547 proteins identified through MS analysis in samples from C . E, Correlations of the 110 unique HepG2- FADD nuclear proteins with FADD expression, positive regulation of IκB kinase/NF-κB signaling pathway signatures, and positive regulation of NF-κB TF activity in samples from the TCGA-LIHC dataset. F, Protein–protein interaction network analysis of SAM68 with eight nodes. An average node degree of 4.25 with a median (0.4) level of confidence is required as the minimum required interaction score. G, Co-IP of nuclear FADD and SAM68 in HepG2-vector, HepG2-FADD, and HepG2-FADD-S194A stable cell lines, followed by Western blotting analysis of p-FADD Ser194 , FADD, SAM68, NF-κB-p50, p-NF-κB-p65 Ser536 , and NF-κB-p65. Lamin B serves as the loading control for nuclear lysate input, and IgG is the control for the IP assay. L, ladder. H, Western blotting analysis of SAM68, p-FADD Ser194 , FADD, p-IκBα Ser32 , IκBα, NF-κB-p50, p-NF-κB-p65 Ser536 , and NF-κB-p65. I, Relative mRNA levels of FADD and CCL5 in HepG2-vector and HepG2- FADD cells treated with siNC or siSAM68 (#1 and #2). J, Co-IP of nuclear FADD and SAM68 from HepG2-vector, HepG2- FADD , and HepG2-FADD treated with siSAM68 (#2), followed by Western blotting analysis of p-FADD Ser194 , FADD, SAM68, NF-κB-p50, p-NF-κB-p65 Ser536 , and NF-κB-p65. Histone H3 served as the nuclear lysate input loading control, and IgG is the IP assay control. K, Relative induction of NF-κB luciferase in HepG2-vector and HepG2- FADD cells treated with siNC or siSAM68 (#2). Data are presented as the mean ± SD for at least three independent experiments (coimmunofluorescence, Western blotting, and co-IP) and analyzed with the unpaired, two-tailed Student t test. Two-tailed Pearson correlation was used to compute the correlation between variables. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Techniques Used: Activity Assay, Immunofluorescence, Stable Transfection, Western Blot, Staining, Co-Immunoprecipitation Assay, Plasmid Preparation, Expressing, Control, Luciferase, Two Tailed Test

Sequential activation of FADD converts anti–PD-1 responsiveness in ICI-resistant HCC mouse models. A, Schematic of sequential anti–PD-1 treatment and Fadd overexpression in orthotopic PD-1R tumor–bearing C57BL/6 mice. B, Kaplan–Meier survival analysis of mice from the indicated groups ( n = 8–10). C and D, Western blotting analysis of p-Fadd Ser191 and Fadd in tumors from control or AAV- Fadd –treated tumor-bearing mice ( C ) and CTNNB1 OE /MYC OE -induced spontaneous tumors ( D ). E, Schematic of sequential anti–PD-1 and ADT-OH treatment schedule in the CTNNB1 OE /MYC OE -induced spontaneous HCC model. F, Western blotting analysis of p-Fadd Ser191 and Fadd in tumors from control and ADT-OH–treated mice. G and H, Representative photos, hematoxylin and eosin staining ( G ), and enumeration of tumor nodules in the indicated groups on day 80 ( H ). Scale bar, 1,000 μm. I, Uniform Manifold Approximation and Projection (UMAP) plots showing high-dimensional flow cytometry analysis of tumor-infiltrating CD45 + leukocytes from the indicated groups of mice ( n = 6). UMAP plots consist of 12,000 cells each and are representative of concatenated samples within each group. Indicated immune cell clusters are highlighted in the indicated colors, and their proportions as percentages of CD45 + leukocytes are quantified ( J ). DC, dendritic cell; NA, no annotation. K, Heat map showing Pearson correlations among the number of tumor nodules; p-Fadd Ser191 ; Fadd; CCL5; the proportions of total, CCR5 + , IFNγ + , and TNFα + CD8 + T cells; TUNEL scores; and the concentrations of IFNγ and TNFα. L, Kaplan–Meier survival analysis of mice from the indicated groups ( n = 10–14); two-sided log-rank (Mantel–Cox) test. M, The FADD/CCL5/CD8a signature in patients with HCC treated with atezolizumab alone or in combination with bevacizumab (anti-VEGF). Data are presented as the mean ± SD for at least two (mouse models) or three (Western blotting) independent experiments and analyzed with the unpaired, two-tailed Student t test. Correlation analyses were performed using single-tailed Pearson correlations. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Figure Legend Snippet: Sequential activation of FADD converts anti–PD-1 responsiveness in ICI-resistant HCC mouse models. A, Schematic of sequential anti–PD-1 treatment and Fadd overexpression in orthotopic PD-1R tumor–bearing C57BL/6 mice. B, Kaplan–Meier survival analysis of mice from the indicated groups ( n = 8–10). C and D, Western blotting analysis of p-Fadd Ser191 and Fadd in tumors from control or AAV- Fadd –treated tumor-bearing mice ( C ) and CTNNB1 OE /MYC OE -induced spontaneous tumors ( D ). E, Schematic of sequential anti–PD-1 and ADT-OH treatment schedule in the CTNNB1 OE /MYC OE -induced spontaneous HCC model. F, Western blotting analysis of p-Fadd Ser191 and Fadd in tumors from control and ADT-OH–treated mice. G and H, Representative photos, hematoxylin and eosin staining ( G ), and enumeration of tumor nodules in the indicated groups on day 80 ( H ). Scale bar, 1,000 μm. I, Uniform Manifold Approximation and Projection (UMAP) plots showing high-dimensional flow cytometry analysis of tumor-infiltrating CD45 + leukocytes from the indicated groups of mice ( n = 6). UMAP plots consist of 12,000 cells each and are representative of concatenated samples within each group. Indicated immune cell clusters are highlighted in the indicated colors, and their proportions as percentages of CD45 + leukocytes are quantified ( J ). DC, dendritic cell; NA, no annotation. K, Heat map showing Pearson correlations among the number of tumor nodules; p-Fadd Ser191 ; Fadd; CCL5; the proportions of total, CCR5 + , IFNγ + , and TNFα + CD8 + T cells; TUNEL scores; and the concentrations of IFNγ and TNFα. L, Kaplan–Meier survival analysis of mice from the indicated groups ( n = 10–14); two-sided log-rank (Mantel–Cox) test. M, The FADD/CCL5/CD8a signature in patients with HCC treated with atezolizumab alone or in combination with bevacizumab (anti-VEGF). Data are presented as the mean ± SD for at least two (mouse models) or three (Western blotting) independent experiments and analyzed with the unpaired, two-tailed Student t test. Correlation analyses were performed using single-tailed Pearson correlations. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Techniques Used: Activation Assay, Over Expression, Western Blot, Control, Staining, Flow Cytometry, TUNEL Assay, Two Tailed Test

Recombinant:

Article Title: Single-cell transcriptomics reveals the effect of PD-L1/TGF-β blockade on the tumor microenvironment
Article Snippet: .. The treatment groups were PBS, recombinant human CCL5 (R&D systems, 278-RN-050/CF), PBS plus anti-PD-L1 (atezolizumab, Roche), and CCL5 plus anti-PD-L1. ..

Article Title: CCL5 persists in RSV stocks following sucrose-gradient purification
Article Snippet: 1Departments ofMedicine, University of Alberta, Edmonton, Alberta, Canada 2Pediatrics, University of Alberta, Edmonton, Alberta, Canada 3Department of Immunology, University of Manitoba,Winnipeg, Manitoba, Canada 4Departments of Pediatrics, University of Saskatchewan, Saskatoon, Saskatchewan, Canada Correspondence Darryl J. Adamko,DepartmentsofPediatric PulmonaryMedicine, Rm2742,RoyalUniversity HospitalUniversity of Saskatchewan, Saskatoon, SaskatchewanS7N0W8,Canada.. E-mail: darryl.adamko@usask.ca Abstract Respiratory syncytial virus (RSV) is associated with bronchiolitis in infancy and the later development of asthma.. Research on RSV in vitro requires preparation of a purified RSV stock.

Article Title: FADD Activation in Hepatocellular Carcinoma Potentiates CD8 + T-cell Responses and Sensitizes to Immune Checkpoint Inhibitors
Article Snippet: .. HepG2- FADD or Huh7-sh FADD cells were then treated with CCL5-neutralizing antibodies (nAb; 100 pg/mL, R&D Systems, #MAB678-SP) or recombinant human CCL5 (rCCL5; 100 pg/mL, R&D Systems, #278-RN-050/CF), respectively, before T cells were added to the top chamber. ..

Article Title: Function of CCL5 in maternal-fetal interface of pig during early pregnancy.
Article Snippet: Chemokines refer to chemoattractant cytokines, which have crucial functions in inflammation and immune responses in multiple cellular processes.. In the present study, we described the potential role of porcine CCL5 in embryo implantation and fetal-maternal environment during early pregnancy.. We first carried out phylogenetic analysis of porcine CCL5, and analyzed the cell specific localization of CCL5 and its receptor CCR3 in a kinetic approach within porcine estrous cycles and early gestation stage.

Article Title: Pericytes augment glioblastoma cell resistance to temozolomide through CCL5-CCR5 paracrine signaling
Article Snippet: Pericytes (5 × 10 4 ) and GBM cells (5 × 10 4 ) were, respectively, cultured in the upper or lower chamber in 6-well transwell apparatus, followed by the treatment of TMZ (500 μmol/L, Selleckchem, S1237). .. To determine the protective effect of pericytes or CCL5 on GBM cells, GBM cells were pretreated with or without pericyte CM, recombinant human CCL5 (10 ng/mL, R&D), or MVC (500 nmol/L, Selleckchem, S2003), followed by TMZ (500 μmol/L) treatment 4 h later. .. Apoptotic analysis was performed using Annexin-V Apoptosis Detection Kit (Invitrogen, 88-8007-74) according to the manufacturer’s instructions.

Article Title: Single cell transcriptomics reveals the effect of PD-L1/TGF-β blockade on the tumor microenvironment
Article Snippet: .. The treatment groups were PBS, recombinant human CCL5 (R&D systems, 278-RN-050/CF), PBS plus anti-PD-L1 (atezolizumab, Roche), and CCL5 plus anti-PD-L1. ..

Article Title: Modulation of the K/BxN arthritis mouse model and the effector functions of human fibroblast-like synoviocytes by liver X receptors.
Article Snippet: StreptavidinHRP-conjugated secondary antibody was from Thermo Fisher Scientific. .. Recombinant human CCL5 and CXCL10 were purchased from R&D Systems. .. Recombinant human TNF, IL-1β, and CXCL12 were obtained from Immunotools.

Article Title: Single-cell transcriptomics reveals the effect of PD-L1/TGF-β blockade on the tumor microenvironment.
Article Snippet: .. The treatment groups were PBS, recombinant human CCL5 (R&D systems, 278-RN-050/CF), PBS plus antiPD-L1 (atezolizumab, Roche), and CCL5 plus anti-PDL1. ..

Positive Control:

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Image Search Results

Journal: Cancer Research

Article Title: FADD Activation in Hepatocellular Carcinoma Potentiates CD8 + T-cell Responses and Sensitizes to Immune Checkpoint Inhibitors

doi: 10.1158/0008-5472.CAN-24-3854

Figure Lengend Snippet: FADD in hepatoma cells directs intratumoral CD8 + T-cell infiltration via the CCL5–CCR5 chemotaxis pathway. A, Schematic of the in vivo T-cell migration assay. B, Tumor weights and relative FADD mRNA levels in HepG2-vector and HepG2- FADD tumors 14 days after inoculation ( n = 8). C, Representative IHC images of CD8 in HepG2-vector and HepG2- FADD tumors and quantification thereof ( n = 10). Scale bar, 100 μm. D, Tumor weights and relative FADD mRNA levels in Huh7-sh Ctrl and Huh7-sh FADD tumors 14 days after inoculation ( n = 8). E, Representative IHC images of CD8 in Huh7-sh Ctrl and Huh7-sh FADD tumors and quantification thereof ( n = 10). Scale bar, 100 μm. F, Venn diagram of 521 immune-related genes from and cytokines/chemokines from ImmPort identified 36 overlapping cytokines and chemokines. G, mRNA levels of the 36 cytokines and chemokines in HepG2-vector, HepG2-FADD, Huh7-sh Ctrl , and Huh7-sh FADD cells, as well as tumors generated in A . H, Schematic of NSG-HuPBL humanized mouse model ( n = 8–10). I and J, Representative coimmunofluorescence images of CD8 and CCR5 in HepG2-vector and HepG2- FADD ( I ) and Huh7-sh Ctrl and Huh7-sh FADD tumors ( J ). Hoechst marks cell nuclei. Quantification of CCR5 + CD8 + cell proportions in the indicated groups is also provided. Scale bar, 100 μm. Data are presented as the mean ± SD for at least two (mouse models) or three (Western blotting) independent experiments and analyzed with the paired ( B–E , I and J ) or unpaired ( G ) two-tailed Student t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Article Snippet: HepG2- FADD or Huh7-sh FADD cells were then treated with CCL5-neutralizing antibodies (nAb; 100 pg/mL, R&D Systems, #MAB678-SP) or recombinant human CCL5 (rCCL5; 100 pg/mL, R&D Systems, #278-RN-050/CF), respectively, before T cells were added to the top chamber.

Techniques: Chemotaxis Assay, In Vivo, Cell Migration Assay, Plasmid Preparation, Generated, Western Blot, Two Tailed Test

Journal: Cancer Research

Article Title: FADD Activation in Hepatocellular Carcinoma Potentiates CD8 + T-cell Responses and Sensitizes to Immune Checkpoint Inhibitors

doi: 10.1158/0008-5472.CAN-24-3854

Figure Lengend Snippet: FADD upregulates CCL5 by activating NF-κB transcription in HCC cells. A, Western blotting analysis of p-FADD Ser194 , FADD, p-IκBα Ser32 , IκBα, NF-κB-p50, p-NF-κB-p65 Ser536 , and NF-κB-p65. B, Relative CCL5 mRNA levels in the indicated groups. C, Relative mRNA levels of FADD and CCL5 in HepG2-vector and HepG2-FADD cells treated with siNC, siNF-κB-p50, or siNF-κB-p65. D, ChIP-qPCR analysis of NF-κB-p65 in the CCL5 promoter of HepG2-vector, HepG2- FADD , and HepG2- FADD -S194A stable cells. The CCL5 promoter region for TF binding is also shown. Data are presented as the mean ± SD for at least three (Western blot and qPCR) or two (ChIP-qPCR) independent experiments and analyzed with the unpaired, two-tailed Student t test. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Techniques: Western Blot, Plasmid Preparation, ChIP-qPCR, Binding Assay, Two Tailed Test

Journal: Cancer Research

Article Title: FADD Activation in Hepatocellular Carcinoma Potentiates CD8 + T-cell Responses and Sensitizes to Immune Checkpoint Inhibitors

doi: 10.1158/0008-5472.CAN-24-3854

Figure Lengend Snippet: Phosphorylated FADD promotes NF-κB transcriptional activity via formation of a nuclear p-FADD/SAM68/NF-κB complex in HCC cells. A, Representative co-immunofluorescence images of p-FADD Ser194 (red), FADD (green), and nuclei (DAPI, blue) in HepG2- FADD and HepG2-FADD-S194 stable cell lines. Scale bar, 100 μm. B, Western blotting analysis of p-FADD Ser194 and FADD in the cytoplasmic (Cyto) and nuclear (Nuc) fractions. C, Coomassie brilliant blue staining for co-IP of nuclear proteins pulled down with anti-FADD antibody in HepG2-vector, HepG2-FADD, and HepG2-FADD-S194A stable cell lines. D, Venn diagram of 547 proteins identified through MS analysis in samples from C . E, Correlations of the 110 unique HepG2- FADD nuclear proteins with FADD expression, positive regulation of IκB kinase/NF-κB signaling pathway signatures, and positive regulation of NF-κB TF activity in samples from the TCGA-LIHC dataset. F, Protein–protein interaction network analysis of SAM68 with eight nodes. An average node degree of 4.25 with a median (0.4) level of confidence is required as the minimum required interaction score. G, Co-IP of nuclear FADD and SAM68 in HepG2-vector, HepG2-FADD, and HepG2-FADD-S194A stable cell lines, followed by Western blotting analysis of p-FADD Ser194 , FADD, SAM68, NF-κB-p50, p-NF-κB-p65 Ser536 , and NF-κB-p65. Lamin B serves as the loading control for nuclear lysate input, and IgG is the control for the IP assay. L, ladder. H, Western blotting analysis of SAM68, p-FADD Ser194 , FADD, p-IκBα Ser32 , IκBα, NF-κB-p50, p-NF-κB-p65 Ser536 , and NF-κB-p65. I, Relative mRNA levels of FADD and CCL5 in HepG2-vector and HepG2- FADD cells treated with siNC or siSAM68 (#1 and #2). J, Co-IP of nuclear FADD and SAM68 from HepG2-vector, HepG2- FADD , and HepG2-FADD treated with siSAM68 (#2), followed by Western blotting analysis of p-FADD Ser194 , FADD, SAM68, NF-κB-p50, p-NF-κB-p65 Ser536 , and NF-κB-p65. Histone H3 served as the nuclear lysate input loading control, and IgG is the IP assay control. K, Relative induction of NF-κB luciferase in HepG2-vector and HepG2- FADD cells treated with siNC or siSAM68 (#2). Data are presented as the mean ± SD for at least three independent experiments (coimmunofluorescence, Western blotting, and co-IP) and analyzed with the unpaired, two-tailed Student t test. Two-tailed Pearson correlation was used to compute the correlation between variables. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Techniques: Activity Assay, Immunofluorescence, Stable Transfection, Western Blot, Staining, Co-Immunoprecipitation Assay, Plasmid Preparation, Expressing, Control, Luciferase, Two Tailed Test

Journal: Cancer Research

Article Title: FADD Activation in Hepatocellular Carcinoma Potentiates CD8 + T-cell Responses and Sensitizes to Immune Checkpoint Inhibitors

doi: 10.1158/0008-5472.CAN-24-3854

Figure Lengend Snippet: Sequential activation of FADD converts anti–PD-1 responsiveness in ICI-resistant HCC mouse models. A, Schematic of sequential anti–PD-1 treatment and Fadd overexpression in orthotopic PD-1R tumor–bearing C57BL/6 mice. B, Kaplan–Meier survival analysis of mice from the indicated groups ( n = 8–10). C and D, Western blotting analysis of p-Fadd Ser191 and Fadd in tumors from control or AAV- Fadd –treated tumor-bearing mice ( C ) and CTNNB1 OE /MYC OE -induced spontaneous tumors ( D ). E, Schematic of sequential anti–PD-1 and ADT-OH treatment schedule in the CTNNB1 OE /MYC OE -induced spontaneous HCC model. F, Western blotting analysis of p-Fadd Ser191 and Fadd in tumors from control and ADT-OH–treated mice. G and H, Representative photos, hematoxylin and eosin staining ( G ), and enumeration of tumor nodules in the indicated groups on day 80 ( H ). Scale bar, 1,000 μm. I, Uniform Manifold Approximation and Projection (UMAP) plots showing high-dimensional flow cytometry analysis of tumor-infiltrating CD45 + leukocytes from the indicated groups of mice ( n = 6). UMAP plots consist of 12,000 cells each and are representative of concatenated samples within each group. Indicated immune cell clusters are highlighted in the indicated colors, and their proportions as percentages of CD45 + leukocytes are quantified ( J ). DC, dendritic cell; NA, no annotation. K, Heat map showing Pearson correlations among the number of tumor nodules; p-Fadd Ser191 ; Fadd; CCL5; the proportions of total, CCR5 + , IFNγ + , and TNFα + CD8 + T cells; TUNEL scores; and the concentrations of IFNγ and TNFα. L, Kaplan–Meier survival analysis of mice from the indicated groups ( n = 10–14); two-sided log-rank (Mantel–Cox) test. M, The FADD/CCL5/CD8a signature in patients with HCC treated with atezolizumab alone or in combination with bevacizumab (anti-VEGF). Data are presented as the mean ± SD for at least two (mouse models) or three (Western blotting) independent experiments and analyzed with the unpaired, two-tailed Student t test. Correlation analyses were performed using single-tailed Pearson correlations. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Techniques: Activation Assay, Over Expression, Western Blot, Control, Staining, Flow Cytometry, TUNEL Assay, Two Tailed Test

Serum CCR1 ligand concentrations (pg/mg) at baseline (t = 0 min) and at the end of the experiment (t = 210 min). Light grey bars: vehicle treatment, n = 7. Dark grey bars: 0.5 μmol/kg BX471 treatment, n = 7. ( A ) CCL3, ( B ) CCL4, ( C ) CCL5, and ( D ) CCL7. *: p < 0.05 vs. baseline (t = 0 min).

Journal: Biomedicines

Article Title: The Chemokine (C-C Motif) Receptor 1 Antagonist BX471 Improves Fluid Resuscitation in Rat Models of Hemorrhagic Shock

doi: 10.3390/biomedicines13051241

Figure Lengend Snippet: Serum CCR1 ligand concentrations (pg/mg) at baseline (t = 0 min) and at the end of the experiment (t = 210 min). Light grey bars: vehicle treatment, n = 7. Dark grey bars: 0.5 μmol/kg BX471 treatment, n = 7. ( A ) CCL3, ( B ) CCL4, ( C ) CCL5, and ( D ) CCL7. *: p < 0.05 vs. baseline (t = 0 min).

Article Snippet: Measurements of Chemokine Concentrations: Serum levels of CCL3, CCL4, CCL5, and CCL7 were measured with commercially available rat enzyme-linked immunosorbent assays (ELISA, Boster Bio, Pleasanton, CA, USA) according to the manufacturer’s instructions.

Techniques:

NOX4 enhanced the CD8 + T cells mediate antitumor effect. (A) TIMER2.0 was used to analysis the correlation between NOX4 expression levels and CD8 + T cell infiltration, Scatter plot showing the correlation between NOX4 expression levels and CD8 + T cell infiltration in breast cancer (BRCA) samples (n=1100). Rho=0.346, p=2.57e-26. (B) TISIDB data: Scatter plot showing the correlation between NOX4 expression and central memory CD8 + T cell (Tcm-CD8) infiltration, effector memory CD8+ T cell (Tem-CD8) in BRCA samples (n=1100). Rho=0.44, p<2.2e-16; Rho=0.171, p<1.24e-6. (C) Representative flow cytometry plots showing the percentage of CD8 + T cells within the CD45 + population in EO771 tumors from NOX4 wild-type (WT) and NOX4 knockout (KO) mice. Bar graph quantifying the percentage of CD8 + cells, showing a significant reduction in CD8 + T cell infiltration in NOX4 KO tumors ***p<0.001. n=6 per group. (D) Representative flow cytometry plots showing IFN-γ and Granzyme B expression in CD8 + T cells from EO771 tumors of NOX4 WT and NOX4 KO mice. Bar graphs quantifying the percentage of CD8 + T cells expressing IFN-γ and Granzyme B, ***p<0.001. n=7 per group. (E) Representative flow cytometry plots showing the percentage of DC cells within the EO771 tumors from NOX4 wild-type (WT) and NOX4 knockout (KO) mice. Bar graph quantifying the percentage of DC cells, **p<0.01. n=7 per group. (F) TISIDB data: Scatter plot showing the correlation between NOX4 expression and CCL11 expression in BRCA samples (n=1100). A significant positive correlation is observed. Rho=0.359, p<2.2e-16. Bar graph showing the concentration of CCL11, CCL5 in the tumor microenvironment, *p<0.05. Data are presented as mean ± SEM from 3 independent experiments. Statistical significance was determined using two-tailed Student’s t-test.

Journal: Frontiers in Immunology

Article Title: NOX4 modulates breast cancer progression through cancer cell metabolic reprogramming and CD8 + T cell antitumor activity

doi: 10.3389/fimmu.2025.1534936

Figure Lengend Snippet: NOX4 enhanced the CD8 + T cells mediate antitumor effect. (A) TIMER2.0 was used to analysis the correlation between NOX4 expression levels and CD8 + T cell infiltration, Scatter plot showing the correlation between NOX4 expression levels and CD8 + T cell infiltration in breast cancer (BRCA) samples (n=1100). Rho=0.346, p=2.57e-26. (B) TISIDB data: Scatter plot showing the correlation between NOX4 expression and central memory CD8 + T cell (Tcm-CD8) infiltration, effector memory CD8+ T cell (Tem-CD8) in BRCA samples (n=1100). Rho=0.44, p<2.2e-16; Rho=0.171, p<1.24e-6. (C) Representative flow cytometry plots showing the percentage of CD8 + T cells within the CD45 + population in EO771 tumors from NOX4 wild-type (WT) and NOX4 knockout (KO) mice. Bar graph quantifying the percentage of CD8 + cells, showing a significant reduction in CD8 + T cell infiltration in NOX4 KO tumors ***p<0.001. n=6 per group. (D) Representative flow cytometry plots showing IFN-γ and Granzyme B expression in CD8 + T cells from EO771 tumors of NOX4 WT and NOX4 KO mice. Bar graphs quantifying the percentage of CD8 + T cells expressing IFN-γ and Granzyme B, ***p<0.001. n=7 per group. (E) Representative flow cytometry plots showing the percentage of DC cells within the EO771 tumors from NOX4 wild-type (WT) and NOX4 knockout (KO) mice. Bar graph quantifying the percentage of DC cells, **p<0.01. n=7 per group. (F) TISIDB data: Scatter plot showing the correlation between NOX4 expression and CCL11 expression in BRCA samples (n=1100). A significant positive correlation is observed. Rho=0.359, p<2.2e-16. Bar graph showing the concentration of CCL11, CCL5 in the tumor microenvironment, *p<0.05. Data are presented as mean ± SEM from 3 independent experiments. Statistical significance was determined using two-tailed Student’s t-test.

Article Snippet: The quantity of CCL11, CCL5 (Bosterbio) were determined in tumor tissue using ELISA kits according to the manufacturer’s instructions.

Techniques: Expressing, Flow Cytometry, Knock-Out, Concentration Assay, Two Tailed Test

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