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raw 264.7  (ATCC)


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    Structured Review

    ATCC raw 264.7
    Raw 264.7, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 23838 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tib/custom%40tib-71%4042438786?v=ATCC
    Average 99 stars, based on 23838 article reviews
    raw 264.7 - by Bioz Stars, 2026-08
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    ATCC raw 264 7
    PGE2 blockade modulates immune cell phenotypes in antitumor resp onses. (A) Inflammatory gene expression across cancer types (GEPIA2 database). (B) Gene expression of Il1b , Cxcl8 , and Lif in colon adenocarcinoma (COAD) tumor tissue and normal tissue (GEPIA2 database). (C and D) Correlation between Ptgs2 and inflammatory genes in various cancers (C) and COAD (D) (TIMER 2.0). (E) Schematic of immune cells co-incubated with CXB treated tumor conditional medium (TCM) (Source material from BioRender). (F and G) Cell viability (F) and Cell cycle arrest (G) detection of CT26 tumor cells treated with gradient concentrations of CXB; n = 3. (H) PGE2 concentration in CT26 cell supernatants; n = 3. (I) The proportion of CD103 + DC within BMDCs after CXB treatments in vitro ; n = 3. (J and K) Maturation (J) and Antigen processing capability (K) on BMDCs; n = 3. (L – N) Flow charts of CD86 or CD206 expression on Raw 264.7 cells (L). Quantification of CD86 (M) and CD206 (N) expression on Raw 264.7 cells; n = 3. (O and P) Flow charts (O) and Quantification (P) of CD69 and CD137 expression on splenic T cells exposed to CXB-pretreated TCM; n = 3. (Q) IFN-γ secretion by T cells co-cultured with CXB-pretreated TCM; n = 3. Data are presented as mean ± SD, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Significance was calculated using One-way ANOVA.
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    PGE2 blockade modulates immune cell phenotypes in antitumor resp onses. (A) Inflammatory gene expression across cancer types (GEPIA2 database). (B) Gene expression of Il1b , Cxcl8 , and Lif in colon adenocarcinoma (COAD) tumor tissue and normal tissue (GEPIA2 database). (C and D) Correlation between Ptgs2 and inflammatory genes in various cancers (C) and COAD (D) (TIMER 2.0). (E) Schematic of immune cells co-incubated with CXB treated tumor conditional medium (TCM) (Source material from BioRender). (F and G) Cell viability (F) and Cell cycle arrest (G) detection of CT26 tumor cells treated with gradient concentrations of CXB; n = 3. (H) PGE2 concentration in CT26 cell supernatants; n = 3. (I) The proportion of CD103 + DC within BMDCs after CXB treatments in vitro ; n = 3. (J and K) Maturation (J) and Antigen processing capability (K) on BMDCs; n = 3. (L – N) Flow charts of CD86 or CD206 expression on Raw 264.7 cells (L). Quantification of CD86 (M) and CD206 (N) expression on Raw 264.7 cells; n = 3. (O and P) Flow charts (O) and Quantification (P) of CD69 and CD137 expression on splenic T cells exposed to CXB-pretreated TCM; n = 3. (Q) IFN-γ secretion by T cells co-cultured with CXB-pretreated TCM; n = 3. Data are presented as mean ± SD, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Significance was calculated using One-way ANOVA.
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    ATCC immunomodulation assay
    PGE2 blockade modulates immune cell phenotypes in antitumor resp onses. (A) Inflammatory gene expression across cancer types (GEPIA2 database). (B) Gene expression of Il1b , Cxcl8 , and Lif in colon adenocarcinoma (COAD) tumor tissue and normal tissue (GEPIA2 database). (C and D) Correlation between Ptgs2 and inflammatory genes in various cancers (C) and COAD (D) (TIMER 2.0). (E) Schematic of immune cells co-incubated with CXB treated tumor conditional medium (TCM) (Source material from BioRender). (F and G) Cell viability (F) and Cell cycle arrest (G) detection of CT26 tumor cells treated with gradient concentrations of CXB; n = 3. (H) PGE2 concentration in CT26 cell supernatants; n = 3. (I) The proportion of CD103 + DC within BMDCs after CXB treatments in vitro ; n = 3. (J and K) Maturation (J) and Antigen processing capability (K) on BMDCs; n = 3. (L – N) Flow charts of CD86 or CD206 expression on Raw 264.7 cells (L). Quantification of CD86 (M) and CD206 (N) expression on Raw 264.7 cells; n = 3. (O and P) Flow charts (O) and Quantification (P) of CD69 and CD137 expression on splenic T cells exposed to CXB-pretreated TCM; n = 3. (Q) IFN-γ secretion by T cells co-cultured with CXB-pretreated TCM; n = 3. Data are presented as mean ± SD, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Significance was calculated using One-way ANOVA.
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    ATCC macrophages
    Single-cell and immune-profiling analysis reveals an imbalanced osteo-immune microenvironment in peri-implantitis. (A) Immune infiltration scores of peri-implant tissues. (B) UMAP visualization of peri-implant tissues, colored by cell-type ontology, showing the distribution of major cell populations. (C, D) Expression patterns of key markers Mrc1 and Tnf projected onto the UMAP space. The color gradient from yellow to blue indicates expression levels from low to high. (E) Dot plot showing the expression of M1-associated ( Tnf , Il6 , Nos2 ) and M2-associated ( Mrc1 , Arg1 , Il10 ) <t>macrophage</t> signature genes. The dot size represents the percentage of cells expressing the gene, and color intensity indicates the average expression level. (F, G) Violin plots illustrating the expression distribution of M1/M2 signature genes across different cell types. (H) Osteogenic genes ( Alpl , Col1a1 ) are specifically and highly expressed in osteoblast clusters. Abbreviation: UMAP, Uniform Manifold Approximation and Projection.
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    PGE2 blockade modulates immune cell phenotypes in antitumor resp onses. (A) Inflammatory gene expression across cancer types (GEPIA2 database). (B) Gene expression of Il1b , Cxcl8 , and Lif in colon adenocarcinoma (COAD) tumor tissue and normal tissue (GEPIA2 database). (C and D) Correlation between Ptgs2 and inflammatory genes in various cancers (C) and COAD (D) (TIMER 2.0). (E) Schematic of immune cells co-incubated with CXB treated tumor conditional medium (TCM) (Source material from BioRender). (F and G) Cell viability (F) and Cell cycle arrest (G) detection of CT26 tumor cells treated with gradient concentrations of CXB; n = 3. (H) PGE2 concentration in CT26 cell supernatants; n = 3. (I) The proportion of CD103 + DC within BMDCs after CXB treatments in vitro ; n = 3. (J and K) Maturation (J) and Antigen processing capability (K) on BMDCs; n = 3. (L – N) Flow charts of CD86 or CD206 expression on Raw 264.7 cells (L). Quantification of CD86 (M) and CD206 (N) expression on Raw 264.7 cells; n = 3. (O and P) Flow charts (O) and Quantification (P) of CD69 and CD137 expression on splenic T cells exposed to CXB-pretreated TCM; n = 3. (Q) IFN-γ secretion by T cells co-cultured with CXB-pretreated TCM; n = 3. Data are presented as mean ± SD, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Significance was calculated using One-way ANOVA.

    Journal: Bioactive Materials

    Article Title: Chronic inflammation-responsive hydrogel restores myeloid-T cell crosstalk to reinvigorate antitumor immunity against metastatic colorectal cancer

    doi: 10.1016/j.bioactmat.2026.03.012

    Figure Lengend Snippet: PGE2 blockade modulates immune cell phenotypes in antitumor resp onses. (A) Inflammatory gene expression across cancer types (GEPIA2 database). (B) Gene expression of Il1b , Cxcl8 , and Lif in colon adenocarcinoma (COAD) tumor tissue and normal tissue (GEPIA2 database). (C and D) Correlation between Ptgs2 and inflammatory genes in various cancers (C) and COAD (D) (TIMER 2.0). (E) Schematic of immune cells co-incubated with CXB treated tumor conditional medium (TCM) (Source material from BioRender). (F and G) Cell viability (F) and Cell cycle arrest (G) detection of CT26 tumor cells treated with gradient concentrations of CXB; n = 3. (H) PGE2 concentration in CT26 cell supernatants; n = 3. (I) The proportion of CD103 + DC within BMDCs after CXB treatments in vitro ; n = 3. (J and K) Maturation (J) and Antigen processing capability (K) on BMDCs; n = 3. (L – N) Flow charts of CD86 or CD206 expression on Raw 264.7 cells (L). Quantification of CD86 (M) and CD206 (N) expression on Raw 264.7 cells; n = 3. (O and P) Flow charts (O) and Quantification (P) of CD69 and CD137 expression on splenic T cells exposed to CXB-pretreated TCM; n = 3. (Q) IFN-γ secretion by T cells co-cultured with CXB-pretreated TCM; n = 3. Data are presented as mean ± SD, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Significance was calculated using One-way ANOVA.

    Article Snippet: CT26 cells and Raw 264.7 were purchased from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Gene Expression, Incubation, Concentration Assay, In Vitro, Expressing, Cell Culture

    TRANS modulates macrophage polarization and promotes antigen present ation. (A) Uniform manifold approximation and projection (UMAP) visualization of myeloid cells in the TME following PBS or TRANS treatment. (B) UMAP clusters of myeloid cells. (C) Cell-type-specific marker genes expression of different clusters. (D) Proportion distribution of myeloid cell clusters. (E) KEGG enrichment in M1 macrophages (TRANS vs PBS). (F) GSEA of NOD-like receptor and JAK-STAT signaling pathways in M1. (G) KEGG enrichment in M2 macrophages (TRANS vs PBS). (H) Glycolysis/Gluconeogenesis and antigen processing/presentation in M2. (I) Scheme of M0 macrophages treated with different TCM. (J) M1 and M2 polarization from M0 macrophages under various treatments; n = 3. (K) STAT1 expression in Raw 264.7 cells. (L) Scheme of M2 macrophages treated with different TCM. (M) Repolarization of M2 macrophages under different treatments; n = 3. (N) H-2K b /SIINFEKL + macrophages in vitro ; n = 3. (O and P) Relative expression of antitumor genes (O) and inflammatory genes (P) in macrophages under different treatments in vitro ; n = 3. (Q) CD69 expression on T cells after co-incubating TCM-treated macrophages and anti-CD3/CD28-stimulated splenic T cells; n = 3. Data are presented as mean ± SD, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Significance of multiple-group comparisons was calculated using One-way ANOVA. Significance of two-group comparison was calculated using Student's t -test.

    Journal: Bioactive Materials

    Article Title: Chronic inflammation-responsive hydrogel restores myeloid-T cell crosstalk to reinvigorate antitumor immunity against metastatic colorectal cancer

    doi: 10.1016/j.bioactmat.2026.03.012

    Figure Lengend Snippet: TRANS modulates macrophage polarization and promotes antigen present ation. (A) Uniform manifold approximation and projection (UMAP) visualization of myeloid cells in the TME following PBS or TRANS treatment. (B) UMAP clusters of myeloid cells. (C) Cell-type-specific marker genes expression of different clusters. (D) Proportion distribution of myeloid cell clusters. (E) KEGG enrichment in M1 macrophages (TRANS vs PBS). (F) GSEA of NOD-like receptor and JAK-STAT signaling pathways in M1. (G) KEGG enrichment in M2 macrophages (TRANS vs PBS). (H) Glycolysis/Gluconeogenesis and antigen processing/presentation in M2. (I) Scheme of M0 macrophages treated with different TCM. (J) M1 and M2 polarization from M0 macrophages under various treatments; n = 3. (K) STAT1 expression in Raw 264.7 cells. (L) Scheme of M2 macrophages treated with different TCM. (M) Repolarization of M2 macrophages under different treatments; n = 3. (N) H-2K b /SIINFEKL + macrophages in vitro ; n = 3. (O and P) Relative expression of antitumor genes (O) and inflammatory genes (P) in macrophages under different treatments in vitro ; n = 3. (Q) CD69 expression on T cells after co-incubating TCM-treated macrophages and anti-CD3/CD28-stimulated splenic T cells; n = 3. Data are presented as mean ± SD, ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Significance of multiple-group comparisons was calculated using One-way ANOVA. Significance of two-group comparison was calculated using Student's t -test.

    Article Snippet: CT26 cells and Raw 264.7 were purchased from the American Type Culture Collection (ATCC; Manassas, VA, USA).

    Techniques: Marker, Expressing, Protein-Protein interactions, In Vitro, Comparison

    Single-cell and immune-profiling analysis reveals an imbalanced osteo-immune microenvironment in peri-implantitis. (A) Immune infiltration scores of peri-implant tissues. (B) UMAP visualization of peri-implant tissues, colored by cell-type ontology, showing the distribution of major cell populations. (C, D) Expression patterns of key markers Mrc1 and Tnf projected onto the UMAP space. The color gradient from yellow to blue indicates expression levels from low to high. (E) Dot plot showing the expression of M1-associated ( Tnf , Il6 , Nos2 ) and M2-associated ( Mrc1 , Arg1 , Il10 ) macrophage signature genes. The dot size represents the percentage of cells expressing the gene, and color intensity indicates the average expression level. (F, G) Violin plots illustrating the expression distribution of M1/M2 signature genes across different cell types. (H) Osteogenic genes ( Alpl , Col1a1 ) are specifically and highly expressed in osteoblast clusters. Abbreviation: UMAP, Uniform Manifold Approximation and Projection.

    Journal: Bioactive Materials

    Article Title: Chiral Fe 3 O 4 /GelMA hydrogels regulate the osteoimmune microenvironment via Itgb3-mediated macrophage polarization to combat peri-implantitis

    doi: 10.1016/j.bioactmat.2026.03.055

    Figure Lengend Snippet: Single-cell and immune-profiling analysis reveals an imbalanced osteo-immune microenvironment in peri-implantitis. (A) Immune infiltration scores of peri-implant tissues. (B) UMAP visualization of peri-implant tissues, colored by cell-type ontology, showing the distribution of major cell populations. (C, D) Expression patterns of key markers Mrc1 and Tnf projected onto the UMAP space. The color gradient from yellow to blue indicates expression levels from low to high. (E) Dot plot showing the expression of M1-associated ( Tnf , Il6 , Nos2 ) and M2-associated ( Mrc1 , Arg1 , Il10 ) macrophage signature genes. The dot size represents the percentage of cells expressing the gene, and color intensity indicates the average expression level. (F, G) Violin plots illustrating the expression distribution of M1/M2 signature genes across different cell types. (H) Osteogenic genes ( Alpl , Col1a1 ) are specifically and highly expressed in osteoblast clusters. Abbreviation: UMAP, Uniform Manifold Approximation and Projection.

    Article Snippet: Macrophages (RAW 264.7, ATCC) were cultured in Dulbecco's Modified Eagle Medium (DMEM; Gibco, USA) supplemented with 10% fetal bovine serum (FBS; HyClone, USA) and 1% penicillin-streptomycin (Gibco, USA) at 5% CO 2 and 37 °C.

    Techniques: Single Cell, Expressing

    In vitro experiments validate the mechanism by which chiral hydrogels modulate the bone immune microenvironment. (A) GO and (B) KEGG enrichment analysis of DEGs with elevated D-FG relative to L-FG. (C) Protein expression levels of p-AKT and AKT after 48-h co-culture with different hydrogels. (D, E) Intracellular ROS fluorescence levels and quantitative analysis after SC79-mediated PI3K/Akt activation. (F, G) ROS levels and quantification in RAW264.7 cells after LPS stimulation and 24 h co-culture with different hydrogels. (H, I) ROS levels and quantification in RAW264.7 cells after 72 h co-culture with different hydrogels. (J, K) Representative fluorescence images and quantitative analysis of Fe 2+ release and ROS kinetics in chiral hydrogel-treated macrophages. Scale bar = 50 μm. (n = 3, compared with the control group, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 vs. GelMA group. # P < 0.05, ## P < 0.01, ### P < 0.001). (L) Schematic representation of the bone immunomodulatory mechanism of chiral hydrogels. Abbreviation: KEGG, Kyoto Encyclopedia of Genes and Genomes; p-AKT, phosphorylated AKT; AKT, protein kinase B.

    Journal: Bioactive Materials

    Article Title: Chiral Fe 3 O 4 /GelMA hydrogels regulate the osteoimmune microenvironment via Itgb3-mediated macrophage polarization to combat peri-implantitis

    doi: 10.1016/j.bioactmat.2026.03.055

    Figure Lengend Snippet: In vitro experiments validate the mechanism by which chiral hydrogels modulate the bone immune microenvironment. (A) GO and (B) KEGG enrichment analysis of DEGs with elevated D-FG relative to L-FG. (C) Protein expression levels of p-AKT and AKT after 48-h co-culture with different hydrogels. (D, E) Intracellular ROS fluorescence levels and quantitative analysis after SC79-mediated PI3K/Akt activation. (F, G) ROS levels and quantification in RAW264.7 cells after LPS stimulation and 24 h co-culture with different hydrogels. (H, I) ROS levels and quantification in RAW264.7 cells after 72 h co-culture with different hydrogels. (J, K) Representative fluorescence images and quantitative analysis of Fe 2+ release and ROS kinetics in chiral hydrogel-treated macrophages. Scale bar = 50 μm. (n = 3, compared with the control group, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 vs. GelMA group. # P < 0.05, ## P < 0.01, ### P < 0.001). (L) Schematic representation of the bone immunomodulatory mechanism of chiral hydrogels. Abbreviation: KEGG, Kyoto Encyclopedia of Genes and Genomes; p-AKT, phosphorylated AKT; AKT, protein kinase B.

    Article Snippet: Macrophages (RAW 264.7, ATCC) were cultured in Dulbecco's Modified Eagle Medium (DMEM; Gibco, USA) supplemented with 10% fetal bovine serum (FBS; HyClone, USA) and 1% penicillin-streptomycin (Gibco, USA) at 5% CO 2 and 37 °C.

    Techniques: In Vitro, Expressing, Co-Culture Assay, Fluorescence, Activation Assay, Control