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ATCC ikk2se inflamed bmsc

a Experimental outline of the delineation of the effects of stromal inflammatory activation on the transcriptome and function of normal HSPCs in a murine system. Created in BioRender. Bian, Y. (2025) https://BioRender.com/x52bgzc . b Effect of stromal inflammation on the transcriptional wiring of normal HSPCs (Hallmark analysis), recapitulating findings in human LR-MDS. Positive NES indicates programs enriched in murine HSPCs cocultured with <t>IKK2SE-transduced</t> (inflamed) BMSCs, while negative scores indicate enrichment in HSPCs cocultured with EV-transduced (non-inflamed) BMSCs. Statistical analysis was performed by a K-S test and adjusted for FDR. c Definition of the Stromal Inflammation-induced Gene alterations in the HSPC Transcriptome (SIGHT) in LR-MDS comprising the set of genes that was differentially expressed in CD34 + HSPCs in LR-MDS in comparison to their counterparts in NBM and significantly dysregulated in HSPCs exposed to inflamed stromal niches ex vivo. d Implication of SIGHT in inflammatory signaling (MAPK, NFĸB and TNFα) and apoptosis by KEGG overrepresentation analysis. Statistical analysis was performed by a hypergeometric test and adjusted for FDR. e – h Attenuation of HSPC number and function by stromal inflammation. e Reduced numbers of HSPCs after co-culture on inflamed BMSCs (replicates from n = 2 mice performed in triplicates). Reduced repopulating ability of HSPCs, as demonstrated by reduced CFU-C forming ability (scale bar, 5 mm) ( f ) and in vivo competitive repopulating ability in PB ( g ) and in BM ( h ) (16 weeks after competitive transplantation; n = 5 mice/group). Statistical analysis was performed by a two-sided unpaired Welch’s t -test in ( e , f , h ); statistical analysis was performed by a two-way ANOVA with Sídák’s multiple testing correction in ( g ). Data are represented as mean ± SEM. Source data are provided as a Source Data file.

Ikk2se Inflamed Bmsc, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 427 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 96 stars, based on 427 article reviews

ikk2se inflamed bmsc - by Bioz Stars, 2026-03

96/100 stars

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1) Product Images from "An inflammatory T-cell-stromal axis contributes to hematopoietic stem/progenitor cell failure and clonal evolution in human myelodysplastic syndrome"

Article Title: An inflammatory T-cell-stromal axis contributes to hematopoietic stem/progenitor cell failure and clonal evolution in human myelodysplastic syndrome

Journal: Nature Communications

doi: 10.1038/s41467-025-65802-z

Figure Legend Snippet: a Experimental outline of the delineation of the effects of stromal inflammatory activation on the transcriptome and function of normal HSPCs in a murine system. Created in BioRender. Bian, Y. (2025) https://BioRender.com/x52bgzc . b Effect of stromal inflammation on the transcriptional wiring of normal HSPCs (Hallmark analysis), recapitulating findings in human LR-MDS. Positive NES indicates programs enriched in murine HSPCs cocultured with IKK2SE-transduced (inflamed) BMSCs, while negative scores indicate enrichment in HSPCs cocultured with EV-transduced (non-inflamed) BMSCs. Statistical analysis was performed by a K-S test and adjusted for FDR. c Definition of the Stromal Inflammation-induced Gene alterations in the HSPC Transcriptome (SIGHT) in LR-MDS comprising the set of genes that was differentially expressed in CD34 + HSPCs in LR-MDS in comparison to their counterparts in NBM and significantly dysregulated in HSPCs exposed to inflamed stromal niches ex vivo. d Implication of SIGHT in inflammatory signaling (MAPK, NFĸB and TNFα) and apoptosis by KEGG overrepresentation analysis. Statistical analysis was performed by a hypergeometric test and adjusted for FDR. e – h Attenuation of HSPC number and function by stromal inflammation. e Reduced numbers of HSPCs after co-culture on inflamed BMSCs (replicates from n = 2 mice performed in triplicates). Reduced repopulating ability of HSPCs, as demonstrated by reduced CFU-C forming ability (scale bar, 5 mm) ( f ) and in vivo competitive repopulating ability in PB ( g ) and in BM ( h ) (16 weeks after competitive transplantation; n = 5 mice/group). Statistical analysis was performed by a two-sided unpaired Welch’s t -test in ( e , f , h ); statistical analysis was performed by a two-way ANOVA with Sídák’s multiple testing correction in ( g ). Data are represented as mean ± SEM. Source data are provided as a Source Data file.

Techniques Used: Activation Assay, Comparison, Ex Vivo, Co-Culture Assay, In Vivo, Transplantation Assay

a Identification and distribution of SF3B1 -mutated cells within the LR-MDS hierarchy. UMAP distribution (left panel) and population-specific frequencies (right panel) of mutant cells. Mutant cells are identified by combining 10X scRNA-seq, RaCHseq and SpliceUp computational analyses. b Distribution of mutant cells within HSPC subsets (left panel) and differentially expressed gene (Hallmark) programs in mutant cells (vs. ‘non-assignable’ cells) (right panel), revealing mitigation of inflammatory stress pathways and enrichment of gene programs implicated in cell cycle progression in mutant cells. Positive NES reflects programs enriched in mutant HSPCs, while negative scores indicate enrichment in non-assignable HSPCs. All cells in HSC/MPPs, LMPPs, MEPs, and GMP clusters were used in the analysis. Statistical analysis was performed by a K-S test and adjusted for FDR. c , d Distribution of mutant cells within HSC subsets. c UMAP and d distribution per sample indicating relative abundance of Mutant cells in the ‘high-output’ (HSC-2) subset in comparison to the residual normal (‘non-assignable’) subset. LR-MDS ( n = 4). Data are presented as boxplots: the central line marks the median, the box spans the 25th to 75th percentiles (interquartile range), and whiskers extend to the smallest and largest values within 1.5× the interquartile range. Data points beyond this range are shown individually as outliers ( d ). e HSPC numbers upon co-culture on inflamed (IKK2SE) stromal cells (relative to EV-transduced BMSCs), demonstrating a relative preservation of SF3B1 -mutant immunophenotypic HSPCs (CD34 + and CD34 + CD38 – CD45RA – CD90 + ). Data represents replicates from NBM ( n = 2) and SF3B1 -mutated LR-MDS ( n = 3), experiments performed in dupli/triplicates for each bone marrow sample. Statistical analysis was performed by a two-sided unpaired Welch’s t -test. Data are presented as mean ± SEM. Source data are provided as a Source Data file.

Figure Legend Snippet: a Identification and distribution of SF3B1 -mutated cells within the LR-MDS hierarchy. UMAP distribution (left panel) and population-specific frequencies (right panel) of mutant cells. Mutant cells are identified by combining 10X scRNA-seq, RaCHseq and SpliceUp computational analyses. b Distribution of mutant cells within HSPC subsets (left panel) and differentially expressed gene (Hallmark) programs in mutant cells (vs. ‘non-assignable’ cells) (right panel), revealing mitigation of inflammatory stress pathways and enrichment of gene programs implicated in cell cycle progression in mutant cells. Positive NES reflects programs enriched in mutant HSPCs, while negative scores indicate enrichment in non-assignable HSPCs. All cells in HSC/MPPs, LMPPs, MEPs, and GMP clusters were used in the analysis. Statistical analysis was performed by a K-S test and adjusted for FDR. c , d Distribution of mutant cells within HSC subsets. c UMAP and d distribution per sample indicating relative abundance of Mutant cells in the ‘high-output’ (HSC-2) subset in comparison to the residual normal (‘non-assignable’) subset. LR-MDS ( n = 4). Data are presented as boxplots: the central line marks the median, the box spans the 25th to 75th percentiles (interquartile range), and whiskers extend to the smallest and largest values within 1.5× the interquartile range. Data points beyond this range are shown individually as outliers ( d ). e HSPC numbers upon co-culture on inflamed (IKK2SE) stromal cells (relative to EV-transduced BMSCs), demonstrating a relative preservation of SF3B1 -mutant immunophenotypic HSPCs (CD34 + and CD34 + CD38 – CD45RA – CD90 + ). Data represents replicates from NBM ( n = 2) and SF3B1 -mutated LR-MDS ( n = 3), experiments performed in dupli/triplicates for each bone marrow sample. Statistical analysis was performed by a two-sided unpaired Welch’s t -test. Data are presented as mean ± SEM. Source data are provided as a Source Data file.

Techniques Used: Mutagenesis, Comparison, Co-Culture Assay, Preserving

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Journal: Nature Communications

Article Title: An inflammatory T-cell-stromal axis contributes to hematopoietic stem/progenitor cell failure and clonal evolution in human myelodysplastic syndrome

doi: 10.1038/s41467-025-65802-z

Figure Lengend Snippet: a Experimental outline of the delineation of the effects of stromal inflammatory activation on the transcriptome and function of normal HSPCs in a murine system. Created in BioRender. Bian, Y. (2025) https://BioRender.com/x52bgzc . b Effect of stromal inflammation on the transcriptional wiring of normal HSPCs (Hallmark analysis), recapitulating findings in human LR-MDS. Positive NES indicates programs enriched in murine HSPCs cocultured with IKK2SE-transduced (inflamed) BMSCs, while negative scores indicate enrichment in HSPCs cocultured with EV-transduced (non-inflamed) BMSCs. Statistical analysis was performed by a K-S test and adjusted for FDR. c Definition of the Stromal Inflammation-induced Gene alterations in the HSPC Transcriptome (SIGHT) in LR-MDS comprising the set of genes that was differentially expressed in CD34 + HSPCs in LR-MDS in comparison to their counterparts in NBM and significantly dysregulated in HSPCs exposed to inflamed stromal niches ex vivo. d Implication of SIGHT in inflammatory signaling (MAPK, NFĸB and TNFα) and apoptosis by KEGG overrepresentation analysis. Statistical analysis was performed by a hypergeometric test and adjusted for FDR. e – h Attenuation of HSPC number and function by stromal inflammation. e Reduced numbers of HSPCs after co-culture on inflamed BMSCs (replicates from n = 2 mice performed in triplicates). Reduced repopulating ability of HSPCs, as demonstrated by reduced CFU-C forming ability (scale bar, 5 mm) ( f ) and in vivo competitive repopulating ability in PB ( g ) and in BM ( h ) (16 weeks after competitive transplantation; n = 5 mice/group). Statistical analysis was performed by a two-sided unpaired Welch’s t -test in ( e , f , h ); statistical analysis was performed by a two-way ANOVA with Sídák’s multiple testing correction in ( g ). Data are represented as mean ± SEM. Source data are provided as a Source Data file.

Article Snippet: For flow cytometry analysis of mouse Lin – co-cultured with or without IKK2SE inflamed BMSC (OP9 (ATCC, CRL-2749)): Lin – cells were stained with following antibodies: lineage cocktail containing biotinylated antibodies against-Biotin-BV510 (B220 Biotin, 1:25, clone: RA3-6B2, BD Biosciences; CD3e Biotin, 1:25, clone: 145-2C11, BD Biosciences; CD4 Biotin, 1:25, clone: GK1.5, BD Biosciences; CD8a Biotin, 1:25, clone: 53-6.7, BD Biosciences; Ly-6G Ly-6C/Gr1 Biotin, 1:25, clone: RB6-8C5, BD Biosciences; CD11b/Mac1 Biotin, 1:25, clone: M1/70, BD Biosciences; TER-119 Biotin, 1:25, clone: TER-119, BD Biosciences), Sca-1-BV421 (1:100, clone: D7, BioLegend), c-Kit-PE-TR(1:100, clone: 2B8, BD Biosciences), CD48-AF700 (1:100, clone: HM48-1, BioLegend), CD150-PE (1:100, clone: TC15-12F12.2, BioLegend), CD45.1-APC (1:100, clone: A20, Sony), CD45.2-PE-Cy7 (1:50, clone: 104, BioLegend); Streptavidin Pacific Orange (1:200, Life Technologies), 7AAD-Percpcy5.5 (1:100, Beckman Coulter).

Techniques: Activation Assay, Comparison, Ex Vivo, Co-Culture Assay, In Vivo, Transplantation Assay

Journal: Nature Communications

Article Title: An inflammatory T-cell-stromal axis contributes to hematopoietic stem/progenitor cell failure and clonal evolution in human myelodysplastic syndrome

doi: 10.1038/s41467-025-65802-z

Figure Lengend Snippet: a Identification and distribution of SF3B1 -mutated cells within the LR-MDS hierarchy. UMAP distribution (left panel) and population-specific frequencies (right panel) of mutant cells. Mutant cells are identified by combining 10X scRNA-seq, RaCHseq and SpliceUp computational analyses. b Distribution of mutant cells within HSPC subsets (left panel) and differentially expressed gene (Hallmark) programs in mutant cells (vs. ‘non-assignable’ cells) (right panel), revealing mitigation of inflammatory stress pathways and enrichment of gene programs implicated in cell cycle progression in mutant cells. Positive NES reflects programs enriched in mutant HSPCs, while negative scores indicate enrichment in non-assignable HSPCs. All cells in HSC/MPPs, LMPPs, MEPs, and GMP clusters were used in the analysis. Statistical analysis was performed by a K-S test and adjusted for FDR. c , d Distribution of mutant cells within HSC subsets. c UMAP and d distribution per sample indicating relative abundance of Mutant cells in the ‘high-output’ (HSC-2) subset in comparison to the residual normal (‘non-assignable’) subset. LR-MDS ( n = 4). Data are presented as boxplots: the central line marks the median, the box spans the 25th to 75th percentiles (interquartile range), and whiskers extend to the smallest and largest values within 1.5× the interquartile range. Data points beyond this range are shown individually as outliers ( d ). e HSPC numbers upon co-culture on inflamed (IKK2SE) stromal cells (relative to EV-transduced BMSCs), demonstrating a relative preservation of SF3B1 -mutant immunophenotypic HSPCs (CD34 + and CD34 + CD38 – CD45RA – CD90 + ). Data represents replicates from NBM ( n = 2) and SF3B1 -mutated LR-MDS ( n = 3), experiments performed in dupli/triplicates for each bone marrow sample. Statistical analysis was performed by a two-sided unpaired Welch’s t -test. Data are presented as mean ± SEM. Source data are provided as a Source Data file.

Techniques: Mutagenesis, Comparison, Co-Culture Assay, Preserving

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1) Product Images from "An inflammatory T-cell-stromal axis contributes to hematopoietic stem/progenitor cell failure and clonal evolution in human myelodysplastic syndrome"

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