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containing torin1  (Selleck Chemicals)


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    Structured Review

    Selleck Chemicals containing torin1
    mTORC2 inhibition prevents proliferation and self-renewal in GSCs (A) IB analysis of CD97, p-S6K, p-AKT, S6K, AKT, ARHGAP1, BZW1, and BZW2 levels in three different GSCs (83, X01, and 528 cells) infected with shCtrl or shCD97 lentivirus. (B) RT-qPCR of BZW1 expression (left), cell proliferation assay (middle), and LDAs (right) in 83 and X01 GSCs infected with shCtrl and shCD97 lentivirus, followed by BZW1 lentivirus infection. (C–F) IB analysis of p-S6K, p-AKT, S6K, AKT, ARHGAP1, BZW1, and BZW2 levels in three different GSCs (83, X01, and 528 cells) treated with <t>Torin1</t> 48 h (C), AKT inhibitor IV 24 h (D), 24 h rapamycin (E), and JR-AB2-011 24 h (F). (G) Cell proliferation assays (left) and LDAs (right) were performed on 83 and X01 GSCs after treatment with JR-AB2-011. (H) Kaplan-Meier survival curves of mice orthotopically implanted with X01-Luc cells ( n = 5, 1 × 10 5 cells/mouse) and intraperitoneally (i.p.) treated with JR-AB2-011 (4 mg/kg) or vehicle. MST, median survival time. Log rank (Mantel-Cox) test. (I) Schematic representation of the CD97-related signaling pathway regulating the proliferation, self-renewal, and tumor progression of GSCs. Vinculin and GAPDH, and β-actin were used as loading controls in IB, β-actin was used as a loading control in RT-PCR. All error bars represent mean ± SD ( n = 3 independent experiments) in (B) and (G). ∗∗∗∗ p < 0.0001, ∗∗∗ p < 0.001, ∗ p < 0.05, t test. See also <xref ref-type=Figures S12–S15 . " width="250" height="auto" />
    Containing Torin1, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 96/100, based on 350 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cell+transcriptomic+sequencing+dataset/Torin+1/pmc11722114-52-0-3
    Average 96 stars, based on 350 article reviews
    containing torin1 - by Bioz Stars, 2026-11
    96/100 stars

    Images

    1) Product Images from "CD97 maintains tumorigenicity of glioblastoma stem cells via mTORC2 signaling and is targeted by CAR Th9 cells"

    Article Title: CD97 maintains tumorigenicity of glioblastoma stem cells via mTORC2 signaling and is targeted by CAR Th9 cells

    Journal: Cell Reports Medicine

    doi: 10.1016/j.xcrm.2024.101844

    mTORC2 inhibition prevents proliferation and self-renewal in GSCs (A) IB analysis of CD97, p-S6K, p-AKT, S6K, AKT, ARHGAP1, BZW1, and BZW2 levels in three different GSCs (83, X01, and 528 cells) infected with shCtrl or shCD97 lentivirus. (B) RT-qPCR of BZW1 expression (left), cell proliferation assay (middle), and LDAs (right) in 83 and X01 GSCs infected with shCtrl and shCD97 lentivirus, followed by BZW1 lentivirus infection. (C–F) IB analysis of p-S6K, p-AKT, S6K, AKT, ARHGAP1, BZW1, and BZW2 levels in three different GSCs (83, X01, and 528 cells) treated with Torin1 48 h (C), AKT inhibitor IV 24 h (D), 24 h rapamycin (E), and JR-AB2-011 24 h (F). (G) Cell proliferation assays (left) and LDAs (right) were performed on 83 and X01 GSCs after treatment with JR-AB2-011. (H) Kaplan-Meier survival curves of mice orthotopically implanted with X01-Luc cells ( n = 5, 1 × 10 5 cells/mouse) and intraperitoneally (i.p.) treated with JR-AB2-011 (4 mg/kg) or vehicle. MST, median survival time. Log rank (Mantel-Cox) test. (I) Schematic representation of the CD97-related signaling pathway regulating the proliferation, self-renewal, and tumor progression of GSCs. Vinculin and GAPDH, and β-actin were used as loading controls in IB, β-actin was used as a loading control in RT-PCR. All error bars represent mean ± SD ( n = 3 independent experiments) in (B) and (G). ∗∗∗∗ p < 0.0001, ∗∗∗ p < 0.001, ∗ p < 0.05, t test. See also <xref ref-type=Figures S12–S15 . " title="... GSCs (83, X01, and 528 cells) treated with Torin1 48 h (C), AKT inhibitor IV 24 h ..." property="contentUrl" width="100%" height="100%"/>
    Figure Legend Snippet: mTORC2 inhibition prevents proliferation and self-renewal in GSCs (A) IB analysis of CD97, p-S6K, p-AKT, S6K, AKT, ARHGAP1, BZW1, and BZW2 levels in three different GSCs (83, X01, and 528 cells) infected with shCtrl or shCD97 lentivirus. (B) RT-qPCR of BZW1 expression (left), cell proliferation assay (middle), and LDAs (right) in 83 and X01 GSCs infected with shCtrl and shCD97 lentivirus, followed by BZW1 lentivirus infection. (C–F) IB analysis of p-S6K, p-AKT, S6K, AKT, ARHGAP1, BZW1, and BZW2 levels in three different GSCs (83, X01, and 528 cells) treated with Torin1 48 h (C), AKT inhibitor IV 24 h (D), 24 h rapamycin (E), and JR-AB2-011 24 h (F). (G) Cell proliferation assays (left) and LDAs (right) were performed on 83 and X01 GSCs after treatment with JR-AB2-011. (H) Kaplan-Meier survival curves of mice orthotopically implanted with X01-Luc cells ( n = 5, 1 × 10 5 cells/mouse) and intraperitoneally (i.p.) treated with JR-AB2-011 (4 mg/kg) or vehicle. MST, median survival time. Log rank (Mantel-Cox) test. (I) Schematic representation of the CD97-related signaling pathway regulating the proliferation, self-renewal, and tumor progression of GSCs. Vinculin and GAPDH, and β-actin were used as loading controls in IB, β-actin was used as a loading control in RT-PCR. All error bars represent mean ± SD ( n = 3 independent experiments) in (B) and (G). ∗∗∗∗ p < 0.0001, ∗∗∗ p < 0.001, ∗ p < 0.05, t test. See also Figures S12–S15 .

    Techniques Used: Inhibition, Infection, Quantitative RT-PCR, Expressing, Proliferation Assay, Control, Reverse Transcription Polymerase Chain Reaction


    Figure Legend Snippet:

    Techniques Used: Produced, Virus, Plasmid Preparation, Recombinant, Purification, Cell Culture, Cell Isolation, Reporter Gene Assay, cDNA Synthesis, Apoptosis Assay, Cytotoxicity Assay, Gene Expression, shRNA, Sequencing, Amplification, Software, Microscopy, Western Blot

    Related Articles

    Transfection:

    Article Title: ALKBH5-Driven m6A Demethylation Boosts Inflammation and Autophagy in LPS-Stimulated Macrophages.
    Article Snippet: .. After 48 h of transfection, cells were treated with LPS (100 ng/mL) for 6 h. Where indicated, Torin1 (100 nM, #S2827, Selleckchem) was used as a positive control for autophagy induction, and Bafilomycin A1 (100 nM, #S1413, Selleckchem) was added for the final 4 h to inhibit autophagosome‐lysosome fusion. .. Cells were then fixed with 4% paraformaldehyde for 15 min at room temperature, permeabilized with 0.1% Triton X‐100 for 10 min, and blocked with 5% BSA for 1 h. Nuclei were counterstained with DAPI (#8961, CST) for 10 min. Coverslips were mounted using ProLong Gold Antifade reagent (#P36930, Thermo Fisher).

    Positive Control:

    Article Title: ALKBH5-Driven m6A Demethylation Boosts Inflammation and Autophagy in LPS-Stimulated Macrophages.
    Article Snippet: .. After 48 h of transfection, cells were treated with LPS (100 ng/mL) for 6 h. Where indicated, Torin1 (100 nM, #S2827, Selleckchem) was used as a positive control for autophagy induction, and Bafilomycin A1 (100 nM, #S1413, Selleckchem) was added for the final 4 h to inhibit autophagosome‐lysosome fusion. .. Cells were then fixed with 4% paraformaldehyde for 15 min at room temperature, permeabilized with 0.1% Triton X‐100 for 10 min, and blocked with 5% BSA for 1 h. Nuclei were counterstained with DAPI (#8961, CST) for 10 min. Coverslips were mounted using ProLong Gold Antifade reagent (#P36930, Thermo Fisher).

    other:

    Article Title: BCR::ABL1 tyrosine kinase inhibitors induce ribosome collisions to activate ZAK-dependent ribotoxic stress and apoptosis in chronic myeloid leukemia.
    Article Snippet: Gene-specific siRNAs were synthesized (Genolution and Bioneer) as listed in Supplementary Table S1.



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    10X Genomics cell transcriptomic sequencing dataset
    <t>Transcriptomic</t> and TME characteristics associated with ECMSig in TCGA-GBM cohort (A) Volcano plot showing DEGs between ECMSig-high and ECMSig-low groups. Red dots: upregulated in high-risk; blue dots: upregulated in low-risk. Benjamini-Hochberg adjusted. (B) Gene set enrichment analysis (GSEA) plots showing enrichment of hallmark pathways. Pathways enriched in ECMSig-high and ECMSig-low groups are shown with their running enrichment scores (ESs) and ranked gene lists. Benjamini-Hochberg adjusted. (C) Heatmap showing the activity scores of selected oncogenic and tumor-related signaling pathways (rows) across TCGA-GBM samples (columns), annotated by ECMSig group and ECMSig score. Red indicates high activity, blue indicates low activity. ∗ p < 0.05. Wilcoxon signed-rank test. (D) Heatmap depicting the estimated infiltration levels of various immune and stromal cell types (rows) in TCGA-GBM samples (columns), stratified by ECMSig group and score. Red indicates high infiltration, blue indicates low infiltration. Cells significantly highly infiltrated in ECMSig-high are labeled in red, and those high in ECMSig-low group are in blue. ∗q < 0.05, ∗∗q < 0.01, ∗∗∗q < 0.001. Wilcoxon signed-rank test. Benjamini-Hochberg adjusted. (E and F) Scatterplots showing the spearman correlation between ECMSig score and (E) Macrophage_XCELL infiltration score and (F) immune_score_XCELL. The blue line represents the linear regression fit with 95% confidence interval bands. Spearman correlation test.
    Cell Transcriptomic Sequencing Dataset, supplied by 10X Genomics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cell+transcriptomic+sequencing+dataset/cell+copy+genomic+number+profiling+single+technologies/pmc13197639-319-1-9
    Average 86 stars, based on 1 article reviews
    cell transcriptomic sequencing dataset - by Bioz Stars, 2026-11
    86/100 stars
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    Transcriptomic and TME characteristics associated with ECMSig in TCGA-GBM cohort (A) Volcano plot showing DEGs between ECMSig-high and ECMSig-low groups. Red dots: upregulated in high-risk; blue dots: upregulated in low-risk. Benjamini-Hochberg adjusted. (B) Gene set enrichment analysis (GSEA) plots showing enrichment of hallmark pathways. Pathways enriched in ECMSig-high and ECMSig-low groups are shown with their running enrichment scores (ESs) and ranked gene lists. Benjamini-Hochberg adjusted. (C) Heatmap showing the activity scores of selected oncogenic and tumor-related signaling pathways (rows) across TCGA-GBM samples (columns), annotated by ECMSig group and ECMSig score. Red indicates high activity, blue indicates low activity. ∗ p < 0.05. Wilcoxon signed-rank test. (D) Heatmap depicting the estimated infiltration levels of various immune and stromal cell types (rows) in TCGA-GBM samples (columns), stratified by ECMSig group and score. Red indicates high infiltration, blue indicates low infiltration. Cells significantly highly infiltrated in ECMSig-high are labeled in red, and those high in ECMSig-low group are in blue. ∗q < 0.05, ∗∗q < 0.01, ∗∗∗q < 0.001. Wilcoxon signed-rank test. Benjamini-Hochberg adjusted. (E and F) Scatterplots showing the spearman correlation between ECMSig score and (E) Macrophage_XCELL infiltration score and (F) immune_score_XCELL. The blue line represents the linear regression fit with 95% confidence interval bands. Spearman correlation test.

    Journal: iScience

    Article Title: Multi-omics profiling-derived signature links cellular ecosystem to glioblastoma prognosis

    doi: 10.1016/j.isci.2026.115982

    Figure Lengend Snippet: Transcriptomic and TME characteristics associated with ECMSig in TCGA-GBM cohort (A) Volcano plot showing DEGs between ECMSig-high and ECMSig-low groups. Red dots: upregulated in high-risk; blue dots: upregulated in low-risk. Benjamini-Hochberg adjusted. (B) Gene set enrichment analysis (GSEA) plots showing enrichment of hallmark pathways. Pathways enriched in ECMSig-high and ECMSig-low groups are shown with their running enrichment scores (ESs) and ranked gene lists. Benjamini-Hochberg adjusted. (C) Heatmap showing the activity scores of selected oncogenic and tumor-related signaling pathways (rows) across TCGA-GBM samples (columns), annotated by ECMSig group and ECMSig score. Red indicates high activity, blue indicates low activity. ∗ p < 0.05. Wilcoxon signed-rank test. (D) Heatmap depicting the estimated infiltration levels of various immune and stromal cell types (rows) in TCGA-GBM samples (columns), stratified by ECMSig group and score. Red indicates high infiltration, blue indicates low infiltration. Cells significantly highly infiltrated in ECMSig-high are labeled in red, and those high in ECMSig-low group are in blue. ∗q < 0.05, ∗∗q < 0.01, ∗∗∗q < 0.001. Wilcoxon signed-rank test. Benjamini-Hochberg adjusted. (E and F) Scatterplots showing the spearman correlation between ECMSig score and (E) Macrophage_XCELL infiltration score and (F) immune_score_XCELL. The blue line represents the linear regression fit with 95% confidence interval bands. Spearman correlation test.

    Article Snippet: The single-cell transcriptomic sequencing dataset utilizing technology from the 10X Genomics platform was available under the accession number GEO: GSE182109 at the Gene Expression Omnibus (GEO) repository.

    Techniques: Activity Assay, Protein-Protein interactions, Labeling

    Single-cell RNA sequencing analysis revealing ECMSig expression across cell types and identification of prognostically relevant cell states in GBM (A) UMAP visualization of major cell types identified in GBM scRNA-seq data. (B) Dot plot showing the scaled average expression (color intensity) and percentage of cells expressing (dot size) canonical marker genes for each major cell type. (C) Dot plot showing the scaled average expression and percentage of cells expressing the seven ECMSig genes across major cell types. (D) UMAP plots showing the expression levels of individual ECMSig genes and overall ECMSig score across all cells. (E–G) UMAP plots illustrating Scissor-identified prognostically unfavorable (Scissor_Pos, red dashed circle) and favorable (Scissor_Neg, blue dashed circle; Scissor_Others, gray) cell subpopulations within (E) tumor cells, (F) myeloid cells, and (G) endothelial cells. (H–K) Violin plots comparing ECMSig scores among tumor cells grouped by Scissor status (H) and tumor type (I), and myeloid cells (J) or endothelial cells (K) grouped by Scissor status. ∗∗∗∗ p < 0.0001. Wilcoxon signed-rank test. (L) Dot plot showing differentially expressed marker genes between myeloid Scissor_Pos and other myeloid cells. Dot size indicates the fraction of cells in the group expressing the gene; color indicates average expression level.

    Journal: iScience

    Article Title: Multi-omics profiling-derived signature links cellular ecosystem to glioblastoma prognosis

    doi: 10.1016/j.isci.2026.115982

    Figure Lengend Snippet: Single-cell RNA sequencing analysis revealing ECMSig expression across cell types and identification of prognostically relevant cell states in GBM (A) UMAP visualization of major cell types identified in GBM scRNA-seq data. (B) Dot plot showing the scaled average expression (color intensity) and percentage of cells expressing (dot size) canonical marker genes for each major cell type. (C) Dot plot showing the scaled average expression and percentage of cells expressing the seven ECMSig genes across major cell types. (D) UMAP plots showing the expression levels of individual ECMSig genes and overall ECMSig score across all cells. (E–G) UMAP plots illustrating Scissor-identified prognostically unfavorable (Scissor_Pos, red dashed circle) and favorable (Scissor_Neg, blue dashed circle; Scissor_Others, gray) cell subpopulations within (E) tumor cells, (F) myeloid cells, and (G) endothelial cells. (H–K) Violin plots comparing ECMSig scores among tumor cells grouped by Scissor status (H) and tumor type (I), and myeloid cells (J) or endothelial cells (K) grouped by Scissor status. ∗∗∗∗ p < 0.0001. Wilcoxon signed-rank test. (L) Dot plot showing differentially expressed marker genes between myeloid Scissor_Pos and other myeloid cells. Dot size indicates the fraction of cells in the group expressing the gene; color indicates average expression level.

    Article Snippet: The single-cell transcriptomic sequencing dataset utilizing technology from the 10X Genomics platform was available under the accession number GEO: GSE182109 at the Gene Expression Omnibus (GEO) repository.

    Techniques: Single Cell, RNA Sequencing, Expressing, Marker

    Spatial transcriptomic analysis revealing co-localization of ECMSig, hypoxia, Scissor-Positive cells, and pericytes in GBM (A) Spatial feature plots for four GBM samples. Each row represents a sample. Columns show spatial heatmaps of: ECMSig score, hypoxia signature score, tumor Scissor_Pos signature score, myeloid Scissor_Pos signature score, endothelial Scissor Pos signature score, and pericyte marker signature score. Color scale indicates scaled expression or score (low to high). Each dot represents a spatial barcoded spot.

    Journal: iScience

    Article Title: Multi-omics profiling-derived signature links cellular ecosystem to glioblastoma prognosis

    doi: 10.1016/j.isci.2026.115982

    Figure Lengend Snippet: Spatial transcriptomic analysis revealing co-localization of ECMSig, hypoxia, Scissor-Positive cells, and pericytes in GBM (A) Spatial feature plots for four GBM samples. Each row represents a sample. Columns show spatial heatmaps of: ECMSig score, hypoxia signature score, tumor Scissor_Pos signature score, myeloid Scissor_Pos signature score, endothelial Scissor Pos signature score, and pericyte marker signature score. Color scale indicates scaled expression or score (low to high). Each dot represents a spatial barcoded spot.

    Article Snippet: The single-cell transcriptomic sequencing dataset utilizing technology from the 10X Genomics platform was available under the accession number GEO: GSE182109 at the Gene Expression Omnibus (GEO) repository.

    Techniques: Marker, Expressing