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primary antibodies targeting terf2  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc primary antibodies targeting terf2
    Elevated <t>TERF2</t> expression in AML patients and its correlation with clinicopathological features. (A) Transcriptional expression of TERF2 in AML analyzed using TCGA database. (B) TERF2 mRNA levels quantified by qRT-PCR in PBMCs from 50 AML patients and 35 healthy donors. (C) UMAP of single cells from an AML patient ( GSE116256 ), single-cell profiling reveals distinct expression patterns of TERF2 across cellular subpopulations in AML. (D) Heatmap depicting the average expression level of TERF2 across distinct cell types within the AML sample. (E) Univariate Cox proportional hazards regression analysis comparing survival outcomes between high- and low-TERF2 expression groups. (F) Prognostic accuracy of TERF2 evaluated using ROC curve analysis. (G) The predictive performance of the novel risk stratification model was evaluated through time-dependent ROC curve analysis, with AUC values calculated at 1-, 3-, and 5-year intervals to quantify sensitivity and specificity in AML prognosis. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; AUC, area under the curve; CI, confidence interval; FPR, false positive rate; HR, hazard ratio; PBMCs, peripheral blood mononuclear cells; qRT-PCR, quantitative reverse transcription polymerase chain reaction; ROC, receiver operating characteristic; TCGA, The Cancer Genome Atlas; TPM, transcripts per million; TPR, true positive rate; UMAP, uniform manifold approximation and projection.
    Primary Antibodies Targeting Terf2, supplied by Cell Signaling Technology Inc, 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/result/primary antibodies targeting terf2/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    primary antibodies targeting terf2 - by Bioz Stars, 2026-06
    86/100 stars

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    1) Product Images from "High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia"

    Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

    Journal: Translational Cancer Research

    doi: 10.21037/tcr-2025-1226

    Elevated TERF2 expression in AML patients and its correlation with clinicopathological features. (A) Transcriptional expression of TERF2 in AML analyzed using TCGA database. (B) TERF2 mRNA levels quantified by qRT-PCR in PBMCs from 50 AML patients and 35 healthy donors. (C) UMAP of single cells from an AML patient ( GSE116256 ), single-cell profiling reveals distinct expression patterns of TERF2 across cellular subpopulations in AML. (D) Heatmap depicting the average expression level of TERF2 across distinct cell types within the AML sample. (E) Univariate Cox proportional hazards regression analysis comparing survival outcomes between high- and low-TERF2 expression groups. (F) Prognostic accuracy of TERF2 evaluated using ROC curve analysis. (G) The predictive performance of the novel risk stratification model was evaluated through time-dependent ROC curve analysis, with AUC values calculated at 1-, 3-, and 5-year intervals to quantify sensitivity and specificity in AML prognosis. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; AUC, area under the curve; CI, confidence interval; FPR, false positive rate; HR, hazard ratio; PBMCs, peripheral blood mononuclear cells; qRT-PCR, quantitative reverse transcription polymerase chain reaction; ROC, receiver operating characteristic; TCGA, The Cancer Genome Atlas; TPM, transcripts per million; TPR, true positive rate; UMAP, uniform manifold approximation and projection.
    Figure Legend Snippet: Elevated TERF2 expression in AML patients and its correlation with clinicopathological features. (A) Transcriptional expression of TERF2 in AML analyzed using TCGA database. (B) TERF2 mRNA levels quantified by qRT-PCR in PBMCs from 50 AML patients and 35 healthy donors. (C) UMAP of single cells from an AML patient ( GSE116256 ), single-cell profiling reveals distinct expression patterns of TERF2 across cellular subpopulations in AML. (D) Heatmap depicting the average expression level of TERF2 across distinct cell types within the AML sample. (E) Univariate Cox proportional hazards regression analysis comparing survival outcomes between high- and low-TERF2 expression groups. (F) Prognostic accuracy of TERF2 evaluated using ROC curve analysis. (G) The predictive performance of the novel risk stratification model was evaluated through time-dependent ROC curve analysis, with AUC values calculated at 1-, 3-, and 5-year intervals to quantify sensitivity and specificity in AML prognosis. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; AUC, area under the curve; CI, confidence interval; FPR, false positive rate; HR, hazard ratio; PBMCs, peripheral blood mononuclear cells; qRT-PCR, quantitative reverse transcription polymerase chain reaction; ROC, receiver operating characteristic; TCGA, The Cancer Genome Atlas; TPM, transcripts per million; TPR, true positive rate; UMAP, uniform manifold approximation and projection.

    Techniques Used: Expressing, Quantitative RT-PCR, Reverse Transcription, Polymerase Chain Reaction

    Downregulation of TERF2 suppresses AML cells viability and proliferation. (A) qRT-PCR assays analyzed TERF2 mRNA levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (B) Western blot assays detected TERF2 protein levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (C,D) CCK-8 assay showing the viability of NC or TERF2-knockdown MOLM13 cells (C) and THP1 cells (D). (E-H) Flow cytometry assay analyzed cell cycle in NC or TERF2-knockdown MOLM13 cells (E,F) and THP1 cells (G,H). **, P<0.01; ****, P<0.0001; ns, not significant. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; NC, negative control; qRT-PCR, quantitative reverse transcription polymerase chain reaction.
    Figure Legend Snippet: Downregulation of TERF2 suppresses AML cells viability and proliferation. (A) qRT-PCR assays analyzed TERF2 mRNA levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (B) Western blot assays detected TERF2 protein levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (C,D) CCK-8 assay showing the viability of NC or TERF2-knockdown MOLM13 cells (C) and THP1 cells (D). (E-H) Flow cytometry assay analyzed cell cycle in NC or TERF2-knockdown MOLM13 cells (E,F) and THP1 cells (G,H). **, P<0.01; ****, P<0.0001; ns, not significant. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; NC, negative control; qRT-PCR, quantitative reverse transcription polymerase chain reaction.

    Techniques Used: Quantitative RT-PCR, Knockdown, Western Blot, CCK-8 Assay, Flow Cytometry, Cell Counting, Negative Control, Reverse Transcription, Polymerase Chain Reaction

    TERF2 deficiency promotes apoptosis in AML cells. (A-D) Flow cytometry assay analyzed apoptosis in NC or TERF2-knockdown MOLM13 cells (A,B) or THP1 cells (C,D). (E-H) Western blot detected cleaved caspase 3 levels of NC or TERF2-knockdown MOLM13 cells (E,F) or THP1 cells (G,H). ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; NC, negative control.
    Figure Legend Snippet: TERF2 deficiency promotes apoptosis in AML cells. (A-D) Flow cytometry assay analyzed apoptosis in NC or TERF2-knockdown MOLM13 cells (A,B) or THP1 cells (C,D). (E-H) Western blot detected cleaved caspase 3 levels of NC or TERF2-knockdown MOLM13 cells (E,F) or THP1 cells (G,H). ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; NC, negative control.

    Techniques Used: Flow Cytometry, Knockdown, Western Blot, Negative Control

    TERF2 involved in cuproptosis through E2F pathway in AML. (A) Bar graphs illustrate the associations between TERF2 expression levels and gene hallmark sets in AML patients. (B) GSEA for AML patients with high TERF2 expression in TCGA database. (C-E) Western blot analysis of E2F1, CDK4, CDK6, CDKN2A levels in MOLM13 cells and NB4 cells with or without TERF2 silence. (F,G) MOLM13 (F) and NB4 (G) cells with TERF2 knockdown were treated with specified concentrations of ES-Cu (1:1 ratio) for 48 hours, followed by cell viability assessment using the CCK-8 assay. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; ES-Cu, elesclomol-copper; GSEA, gene set enrichment analysis; IC 50 , half-maximal inhibitory concentration; TCGA, The Cancer Genome Atlas.
    Figure Legend Snippet: TERF2 involved in cuproptosis through E2F pathway in AML. (A) Bar graphs illustrate the associations between TERF2 expression levels and gene hallmark sets in AML patients. (B) GSEA for AML patients with high TERF2 expression in TCGA database. (C-E) Western blot analysis of E2F1, CDK4, CDK6, CDKN2A levels in MOLM13 cells and NB4 cells with or without TERF2 silence. (F,G) MOLM13 (F) and NB4 (G) cells with TERF2 knockdown were treated with specified concentrations of ES-Cu (1:1 ratio) for 48 hours, followed by cell viability assessment using the CCK-8 assay. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; ES-Cu, elesclomol-copper; GSEA, gene set enrichment analysis; IC 50 , half-maximal inhibitory concentration; TCGA, The Cancer Genome Atlas.

    Techniques Used: Expressing, Western Blot, Knockdown, CCK-8 Assay, Cell Counting, Concentration Assay

    Knockdown of TERF2 suppresses AML progression and enhances cuproptosis sensitivity in vivo . (A,B) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted NSG mice (A) and the quantification of luciferase signals for all mice per group (B). (C) Kaplan-Meier analysis of survival of MOLM13-engrafted mice, log rank test. (D,E) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted mice treated with elesclomol (D) and the quantification of luciferase signals for all mice per group (E). (F) Kaplan-Meier analysis of survival of MOLM13-engrafted mice treated with elesclomol, log rank test. **, P<0.01. AML, acute myeloid leukemia; NSG, NOD-SCID IL2rg.
    Figure Legend Snippet: Knockdown of TERF2 suppresses AML progression and enhances cuproptosis sensitivity in vivo . (A,B) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted NSG mice (A) and the quantification of luciferase signals for all mice per group (B). (C) Kaplan-Meier analysis of survival of MOLM13-engrafted mice, log rank test. (D,E) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted mice treated with elesclomol (D) and the quantification of luciferase signals for all mice per group (E). (F) Kaplan-Meier analysis of survival of MOLM13-engrafted mice treated with elesclomol, log rank test. **, P<0.01. AML, acute myeloid leukemia; NSG, NOD-SCID IL2rg.

    Techniques Used: Knockdown, In Vivo, Imaging, Luciferase



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    Cell Signaling Technology Inc primary antibodies targeting terf2
    Elevated <t>TERF2</t> expression in AML patients and its correlation with clinicopathological features. (A) Transcriptional expression of TERF2 in AML analyzed using TCGA database. (B) TERF2 mRNA levels quantified by qRT-PCR in PBMCs from 50 AML patients and 35 healthy donors. (C) UMAP of single cells from an AML patient ( GSE116256 ), single-cell profiling reveals distinct expression patterns of TERF2 across cellular subpopulations in AML. (D) Heatmap depicting the average expression level of TERF2 across distinct cell types within the AML sample. (E) Univariate Cox proportional hazards regression analysis comparing survival outcomes between high- and low-TERF2 expression groups. (F) Prognostic accuracy of TERF2 evaluated using ROC curve analysis. (G) The predictive performance of the novel risk stratification model was evaluated through time-dependent ROC curve analysis, with AUC values calculated at 1-, 3-, and 5-year intervals to quantify sensitivity and specificity in AML prognosis. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; AUC, area under the curve; CI, confidence interval; FPR, false positive rate; HR, hazard ratio; PBMCs, peripheral blood mononuclear cells; qRT-PCR, quantitative reverse transcription polymerase chain reaction; ROC, receiver operating characteristic; TCGA, The Cancer Genome Atlas; TPM, transcripts per million; TPR, true positive rate; UMAP, uniform manifold approximation and projection.
    Primary Antibodies Targeting Terf2, supplied by Cell Signaling Technology Inc, 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/result/primary antibodies targeting terf2/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
    primary antibodies targeting terf2 - by Bioz Stars, 2026-06
    86/100 stars
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    Elevated TERF2 expression in AML patients and its correlation with clinicopathological features. (A) Transcriptional expression of TERF2 in AML analyzed using TCGA database. (B) TERF2 mRNA levels quantified by qRT-PCR in PBMCs from 50 AML patients and 35 healthy donors. (C) UMAP of single cells from an AML patient ( GSE116256 ), single-cell profiling reveals distinct expression patterns of TERF2 across cellular subpopulations in AML. (D) Heatmap depicting the average expression level of TERF2 across distinct cell types within the AML sample. (E) Univariate Cox proportional hazards regression analysis comparing survival outcomes between high- and low-TERF2 expression groups. (F) Prognostic accuracy of TERF2 evaluated using ROC curve analysis. (G) The predictive performance of the novel risk stratification model was evaluated through time-dependent ROC curve analysis, with AUC values calculated at 1-, 3-, and 5-year intervals to quantify sensitivity and specificity in AML prognosis. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; AUC, area under the curve; CI, confidence interval; FPR, false positive rate; HR, hazard ratio; PBMCs, peripheral blood mononuclear cells; qRT-PCR, quantitative reverse transcription polymerase chain reaction; ROC, receiver operating characteristic; TCGA, The Cancer Genome Atlas; TPM, transcripts per million; TPR, true positive rate; UMAP, uniform manifold approximation and projection.

    Journal: Translational Cancer Research

    Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

    doi: 10.21037/tcr-2025-1226

    Figure Lengend Snippet: Elevated TERF2 expression in AML patients and its correlation with clinicopathological features. (A) Transcriptional expression of TERF2 in AML analyzed using TCGA database. (B) TERF2 mRNA levels quantified by qRT-PCR in PBMCs from 50 AML patients and 35 healthy donors. (C) UMAP of single cells from an AML patient ( GSE116256 ), single-cell profiling reveals distinct expression patterns of TERF2 across cellular subpopulations in AML. (D) Heatmap depicting the average expression level of TERF2 across distinct cell types within the AML sample. (E) Univariate Cox proportional hazards regression analysis comparing survival outcomes between high- and low-TERF2 expression groups. (F) Prognostic accuracy of TERF2 evaluated using ROC curve analysis. (G) The predictive performance of the novel risk stratification model was evaluated through time-dependent ROC curve analysis, with AUC values calculated at 1-, 3-, and 5-year intervals to quantify sensitivity and specificity in AML prognosis. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; AUC, area under the curve; CI, confidence interval; FPR, false positive rate; HR, hazard ratio; PBMCs, peripheral blood mononuclear cells; qRT-PCR, quantitative reverse transcription polymerase chain reaction; ROC, receiver operating characteristic; TCGA, The Cancer Genome Atlas; TPM, transcripts per million; TPR, true positive rate; UMAP, uniform manifold approximation and projection.

    Article Snippet: Primary antibodies targeting TERF2 (#13136, 1:500 dilution), CDK4 (#12790, 1:500), CDK6 (#1331, 1:500), and CDKN2A (#80772, 1:500) were commercially obtained from CST (Danvers, MA, USA).

    Techniques: Expressing, Quantitative RT-PCR, Reverse Transcription, Polymerase Chain Reaction

    Downregulation of TERF2 suppresses AML cells viability and proliferation. (A) qRT-PCR assays analyzed TERF2 mRNA levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (B) Western blot assays detected TERF2 protein levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (C,D) CCK-8 assay showing the viability of NC or TERF2-knockdown MOLM13 cells (C) and THP1 cells (D). (E-H) Flow cytometry assay analyzed cell cycle in NC or TERF2-knockdown MOLM13 cells (E,F) and THP1 cells (G,H). **, P<0.01; ****, P<0.0001; ns, not significant. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; NC, negative control; qRT-PCR, quantitative reverse transcription polymerase chain reaction.

    Journal: Translational Cancer Research

    Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

    doi: 10.21037/tcr-2025-1226

    Figure Lengend Snippet: Downregulation of TERF2 suppresses AML cells viability and proliferation. (A) qRT-PCR assays analyzed TERF2 mRNA levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (B) Western blot assays detected TERF2 protein levels of NC or TERF2-knockdown MOLM13 cells and THP1 cells. (C,D) CCK-8 assay showing the viability of NC or TERF2-knockdown MOLM13 cells (C) and THP1 cells (D). (E-H) Flow cytometry assay analyzed cell cycle in NC or TERF2-knockdown MOLM13 cells (E,F) and THP1 cells (G,H). **, P<0.01; ****, P<0.0001; ns, not significant. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; NC, negative control; qRT-PCR, quantitative reverse transcription polymerase chain reaction.

    Article Snippet: Primary antibodies targeting TERF2 (#13136, 1:500 dilution), CDK4 (#12790, 1:500), CDK6 (#1331, 1:500), and CDKN2A (#80772, 1:500) were commercially obtained from CST (Danvers, MA, USA).

    Techniques: Quantitative RT-PCR, Knockdown, Western Blot, CCK-8 Assay, Flow Cytometry, Cell Counting, Negative Control, Reverse Transcription, Polymerase Chain Reaction

    TERF2 deficiency promotes apoptosis in AML cells. (A-D) Flow cytometry assay analyzed apoptosis in NC or TERF2-knockdown MOLM13 cells (A,B) or THP1 cells (C,D). (E-H) Western blot detected cleaved caspase 3 levels of NC or TERF2-knockdown MOLM13 cells (E,F) or THP1 cells (G,H). ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; NC, negative control.

    Journal: Translational Cancer Research

    Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

    doi: 10.21037/tcr-2025-1226

    Figure Lengend Snippet: TERF2 deficiency promotes apoptosis in AML cells. (A-D) Flow cytometry assay analyzed apoptosis in NC or TERF2-knockdown MOLM13 cells (A,B) or THP1 cells (C,D). (E-H) Western blot detected cleaved caspase 3 levels of NC or TERF2-knockdown MOLM13 cells (E,F) or THP1 cells (G,H). ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; NC, negative control.

    Article Snippet: Primary antibodies targeting TERF2 (#13136, 1:500 dilution), CDK4 (#12790, 1:500), CDK6 (#1331, 1:500), and CDKN2A (#80772, 1:500) were commercially obtained from CST (Danvers, MA, USA).

    Techniques: Flow Cytometry, Knockdown, Western Blot, Negative Control

    TERF2 involved in cuproptosis through E2F pathway in AML. (A) Bar graphs illustrate the associations between TERF2 expression levels and gene hallmark sets in AML patients. (B) GSEA for AML patients with high TERF2 expression in TCGA database. (C-E) Western blot analysis of E2F1, CDK4, CDK6, CDKN2A levels in MOLM13 cells and NB4 cells with or without TERF2 silence. (F,G) MOLM13 (F) and NB4 (G) cells with TERF2 knockdown were treated with specified concentrations of ES-Cu (1:1 ratio) for 48 hours, followed by cell viability assessment using the CCK-8 assay. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; ES-Cu, elesclomol-copper; GSEA, gene set enrichment analysis; IC 50 , half-maximal inhibitory concentration; TCGA, The Cancer Genome Atlas.

    Journal: Translational Cancer Research

    Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

    doi: 10.21037/tcr-2025-1226

    Figure Lengend Snippet: TERF2 involved in cuproptosis through E2F pathway in AML. (A) Bar graphs illustrate the associations between TERF2 expression levels and gene hallmark sets in AML patients. (B) GSEA for AML patients with high TERF2 expression in TCGA database. (C-E) Western blot analysis of E2F1, CDK4, CDK6, CDKN2A levels in MOLM13 cells and NB4 cells with or without TERF2 silence. (F,G) MOLM13 (F) and NB4 (G) cells with TERF2 knockdown were treated with specified concentrations of ES-Cu (1:1 ratio) for 48 hours, followed by cell viability assessment using the CCK-8 assay. ***, P<0.001; ****, P<0.0001. AML, acute myeloid leukemia; CCK-8, Cell Counting Kit-8; ES-Cu, elesclomol-copper; GSEA, gene set enrichment analysis; IC 50 , half-maximal inhibitory concentration; TCGA, The Cancer Genome Atlas.

    Article Snippet: Primary antibodies targeting TERF2 (#13136, 1:500 dilution), CDK4 (#12790, 1:500), CDK6 (#1331, 1:500), and CDKN2A (#80772, 1:500) were commercially obtained from CST (Danvers, MA, USA).

    Techniques: Expressing, Western Blot, Knockdown, CCK-8 Assay, Cell Counting, Concentration Assay

    Knockdown of TERF2 suppresses AML progression and enhances cuproptosis sensitivity in vivo . (A,B) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted NSG mice (A) and the quantification of luciferase signals for all mice per group (B). (C) Kaplan-Meier analysis of survival of MOLM13-engrafted mice, log rank test. (D,E) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted mice treated with elesclomol (D) and the quantification of luciferase signals for all mice per group (E). (F) Kaplan-Meier analysis of survival of MOLM13-engrafted mice treated with elesclomol, log rank test. **, P<0.01. AML, acute myeloid leukemia; NSG, NOD-SCID IL2rg.

    Journal: Translational Cancer Research

    Article Title: High TERF2 expression is associated with poor prognosis and its suppression attenuates progression in acute myeloid leukemia

    doi: 10.21037/tcr-2025-1226

    Figure Lengend Snippet: Knockdown of TERF2 suppresses AML progression and enhances cuproptosis sensitivity in vivo . (A,B) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted NSG mice (A) and the quantification of luciferase signals for all mice per group (B). (C) Kaplan-Meier analysis of survival of MOLM13-engrafted mice, log rank test. (D,E) Tumor growth was monitored by bioluminescence imaging in MOLM13-engrafted mice treated with elesclomol (D) and the quantification of luciferase signals for all mice per group (E). (F) Kaplan-Meier analysis of survival of MOLM13-engrafted mice treated with elesclomol, log rank test. **, P<0.01. AML, acute myeloid leukemia; NSG, NOD-SCID IL2rg.

    Article Snippet: Primary antibodies targeting TERF2 (#13136, 1:500 dilution), CDK4 (#12790, 1:500), CDK6 (#1331, 1:500), and CDKN2A (#80772, 1:500) were commercially obtained from CST (Danvers, MA, USA).

    Techniques: Knockdown, In Vivo, Imaging, Luciferase