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Addgene inc foxo1 open reading frame
Foxo1 Open Reading Frame, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/foxo1+open+reading+frame/Flag+FoxO1+(Plasmid+%2366147)/pm27132507-179-1-21
Average 93 stars, based on 13 article reviews

foxo1 open reading frame - by Bioz Stars, 2026-09

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Figure 4. The impact of p300 on FOXO1 acetylation and its transcriptional activity. (a) p300-mediated FOXO1 acetylation. HEK293T cells with exogenous FOXO1-WT and p300-WT or -ΔHAT expression were treated with 300 μM H2O2 for 30 min. Where indicated, cells were pre- incubated with 10 μM tenovin-6 for 2 h. (b, c) The effect of C612S mutation of FOXO1 on its interaction with p300 and acetylation. HEK293T cells with exogenous p300-WT and FOXO1-WT or -C612S expression were treated with 300 μM H2O2 for 30 min; thereafter, cells were lysed and FOXO1 acetylation was assessed by immunoblotting (c). Proteins interacting with FOXO1 variants were separated by co- immunoprecipitation with anti-FLAG antibody and analyzed by immunoblotting (b). (d) The effect of TXN activity on FOXO1 acetylation. HEK293T cells with exogenous FOXO1-WT, p300-WT and TXN-WT or -dominant negative (DN) expression were treated with 300 μM H2O2 for 30 min, and protein abundance was assessed by immunoblotting. (e) The effect of TXN inhibitor, PX-12, on FOXO1 acetylation. HEK293T cells with exogenous FOXO1-WT and p300-WT expression were pre-incubated with 5 μM PX-12 for 18 h and treated with 300 μM H2O2 for 30 min. (f) The impact of FOXO1-C612S mutation on induction of FOXO1 target genes after oxidative stress. HEK293T cells transfected with vectors coding p300-WT and FOXO1-WT or -C612S were treated with 300 μM H2O2. Thereafter, mRNA expression was determined with RT–qPCR. Error bars represent s.d. of three independent replicates in a representative experiment. P-values were calculated using Welch’s t-test. (g) Endogenous FOXO1 acetylation after oxidative stress in OxPhos-DLBCL cells. K422 control cells (SCR) or those with shRNA-mediated TXN knockdown were treated with 300 μM H2O2 for 30 min. Quantitative differences in the Ac-FOXO1 protein level based on densitometric analysis, normalized to the total FOXO1 protein and GAPDH expression levels are indicated below the blots. See also Supplementary Figure S3.

Journal: Oncogene

Article Title: FOXO1 is a TXN- and p300-dependent sensor and effector of oxidative stress in diffuse large B-cell lymphomas characterized by increased oxidative metabolism.

doi: 10.1038/onc.2016.126

Figure Lengend Snippet: Figure 4. The impact of p300 on FOXO1 acetylation and its transcriptional activity. (a) p300-mediated FOXO1 acetylation. HEK293T cells with exogenous FOXO1-WT and p300-WT or -ΔHAT expression were treated with 300 μM H2O2 for 30 min. Where indicated, cells were pre- incubated with 10 μM tenovin-6 for 2 h. (b, c) The effect of C612S mutation of FOXO1 on its interaction with p300 and acetylation. HEK293T cells with exogenous p300-WT and FOXO1-WT or -C612S expression were treated with 300 μM H2O2 for 30 min; thereafter, cells were lysed and FOXO1 acetylation was assessed by immunoblotting (c). Proteins interacting with FOXO1 variants were separated by co- immunoprecipitation with anti-FLAG antibody and analyzed by immunoblotting (b). (d) The effect of TXN activity on FOXO1 acetylation. HEK293T cells with exogenous FOXO1-WT, p300-WT and TXN-WT or -dominant negative (DN) expression were treated with 300 μM H2O2 for 30 min, and protein abundance was assessed by immunoblotting. (e) The effect of TXN inhibitor, PX-12, on FOXO1 acetylation. HEK293T cells with exogenous FOXO1-WT and p300-WT expression were pre-incubated with 5 μM PX-12 for 18 h and treated with 300 μM H2O2 for 30 min. (f) The impact of FOXO1-C612S mutation on induction of FOXO1 target genes after oxidative stress. HEK293T cells transfected with vectors coding p300-WT and FOXO1-WT or -C612S were treated with 300 μM H2O2. Thereafter, mRNA expression was determined with RT–qPCR. Error bars represent s.d. of three independent replicates in a representative experiment. P-values were calculated using Welch’s t-test. (g) Endogenous FOXO1 acetylation after oxidative stress in OxPhos-DLBCL cells. K422 control cells (SCR) or those with shRNA-mediated TXN knockdown were treated with 300 μM H2O2 for 30 min. Quantitative differences in the Ac-FOXO1 protein level based on densitometric analysis, normalized to the total FOXO1 protein and GAPDH expression levels are indicated below the blots. See also Supplementary Figure S3.

Article Snippet: FLAG-tagged FOXO1 open reading frame was first fused with the estrogen receptor by replacing FOXO3A in the pECE-FOXO3a-TMER vector (obtained from Addgene, plasmid #8353).51 Next, the p300-acetylated lysines at sites 245, 248, 262 and 265 in FOXO1 were mutated to arginines using site-directed mutagenesis (FOXO1-3A4KR).

Techniques: Activity Assay, Expressing, Incubation, Mutagenesis, Western Blot, Immunoprecipitation, Dominant Negative Mutation, Quantitative Proteomics, Transfection, Quantitative RT-PCR, Control, shRNA, Knockdown

Figure 5. Activity of WT and acetylation-deﬁcient FOXO1 in DLBCL cells. DHL4 cells were transfected with vectors coding constitutively nuclear FOXO1-3A or constitutively nuclear, acetylation-deﬁcient FOXO1-3A4KR; thereafter, cells were incubated with 1 μM 4-hydroxytamoxifen (4-OHT) for the induction of FOXO1 nuclear localization. (a) Cell viability was assessed after 72 h incubation; error bars represent s.d. of three independent replicates in a representative experiment. (b) Apoptosis was determined by Annexin V/7-AAD staining after 96 h. (c) Graphs present an increase in apoptosis relative to control cells. (d) FOXO1 target genes mRNA abundance was determined using RT–qPCR, relative to GAPDH. Graphs illustrate fold change from untreated control; error bars represent s.d. of three independent replicates in a representative experiment. P-values were calculated using Welch’s t-test. See also Supplementary Figure S4.

Journal: Oncogene

Article Title: FOXO1 is a TXN- and p300-dependent sensor and effector of oxidative stress in diffuse large B-cell lymphomas characterized by increased oxidative metabolism.

doi: 10.1038/onc.2016.126

Figure Lengend Snippet: Figure 5. Activity of WT and acetylation-deﬁcient FOXO1 in DLBCL cells. DHL4 cells were transfected with vectors coding constitutively nuclear FOXO1-3A or constitutively nuclear, acetylation-deﬁcient FOXO1-3A4KR; thereafter, cells were incubated with 1 μM 4-hydroxytamoxifen (4-OHT) for the induction of FOXO1 nuclear localization. (a) Cell viability was assessed after 72 h incubation; error bars represent s.d. of three independent replicates in a representative experiment. (b) Apoptosis was determined by Annexin V/7-AAD staining after 96 h. (c) Graphs present an increase in apoptosis relative to control cells. (d) FOXO1 target genes mRNA abundance was determined using RT–qPCR, relative to GAPDH. Graphs illustrate fold change from untreated control; error bars represent s.d. of three independent replicates in a representative experiment. P-values were calculated using Welch’s t-test. See also Supplementary Figure S4.

Techniques: Activity Assay, Transfection, Incubation, Staining, Control, Quantitative RT-PCR

Figure 6. Changes in FOXO1 subcellular localization in response to oxidative stress in OxPhos-DLBCL cells. (a) Subcellular FOXO1 localization in the K422 cell line with respect to TXN expression after oxidative stress. Cells were transfected with vectors coding control (SCR) or TXN-targeting shRNA and incubated with 1 mU/ml GO for 3 h. Cells were visualized with confocal microscope; DRAQ5–DNA, Alexa-488–FOXO1. Scale bar represents 20 μm. (b) Changes in the activity of MST1 kinase involved in cellular localization of FOXO1 in K422 and Pfeiffer cells with silenced TXN expression after oxidative stress. Cells were incubated with 1 mU/ml GO for 12 h, and protein abundance was assessed by immunoblotting. In all tested cell lines with TXN knockdown, oxidative stress exposure markedly increased the level of oxidized (more stable) peroxiredoxins (PRDXs), conﬁrming lower antioxidant capacity of these cells compared with control cells. (c, d) Apoptosis increase in the K422 cell line with silenced TXN and FOXO1 expression in response to oxidative stress. K422 cells with silenced TXN expression and WT or knocked down FOXO1 expression were treated with 1 mU/ml GO for 24 h; thereafter, percentage of apoptotic cells was determined with Annexin V/7-AAD staining. (c) Dot plots from a representative experiment and (d) bar graph summary (normalized to untreated controls). See also Supplementary Figures S5–S6.

Journal: Oncogene

Article Title: FOXO1 is a TXN- and p300-dependent sensor and effector of oxidative stress in diffuse large B-cell lymphomas characterized by increased oxidative metabolism.

doi: 10.1038/onc.2016.126

Figure Lengend Snippet: Figure 6. Changes in FOXO1 subcellular localization in response to oxidative stress in OxPhos-DLBCL cells. (a) Subcellular FOXO1 localization in the K422 cell line with respect to TXN expression after oxidative stress. Cells were transfected with vectors coding control (SCR) or TXN-targeting shRNA and incubated with 1 mU/ml GO for 3 h. Cells were visualized with confocal microscope; DRAQ5–DNA, Alexa-488–FOXO1. Scale bar represents 20 μm. (b) Changes in the activity of MST1 kinase involved in cellular localization of FOXO1 in K422 and Pfeiffer cells with silenced TXN expression after oxidative stress. Cells were incubated with 1 mU/ml GO for 12 h, and protein abundance was assessed by immunoblotting. In all tested cell lines with TXN knockdown, oxidative stress exposure markedly increased the level of oxidized (more stable) peroxiredoxins (PRDXs), conﬁrming lower antioxidant capacity of these cells compared with control cells. (c, d) Apoptosis increase in the K422 cell line with silenced TXN and FOXO1 expression in response to oxidative stress. K422 cells with silenced TXN expression and WT or knocked down FOXO1 expression were treated with 1 mU/ml GO for 24 h; thereafter, percentage of apoptotic cells was determined with Annexin V/7-AAD staining. (c) Dot plots from a representative experiment and (d) bar graph summary (normalized to untreated controls). See also Supplementary Figures S5–S6.

Techniques: Expressing, Transfection, Control, shRNA, Incubation, Microscopy, Activity Assay, Quantitative Proteomics, Western Blot, Knockdown, Staining

Figure 1. The BCR-SYK-AKT-FOXO1 signaling pathway is operative in tonic BCR signal-dependent DLBCL cell lines and leads to the suppression of FOXO1 activity. (A) The integrity of the BCR-SYK-AKT-FOXO1 axis was determined in BCR-dependent cell lines DHL4, DHL6, Ly1, and Ly7 after crosslinking of their BCRs, with or without R406 pretreatment. Activity of key signaling components of the pathway was assessed with phospho-specific antibodies against SYK(Y525/6), AKT(S473), and FOXO1(T24 and S256). Blots were next stripped and reprobed with antibodies against total-SYK, total-AKT, and total-FOXO1. GAPDH served as a loading control. Densitometric quantification of band intensities is provided in supplemental Table 4. (B) DLBCL cells were treated with R406 (gray line) or vehicle alone (black line) for 18 hours and subjected to single-cell phospho-flow analysis to detect tonic AKT phosphorylation at S473. Dotted line, isotype control. (C) FOXO1 phosphorylation in DLBCL cell lines treated for 18 hours with R406 or vehicle alone was analyzed by immunoblotting. Densitometric quantification of band intensities is provided in supplemental Table 5.

Journal: Blood

Article Title: FOXO1 activation is an effector of SYK and AKT inhibition in tonic BCR signal-dependent diffuse large B-cell lymphomas.

doi: 10.1182/blood-2015-06-654111

Figure Lengend Snippet: Figure 1. The BCR-SYK-AKT-FOXO1 signaling pathway is operative in tonic BCR signal-dependent DLBCL cell lines and leads to the suppression of FOXO1 activity. (A) The integrity of the BCR-SYK-AKT-FOXO1 axis was determined in BCR-dependent cell lines DHL4, DHL6, Ly1, and Ly7 after crosslinking of their BCRs, with or without R406 pretreatment. Activity of key signaling components of the pathway was assessed with phospho-specific antibodies against SYK(Y525/6), AKT(S473), and FOXO1(T24 and S256). Blots were next stripped and reprobed with antibodies against total-SYK, total-AKT, and total-FOXO1. GAPDH served as a loading control. Densitometric quantification of band intensities is provided in supplemental Table 4. (B) DLBCL cells were treated with R406 (gray line) or vehicle alone (black line) for 18 hours and subjected to single-cell phospho-flow analysis to detect tonic AKT phosphorylation at S473. Dotted line, isotype control. (C) FOXO1 phosphorylation in DLBCL cell lines treated for 18 hours with R406 or vehicle alone was analyzed by immunoblotting. Densitometric quantification of band intensities is provided in supplemental Table 5.

Article Snippet: The pMIG-FOXO1-WTIRES-GFP and pMIG-FOXO1-3A-IRES-GFP were generated by ligating wild-type (WT) or 3A FOXO1 mutant open reading frames (derived from Addgene vectors 13507 and 13508, deposited by Kunliang Guan21) into the pMIG-IRES-GFP vector.

Techniques: Activity Assay, Control, Phospho-proteomics, Western Blot

Figure 2. FOXO1 activation in DLBCL cells induces FOXO1-dependent gene expression, cell cycle arrest, and apoptosis. (A) SYK inhibition induces FOXO1 target gene expression. The heat map shows relative abundance of 40 FOXO1 target genes (GSEA leading edge) in tonic BCR signal-dependent DLBCL cell lines following 24-hour treatment with R406. (B) GSEA enrichment plot of FOXO1 target genes in tonic BCR signal-dependent DLBCL cell lines (DHL4, DHL6, Ly7) treated with DMSO or R406 for 24 hours. Note that the positions of the FOXO1 targets (Vogel et al23) were significantly skewed toward the left end of the sorted list, reflecting their statistically significant induction in R406-treated lines. (C) FOXO1 target gene expression in 4 tonic BCR signal-dependent cell lines following 24-hour treatment with R406 or vehicle, analyzed by qRT-PCR. (P values were determined using 2-sided Gosset’s t test: *P , .05; **P , .01; ***P , .001; ****P , .0001). (D) Protein abundance of key FOXO1 targets, CDKN1B (p27) and BCL2L11 (BIM), in DLBCL cells following 6- to 72-hour treatment with R406 or vehicle, analyzed by western blot. GAPDH served as a loading control. Densitometric quantification of band intensities is provided in supplemental Table 6. (E) FOXO1 nuclear localization induces cell cycle arrest. DHL4 cells were retrovirally transduced with pMIG-FOXO1-WT-IRES-GFP or pMIG-FOXO1-3A-IRES-GFP to express wild-type (FOXO1-WT) or constitutively nuclear FOXO1 mutant (FOXO1-3A). Cell cycle distribution was measured within the GFP1 population by Hoechst blue staining and FACS analysis. (F) FOXO1 nuclear localization induces apoptosis. Cells were transduced as in E; 48 hours after transduction, GFP1 cells were FACS sorted and after another 60 hours were analyzed by AnnexinV/7-AAD staining. Bar graphs are derived from FACS data.

Journal: Blood

Article Title: FOXO1 activation is an effector of SYK and AKT inhibition in tonic BCR signal-dependent diffuse large B-cell lymphomas.

doi: 10.1182/blood-2015-06-654111

Figure Lengend Snippet: Figure 2. FOXO1 activation in DLBCL cells induces FOXO1-dependent gene expression, cell cycle arrest, and apoptosis. (A) SYK inhibition induces FOXO1 target gene expression. The heat map shows relative abundance of 40 FOXO1 target genes (GSEA leading edge) in tonic BCR signal-dependent DLBCL cell lines following 24-hour treatment with R406. (B) GSEA enrichment plot of FOXO1 target genes in tonic BCR signal-dependent DLBCL cell lines (DHL4, DHL6, Ly7) treated with DMSO or R406 for 24 hours. Note that the positions of the FOXO1 targets (Vogel et al23) were significantly skewed toward the left end of the sorted list, reflecting their statistically significant induction in R406-treated lines. (C) FOXO1 target gene expression in 4 tonic BCR signal-dependent cell lines following 24-hour treatment with R406 or vehicle, analyzed by qRT-PCR. (P values were determined using 2-sided Gosset’s t test: *P , .05; **P , .01; ***P , .001; ****P , .0001). (D) Protein abundance of key FOXO1 targets, CDKN1B (p27) and BCL2L11 (BIM), in DLBCL cells following 6- to 72-hour treatment with R406 or vehicle, analyzed by western blot. GAPDH served as a loading control. Densitometric quantification of band intensities is provided in supplemental Table 6. (E) FOXO1 nuclear localization induces cell cycle arrest. DHL4 cells were retrovirally transduced with pMIG-FOXO1-WT-IRES-GFP or pMIG-FOXO1-3A-IRES-GFP to express wild-type (FOXO1-WT) or constitutively nuclear FOXO1 mutant (FOXO1-3A). Cell cycle distribution was measured within the GFP1 population by Hoechst blue staining and FACS analysis. (F) FOXO1 nuclear localization induces apoptosis. Cells were transduced as in E; 48 hours after transduction, GFP1 cells were FACS sorted and after another 60 hours were analyzed by AnnexinV/7-AAD staining. Bar graphs are derived from FACS data.

Techniques: Activation Assay, Gene Expression, Inhibition, Targeted Gene Expression, Quantitative RT-PCR, Quantitative Proteomics, Western Blot, Control, Transduction, Mutagenesis, Staining, Derivative Assay

Figure 3. FOXO1 mediates toxicity of SYK inhibitor in tonic BCR signal-dependent DLBCL cells. DHL4, DHL6, Ly1, and Ly7 cells were transduced with pSiren-RetroQ-scrambled-shRNA (Scr shRNA) or pSiren-RetroQ-FOXO1-shRNA (FOXO1 shRNA), and stable transfectants were selected using puromy- cin. (A) FOXO1, AKT, and SYK protein expression was analyzed by immunoblotting. GAPDH served as a loading control. Densitometric quantification of band intensities is provided in supplemental Table 7. (B) Cells transduced with FOXO1-targeting shRNA vectors were treated with R406 and after 72 hours were analyzed for proliferation using the MTS assay. Please also see supplemental Figure 3 for addi- tional information.

Journal: Blood

Article Title: FOXO1 activation is an effector of SYK and AKT inhibition in tonic BCR signal-dependent diffuse large B-cell lymphomas.

doi: 10.1182/blood-2015-06-654111

Figure Lengend Snippet: Figure 3. FOXO1 mediates toxicity of SYK inhibitor in tonic BCR signal-dependent DLBCL cells. DHL4, DHL6, Ly1, and Ly7 cells were transduced with pSiren-RetroQ-scrambled-shRNA (Scr shRNA) or pSiren-RetroQ-FOXO1-shRNA (FOXO1 shRNA), and stable transfectants were selected using puromy- cin. (A) FOXO1, AKT, and SYK protein expression was analyzed by immunoblotting. GAPDH served as a loading control. Densitometric quantification of band intensities is provided in supplemental Table 7. (B) Cells transduced with FOXO1-targeting shRNA vectors were treated with R406 and after 72 hours were analyzed for proliferation using the MTS assay. Please also see supplemental Figure 3 for addi- tional information.

Techniques: Transduction, shRNA, Expressing, Western Blot, Control, MTS Assay

Figure 4. FOXO1 mediates toxicity of SYK inhibitor in tonic BCR signal-dependent DLBCL cells. (A) Transcript abundance of FOXO1 target genes, BIM, TRAIL, GADD45a, and CDKN1B (p27Kip1) in cell lines transduced with FOXO1-targeting or control shRNA vectors, assessed by qRT-PCR after 24-hour incubation with R406. (B) SREBP1 expression following incubation with R406 was assessed as described above. (C) Transcript abundance of HRK in DHL4 and Ly7 cell lines transduced with scrambled control shRNA (Scr) or FOXO1-targeting shRNA following 24-hour incubation with R406. P values in A to C were determined using a 2-sided Gosset’s t test: *P , .05; **P , .01; ***P , .001; ****P , .0001. (D) HRK expression was determined after 24-hour treatment with vehicle alone (DMSO), R406, or a combination of SYK and pan-caspase inhibitor (Z-VAD-FMK) by qRT-PCR relative to GAPDH. P values were determined using analysis of variance and post hoc Tukey’s test: ****P , .0001. (E) DHL4 stably transduced with indicated shRNAs were further transduced with the pMIG-HA-DREAM-IRES-GFP vector. GFP1 cells were then FACS sorted and treated with R406 or vehicle alone. After 24 hours of incubation, cells were analyzed for FOXO1 and DREAM expression by immunoblotting. GAPDH served as a loading control. Densitometric quantification of band intensities is provided in supplemental Table 8.

Journal: Blood

Article Title: FOXO1 activation is an effector of SYK and AKT inhibition in tonic BCR signal-dependent diffuse large B-cell lymphomas.

doi: 10.1182/blood-2015-06-654111

Figure Lengend Snippet: Figure 4. FOXO1 mediates toxicity of SYK inhibitor in tonic BCR signal-dependent DLBCL cells. (A) Transcript abundance of FOXO1 target genes, BIM, TRAIL, GADD45a, and CDKN1B (p27Kip1) in cell lines transduced with FOXO1-targeting or control shRNA vectors, assessed by qRT-PCR after 24-hour incubation with R406. (B) SREBP1 expression following incubation with R406 was assessed as described above. (C) Transcript abundance of HRK in DHL4 and Ly7 cell lines transduced with scrambled control shRNA (Scr) or FOXO1-targeting shRNA following 24-hour incubation with R406. P values in A to C were determined using a 2-sided Gosset’s t test: *P , .05; **P , .01; ***P , .001; ****P , .0001. (D) HRK expression was determined after 24-hour treatment with vehicle alone (DMSO), R406, or a combination of SYK and pan-caspase inhibitor (Z-VAD-FMK) by qRT-PCR relative to GAPDH. P values were determined using analysis of variance and post hoc Tukey’s test: ****P , .0001. (E) DHL4 stably transduced with indicated shRNAs were further transduced with the pMIG-HA-DREAM-IRES-GFP vector. GFP1 cells were then FACS sorted and treated with R406 or vehicle alone. After 24 hours of incubation, cells were analyzed for FOXO1 and DREAM expression by immunoblotting. GAPDH served as a loading control. Densitometric quantification of band intensities is provided in supplemental Table 8.

Techniques: Transduction, Control, shRNA, Quantitative RT-PCR, Incubation, Expressing, Stable Transfection, Plasmid Preparation, Western Blot

Figure 5. FOXO1 is essential for R406 and the MK2206 synergistic effect in tonic BCR signal-dependent DLBCL cells. (A) Cellular proliferation was assessed in DLBCL cell lines following 72-hour incubation with indicated concentrations of R406 and MK2206 by MTS. (B) DHL4 and Ly7 cells transduced with indicated shRNA vectors were treated and analyzed as described above. For further information please refer to supplemental Tables 9 and 10.

Journal: Blood

Article Title: FOXO1 activation is an effector of SYK and AKT inhibition in tonic BCR signal-dependent diffuse large B-cell lymphomas.

doi: 10.1182/blood-2015-06-654111

Figure Lengend Snippet: Figure 5. FOXO1 is essential for R406 and the MK2206 synergistic effect in tonic BCR signal-dependent DLBCL cells. (A) Cellular proliferation was assessed in DLBCL cell lines following 72-hour incubation with indicated concentrations of R406 and MK2206 by MTS. (B) DHL4 and Ly7 cells transduced with indicated shRNA vectors were treated and analyzed as described above. For further information please refer to supplemental Tables 9 and 10.

Techniques: Incubation, Transduction, shRNA

Figure 6. Expression and clinical significance of FOXO1 in primary DLBCLs. (A) Immunohistochemical analysis of FOXO1 and phospho-SYK (Y525/6) expression in DLBCL samples. Shown are representative cases with positive and negative staining. Pictures were taken with 360 objective. For the tabular represen- tation of the immunohistochemical analysis of FOXO1 and phospho-SYK expression performed in a panel of 60 DLBCL patients, please see supplemental Table 11. (B) Overall survival of DLBCL patients with respect to FOXO1 expression.

Journal: Blood

Article Title: FOXO1 activation is an effector of SYK and AKT inhibition in tonic BCR signal-dependent diffuse large B-cell lymphomas.

doi: 10.1182/blood-2015-06-654111

Figure Lengend Snippet: Figure 6. Expression and clinical significance of FOXO1 in primary DLBCLs. (A) Immunohistochemical analysis of FOXO1 and phospho-SYK (Y525/6) expression in DLBCL samples. Shown are representative cases with positive and negative staining. Pictures were taken with 360 objective. For the tabular represen- tation of the immunohistochemical analysis of FOXO1 and phospho-SYK expression performed in a panel of 60 DLBCL patients, please see supplemental Table 11. (B) Overall survival of DLBCL patients with respect to FOXO1 expression.

Techniques: Expressing, Immunohistochemical staining, Negative Staining

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