anti exportin 5  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti exportin 5
    Anti Exportin 5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti exportin 5/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
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    anti exportin 5  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti exportin 5
    Anti Exportin 5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti exportin 5/product/Cell Signaling Technology Inc
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    anti xpo5  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti xpo5
    Anti Xpo5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti xpo5/product/Cell Signaling Technology Inc
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    xpo5  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc xpo5
    a Diagram showing the Spearman’s correlation of top co-dependent proteins with ANKRD52 or PPP6C in CRISPR (Avana) Public 20Q3 database. Solid lines depict significant positive correlations (Correlation > 0.25, P < 0.001) and dashed lines depict weak correlation (Correlation > 0.1, P < 0.01). b , c Volcano plot showing the Spearman’s correlation and estimated significance of DICER1 ( b ) or <t>XPO5</t> ( c ) with SOCS1 mRNA levels from RNA-seq data across all TCGA cancer types. Each dot represents a cancer type in TCGA; blue dots indicate significant negative correlations ( P < 0.05, TIMER). d SOCS1 mRNA level in MC38 cells with targeted sgRNAs ( n = 3 per group). Data are representative of three independent experiments and represented as mean ± s.e.m., significance was determined using two-tailed unpaired Student’s t -test. e Killing of OVA-treated MC38 cells with targeted sgRNAs by OT-I T cells ( n = 3 per group per condition). Data are representative of two independent experiments and represented as mean ± s.d., significance was determined using two-tailed unpaired Student’s t -test. f Tumor growth curves of Ago2 -null or control MC38 tumors in WT mice treated with PD-1 antibody or not ( n = 5 for NT tumor, n = 6 for NT with anti-PD-1 and n = 7 for Ago2 -null with or without anti-PD-1). Data are represented as mean ± s.e.m., significance was determined using two-tailed unpaired Student’s t -test. g Heatmap showing the Spearman’s correlation of ANKRD52 , AGO2 , DICER1 , XPO5 , DROSHA , PPP6C , or SOCS1 mRNA levels with CD4 + and CD8 + T cell abundance in tumors across all TCGA cancer types. h Model of miRNA machinery in regulation of cancer-intrinsic evasion from T cell attack. See also Supplementary Figs. – . Source data are provided as a source data file.
    Xpo5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    xpo5 - by Bioz Stars, 2023-01
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    1) Product Images from "Tumor evolution selectively inactivates the core microRNA machinery for immune evasion"

    Article Title: Tumor evolution selectively inactivates the core microRNA machinery for immune evasion

    Journal: Nature Communications

    doi: 10.1038/s41467-021-27331-3

    a Diagram showing the Spearman’s correlation of top co-dependent proteins with ANKRD52 or PPP6C in CRISPR (Avana) Public 20Q3 database. Solid lines depict significant positive correlations (Correlation > 0.25, P < 0.001) and dashed lines depict weak correlation (Correlation > 0.1, P < 0.01). b , c Volcano plot showing the Spearman’s correlation and estimated significance of DICER1 ( b ) or XPO5 ( c ) with SOCS1 mRNA levels from RNA-seq data across all TCGA cancer types. Each dot represents a cancer type in TCGA; blue dots indicate significant negative correlations ( P < 0.05, TIMER). d SOCS1 mRNA level in MC38 cells with targeted sgRNAs ( n = 3 per group). Data are representative of three independent experiments and represented as mean ± s.e.m., significance was determined using two-tailed unpaired Student’s t -test. e Killing of OVA-treated MC38 cells with targeted sgRNAs by OT-I T cells ( n = 3 per group per condition). Data are representative of two independent experiments and represented as mean ± s.d., significance was determined using two-tailed unpaired Student’s t -test. f Tumor growth curves of Ago2 -null or control MC38 tumors in WT mice treated with PD-1 antibody or not ( n = 5 for NT tumor, n = 6 for NT with anti-PD-1 and n = 7 for Ago2 -null with or without anti-PD-1). Data are represented as mean ± s.e.m., significance was determined using two-tailed unpaired Student’s t -test. g Heatmap showing the Spearman’s correlation of ANKRD52 , AGO2 , DICER1 , XPO5 , DROSHA , PPP6C , or SOCS1 mRNA levels with CD4 + and CD8 + T cell abundance in tumors across all TCGA cancer types. h Model of miRNA machinery in regulation of cancer-intrinsic evasion from T cell attack. See also Supplementary Figs. – . Source data are provided as a source data file.
    Figure Legend Snippet: a Diagram showing the Spearman’s correlation of top co-dependent proteins with ANKRD52 or PPP6C in CRISPR (Avana) Public 20Q3 database. Solid lines depict significant positive correlations (Correlation > 0.25, P < 0.001) and dashed lines depict weak correlation (Correlation > 0.1, P < 0.01). b , c Volcano plot showing the Spearman’s correlation and estimated significance of DICER1 ( b ) or XPO5 ( c ) with SOCS1 mRNA levels from RNA-seq data across all TCGA cancer types. Each dot represents a cancer type in TCGA; blue dots indicate significant negative correlations ( P < 0.05, TIMER). d SOCS1 mRNA level in MC38 cells with targeted sgRNAs ( n = 3 per group). Data are representative of three independent experiments and represented as mean ± s.e.m., significance was determined using two-tailed unpaired Student’s t -test. e Killing of OVA-treated MC38 cells with targeted sgRNAs by OT-I T cells ( n = 3 per group per condition). Data are representative of two independent experiments and represented as mean ± s.d., significance was determined using two-tailed unpaired Student’s t -test. f Tumor growth curves of Ago2 -null or control MC38 tumors in WT mice treated with PD-1 antibody or not ( n = 5 for NT tumor, n = 6 for NT with anti-PD-1 and n = 7 for Ago2 -null with or without anti-PD-1). Data are represented as mean ± s.e.m., significance was determined using two-tailed unpaired Student’s t -test. g Heatmap showing the Spearman’s correlation of ANKRD52 , AGO2 , DICER1 , XPO5 , DROSHA , PPP6C , or SOCS1 mRNA levels with CD4 + and CD8 + T cell abundance in tumors across all TCGA cancer types. h Model of miRNA machinery in regulation of cancer-intrinsic evasion from T cell attack. See also Supplementary Figs. – . Source data are provided as a source data file.

    Techniques Used: CRISPR, RNA Sequencing Assay, Two Tailed Test

    exportin 5  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc exportin 5
    a Immunoblotting of Dicer, Drosha, DGCR8, <t>Exportin-5,</t> and β-actin in LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer. b Clonogenic survival assays of LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer after X-ray ionizing radiation (IR) treatment. n = 3 wells per group. c Immunoblotting of DGCR8, Drosha, Exportin-5, Dicer, γH2AX, H2AX, and β-actin in LM2 cells collected at the indicated times after X-ray IR treatment. Quantification results were normalized to β-actin. d Immunoblotting of Drosha, DGCR8, and β-actin (left panel) and clonogenic survival assays (right panel) of LM2 stable cell lines overexpressing GFP, wild-type (WT) DGCR8, or Δ692-DGCR8 (the Drosha binding-deficient mutant). n = 3 wells per group. e Schematic representation of the generation of radioresistant sublines (LM2-R and MCF-7-R) from parental LM2 and MCF-7 breast cancer cell lines by three rounds of X-ray irradiation. f Clonogenic survival assays of parental LM2 and LM2-R cells after X-ray IR treatment. n = 3 wells per group. g Immunoblotting of γH2AX, H2AX, and β-actin in parental LM2 and LM2-R cells collected at the indicated times after IR. h Immunoblotting of DGCR8, Drosha, Dicer, Exportin-5, and β-actin in LM2 and LM2-R cells collected at the indicated times after IR. LE long exposure, SE short exposure. Quantification results were normalized to β-actin. i , j Immunoblotting of DGCR8 and β-actin ( i ) and clonogenic survival assays ( j ) of control or DGCR8-knockdown LM2-R cells transduced with GFP, WT DGCR8, or Δ692-DGCR8. n = 3 wells per group. k Tumor size of mice bearing xenograft tumors formed by control or DGCR8-knockdown LM2-R cells transduced with WT DGCR8 or Δ692-DGCR8, with or without fractionated doses of localized X-ray IR treatment (XRT) using an X-RAD 320 irradiator. n = 5 mice per group. l Kaplan–Meier curves of relapse-free survival of breast cancer patients (dataset: GSE2034; n = 286 patients, 87% of whom received radiotherapy), stratified by DGCR8 expression levels. Data were generated from the KM Plotter (probes: 64474_g_at in the left panel and 91617_at in the right panel). The auto-select best cutoff was used in the analysis. Statistical significance was determined by a log-rank test. HR hazard ratio. Statistical significance in b , d , f , j , and k was determined by a two-tailed unpaired t -test. Error bars are mean ± SEM. Source data are provided as a file.
    Exportin 5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/exportin 5/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
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    exportin 5 - by Bioz Stars, 2023-01
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    Images

    1) Product Images from "Non-canonical function of DGCR8 in DNA double-strand break repair signaling and tumor radioresistance"

    Article Title: Non-canonical function of DGCR8 in DNA double-strand break repair signaling and tumor radioresistance

    Journal: Nature Communications

    doi: 10.1038/s41467-021-24298-z

    a Immunoblotting of Dicer, Drosha, DGCR8, Exportin-5, and β-actin in LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer. b Clonogenic survival assays of LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer after X-ray ionizing radiation (IR) treatment. n = 3 wells per group. c Immunoblotting of DGCR8, Drosha, Exportin-5, Dicer, γH2AX, H2AX, and β-actin in LM2 cells collected at the indicated times after X-ray IR treatment. Quantification results were normalized to β-actin. d Immunoblotting of Drosha, DGCR8, and β-actin (left panel) and clonogenic survival assays (right panel) of LM2 stable cell lines overexpressing GFP, wild-type (WT) DGCR8, or Δ692-DGCR8 (the Drosha binding-deficient mutant). n = 3 wells per group. e Schematic representation of the generation of radioresistant sublines (LM2-R and MCF-7-R) from parental LM2 and MCF-7 breast cancer cell lines by three rounds of X-ray irradiation. f Clonogenic survival assays of parental LM2 and LM2-R cells after X-ray IR treatment. n = 3 wells per group. g Immunoblotting of γH2AX, H2AX, and β-actin in parental LM2 and LM2-R cells collected at the indicated times after IR. h Immunoblotting of DGCR8, Drosha, Dicer, Exportin-5, and β-actin in LM2 and LM2-R cells collected at the indicated times after IR. LE long exposure, SE short exposure. Quantification results were normalized to β-actin. i , j Immunoblotting of DGCR8 and β-actin ( i ) and clonogenic survival assays ( j ) of control or DGCR8-knockdown LM2-R cells transduced with GFP, WT DGCR8, or Δ692-DGCR8. n = 3 wells per group. k Tumor size of mice bearing xenograft tumors formed by control or DGCR8-knockdown LM2-R cells transduced with WT DGCR8 or Δ692-DGCR8, with or without fractionated doses of localized X-ray IR treatment (XRT) using an X-RAD 320 irradiator. n = 5 mice per group. l Kaplan–Meier curves of relapse-free survival of breast cancer patients (dataset: GSE2034; n = 286 patients, 87% of whom received radiotherapy), stratified by DGCR8 expression levels. Data were generated from the KM Plotter (probes: 64474_g_at in the left panel and 91617_at in the right panel). The auto-select best cutoff was used in the analysis. Statistical significance was determined by a log-rank test. HR hazard ratio. Statistical significance in b , d , f , j , and k was determined by a two-tailed unpaired t -test. Error bars are mean ± SEM. Source data are provided as a file.
    Figure Legend Snippet: a Immunoblotting of Dicer, Drosha, DGCR8, Exportin-5, and β-actin in LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer. b Clonogenic survival assays of LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer after X-ray ionizing radiation (IR) treatment. n = 3 wells per group. c Immunoblotting of DGCR8, Drosha, Exportin-5, Dicer, γH2AX, H2AX, and β-actin in LM2 cells collected at the indicated times after X-ray IR treatment. Quantification results were normalized to β-actin. d Immunoblotting of Drosha, DGCR8, and β-actin (left panel) and clonogenic survival assays (right panel) of LM2 stable cell lines overexpressing GFP, wild-type (WT) DGCR8, or Δ692-DGCR8 (the Drosha binding-deficient mutant). n = 3 wells per group. e Schematic representation of the generation of radioresistant sublines (LM2-R and MCF-7-R) from parental LM2 and MCF-7 breast cancer cell lines by three rounds of X-ray irradiation. f Clonogenic survival assays of parental LM2 and LM2-R cells after X-ray IR treatment. n = 3 wells per group. g Immunoblotting of γH2AX, H2AX, and β-actin in parental LM2 and LM2-R cells collected at the indicated times after IR. h Immunoblotting of DGCR8, Drosha, Dicer, Exportin-5, and β-actin in LM2 and LM2-R cells collected at the indicated times after IR. LE long exposure, SE short exposure. Quantification results were normalized to β-actin. i , j Immunoblotting of DGCR8 and β-actin ( i ) and clonogenic survival assays ( j ) of control or DGCR8-knockdown LM2-R cells transduced with GFP, WT DGCR8, or Δ692-DGCR8. n = 3 wells per group. k Tumor size of mice bearing xenograft tumors formed by control or DGCR8-knockdown LM2-R cells transduced with WT DGCR8 or Δ692-DGCR8, with or without fractionated doses of localized X-ray IR treatment (XRT) using an X-RAD 320 irradiator. n = 5 mice per group. l Kaplan–Meier curves of relapse-free survival of breast cancer patients (dataset: GSE2034; n = 286 patients, 87% of whom received radiotherapy), stratified by DGCR8 expression levels. Data were generated from the KM Plotter (probes: 64474_g_at in the left panel and 91617_at in the right panel). The auto-select best cutoff was used in the analysis. Statistical significance was determined by a log-rank test. HR hazard ratio. Statistical significance in b , d , f , j , and k was determined by a two-tailed unpaired t -test. Error bars are mean ± SEM. Source data are provided as a file.

    Techniques Used: Western Blot, Transduction, Stable Transfection, Binding Assay, Mutagenesis, Irradiation, Expressing, Generated, Two Tailed Test

    xpo5  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc xpo5
    Erk2 regulates the output of miR-549a via <t>XPO5.</t> (A) Cytosolic and nuclear protein were prepared and analyzed for XPO5 expression in 786-O and 786-O-SR by Western blot. (B) Western blot analysis of Erk1/2 expression in 786-O and 786-O-SR and the detection of overexpression efficiency of Erk2 in 786-O. (C) RT-PCR and gel electrophoresis of PCR products analysis of pre-miR-549a expression in 786-O/786-O-SR cells. (D) Cytosolic and nuclear XPO5 expression in 786-O and Erk2 overexpressing 786-O by Western blotting. (E,F) RT-PCR and gel electrophoresis of PCR products analysis of pre-miR-549a expression in 786-O/786-O-SR exosomes (E) and HUVECs treated with exosomes (F) . ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 according to two-tailed Student’s t -test.
    Xpo5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "TKI-Resistant Renal Cancer Secretes Low-Level Exosomal miR-549a to Induce Vascular Permeability and Angiogenesis to Promote Tumor Metastasis"

    Article Title: TKI-Resistant Renal Cancer Secretes Low-Level Exosomal miR-549a to Induce Vascular Permeability and Angiogenesis to Promote Tumor Metastasis

    Journal: Frontiers in Cell and Developmental Biology

    doi: 10.3389/fcell.2021.689947

    Erk2 regulates the output of miR-549a via XPO5. (A) Cytosolic and nuclear protein were prepared and analyzed for XPO5 expression in 786-O and 786-O-SR by Western blot. (B) Western blot analysis of Erk1/2 expression in 786-O and 786-O-SR and the detection of overexpression efficiency of Erk2 in 786-O. (C) RT-PCR and gel electrophoresis of PCR products analysis of pre-miR-549a expression in 786-O/786-O-SR cells. (D) Cytosolic and nuclear XPO5 expression in 786-O and Erk2 overexpressing 786-O by Western blotting. (E,F) RT-PCR and gel electrophoresis of PCR products analysis of pre-miR-549a expression in 786-O/786-O-SR exosomes (E) and HUVECs treated with exosomes (F) . ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 according to two-tailed Student’s t -test.
    Figure Legend Snippet: Erk2 regulates the output of miR-549a via XPO5. (A) Cytosolic and nuclear protein were prepared and analyzed for XPO5 expression in 786-O and 786-O-SR by Western blot. (B) Western blot analysis of Erk1/2 expression in 786-O and 786-O-SR and the detection of overexpression efficiency of Erk2 in 786-O. (C) RT-PCR and gel electrophoresis of PCR products analysis of pre-miR-549a expression in 786-O/786-O-SR cells. (D) Cytosolic and nuclear XPO5 expression in 786-O and Erk2 overexpressing 786-O by Western blotting. (E,F) RT-PCR and gel electrophoresis of PCR products analysis of pre-miR-549a expression in 786-O/786-O-SR exosomes (E) and HUVECs treated with exosomes (F) . ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001 according to two-tailed Student’s t -test.

    Techniques Used: Expressing, Western Blot, Over Expression, Reverse Transcription Polymerase Chain Reaction, Nucleic Acid Electrophoresis, Two Tailed Test

    exportin 5  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc exportin 5
    IsoSeek has reduced bias in detecting isomiRs A) Distribution of 30 isomiR spike-ins added to pEV RNA prior to library preparation using NEBNext (left) and 5N-adapters without (middle) and with UMI correction (IsoSeek, right). Representative data is shown for each procedure) including the coefficient of variation (CoV). B) NTA distribution in libraries prepared from 293T WT and TUT4/7 DKO cells using NEBNext (left panel) and IsoSeek (middle panel) and HCT116 WT, Drosha KO, <t>XPO5</t> KO, Dicer KO and Ago2 KO cells using IsoSeek (right panel). C) Percentage of uridylation of miRNAs derived from the 3p arm (purple) or the 5p arm (green) in 293T WT and TUT4/7 DKO cells after library preparation using IsoSeek (upper panel) or NEBNext (lower panel). D-E) Differential expression analysis of uridylated miRNAs (NTA#U) in TUT4/7 DKO cells vs 293T WT. Libraries were prepared using IsoSeek (D) and NEBNext (E). Each dot represents an individual uridylated isomiR. All miRNAs detected in the 293T WT cells were included in the analysis. F) Top 10 of the most highly uridylated miRNAs in 293T cells after library preparation using IsoSeek. Data is shown as percentage of total reads and the number of additional uridines is shown separately. Analysis includes miRNAs >= 10 RPM (total reads) in all samples. G) Top 10 of the uridylated miRNAs in 293T cells that mostly depend on TUT4/7 based on IsoSeek. The miRNAs shown decrease the most in TUT4/7 DKO cells compared to WT cells. Data is shown as percentage of total reads and the number of additional uridines is shown separately. Analysis includes miRNAs >= 10 RPM (total reads) in all samples. H) Percentage of uridylation of miR-3127-3p (upper panel) and miR-30e-3p (lower panel) in 293T WT and TUT4/7 DKO cells. Libraries were prepared with NEBNext or IsoSeek as indicated. Analysis includes miRNAs >= 10 RPM (total reads) in all samples.
    Exportin 5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/exportin 5/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    exportin 5 - by Bioz Stars, 2023-01
    94/100 stars

    Images

    1) Product Images from "Unbiased and UMI-informed sequencing of cell-free miRNAs at single-nucleotide resolution"

    Article Title: Unbiased and UMI-informed sequencing of cell-free miRNAs at single-nucleotide resolution

    Journal: bioRxiv

    doi: 10.1101/2021.05.04.442244

    IsoSeek has reduced bias in detecting isomiRs A) Distribution of 30 isomiR spike-ins added to pEV RNA prior to library preparation using NEBNext (left) and 5N-adapters without (middle) and with UMI correction (IsoSeek, right). Representative data is shown for each procedure) including the coefficient of variation (CoV). B) NTA distribution in libraries prepared from 293T WT and TUT4/7 DKO cells using NEBNext (left panel) and IsoSeek (middle panel) and HCT116 WT, Drosha KO, XPO5 KO, Dicer KO and Ago2 KO cells using IsoSeek (right panel). C) Percentage of uridylation of miRNAs derived from the 3p arm (purple) or the 5p arm (green) in 293T WT and TUT4/7 DKO cells after library preparation using IsoSeek (upper panel) or NEBNext (lower panel). D-E) Differential expression analysis of uridylated miRNAs (NTA#U) in TUT4/7 DKO cells vs 293T WT. Libraries were prepared using IsoSeek (D) and NEBNext (E). Each dot represents an individual uridylated isomiR. All miRNAs detected in the 293T WT cells were included in the analysis. F) Top 10 of the most highly uridylated miRNAs in 293T cells after library preparation using IsoSeek. Data is shown as percentage of total reads and the number of additional uridines is shown separately. Analysis includes miRNAs >= 10 RPM (total reads) in all samples. G) Top 10 of the uridylated miRNAs in 293T cells that mostly depend on TUT4/7 based on IsoSeek. The miRNAs shown decrease the most in TUT4/7 DKO cells compared to WT cells. Data is shown as percentage of total reads and the number of additional uridines is shown separately. Analysis includes miRNAs >= 10 RPM (total reads) in all samples. H) Percentage of uridylation of miR-3127-3p (upper panel) and miR-30e-3p (lower panel) in 293T WT and TUT4/7 DKO cells. Libraries were prepared with NEBNext or IsoSeek as indicated. Analysis includes miRNAs >= 10 RPM (total reads) in all samples.
    Figure Legend Snippet: IsoSeek has reduced bias in detecting isomiRs A) Distribution of 30 isomiR spike-ins added to pEV RNA prior to library preparation using NEBNext (left) and 5N-adapters without (middle) and with UMI correction (IsoSeek, right). Representative data is shown for each procedure) including the coefficient of variation (CoV). B) NTA distribution in libraries prepared from 293T WT and TUT4/7 DKO cells using NEBNext (left panel) and IsoSeek (middle panel) and HCT116 WT, Drosha KO, XPO5 KO, Dicer KO and Ago2 KO cells using IsoSeek (right panel). C) Percentage of uridylation of miRNAs derived from the 3p arm (purple) or the 5p arm (green) in 293T WT and TUT4/7 DKO cells after library preparation using IsoSeek (upper panel) or NEBNext (lower panel). D-E) Differential expression analysis of uridylated miRNAs (NTA#U) in TUT4/7 DKO cells vs 293T WT. Libraries were prepared using IsoSeek (D) and NEBNext (E). Each dot represents an individual uridylated isomiR. All miRNAs detected in the 293T WT cells were included in the analysis. F) Top 10 of the most highly uridylated miRNAs in 293T cells after library preparation using IsoSeek. Data is shown as percentage of total reads and the number of additional uridines is shown separately. Analysis includes miRNAs >= 10 RPM (total reads) in all samples. G) Top 10 of the uridylated miRNAs in 293T cells that mostly depend on TUT4/7 based on IsoSeek. The miRNAs shown decrease the most in TUT4/7 DKO cells compared to WT cells. Data is shown as percentage of total reads and the number of additional uridines is shown separately. Analysis includes miRNAs >= 10 RPM (total reads) in all samples. H) Percentage of uridylation of miR-3127-3p (upper panel) and miR-30e-3p (lower panel) in 293T WT and TUT4/7 DKO cells. Libraries were prepared with NEBNext or IsoSeek as indicated. Analysis includes miRNAs >= 10 RPM (total reads) in all samples.

    Techniques Used: Derivative Assay, Expressing

    anti exportin 5  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc anti exportin 5
    Effective suppression of Pin1 in Hep3B cells by GalNAc‐Pin1 siRNA/DP7‐C transfection in vitro. A, Schematic diagram. B, Pin1 mRNA expression in Hep3B cells quantified by qPCR. C, Pin1 protein expression in Hep3B cells quantified by western blot. D, Western blot assay of <t>XPO5</t> subcellular distribution in Hep3B cells. Expression of related mature miRNAs, including (E) miR‐122, (F) miRNA Let‐7a, (G) miR‐146a and (H) miR‐29b, was analyzed using qPCR. Data are expressed as the mean ± SEM. * P < .05, ** P < .01, *** P < .001
    Anti Exportin 5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Sustained and targeted delivery of siRNA/DP7‐C nanoparticles from injectable thermosensitive hydrogel for hepatocellular carcinoma therapy"

    Article Title: Sustained and targeted delivery of siRNA/DP7‐C nanoparticles from injectable thermosensitive hydrogel for hepatocellular carcinoma therapy

    Journal: Cancer Science

    doi: 10.1111/cas.14903

    Effective suppression of Pin1 in Hep3B cells by GalNAc‐Pin1 siRNA/DP7‐C transfection in vitro. A, Schematic diagram. B, Pin1 mRNA expression in Hep3B cells quantified by qPCR. C, Pin1 protein expression in Hep3B cells quantified by western blot. D, Western blot assay of XPO5 subcellular distribution in Hep3B cells. Expression of related mature miRNAs, including (E) miR‐122, (F) miRNA Let‐7a, (G) miR‐146a and (H) miR‐29b, was analyzed using qPCR. Data are expressed as the mean ± SEM. * P < .05, ** P < .01, *** P < .001
    Figure Legend Snippet: Effective suppression of Pin1 in Hep3B cells by GalNAc‐Pin1 siRNA/DP7‐C transfection in vitro. A, Schematic diagram. B, Pin1 mRNA expression in Hep3B cells quantified by qPCR. C, Pin1 protein expression in Hep3B cells quantified by western blot. D, Western blot assay of XPO5 subcellular distribution in Hep3B cells. Expression of related mature miRNAs, including (E) miR‐122, (F) miRNA Let‐7a, (G) miR‐146a and (H) miR‐29b, was analyzed using qPCR. Data are expressed as the mean ± SEM. * P < .05, ** P < .01, *** P < .001

    Techniques Used: Transfection, In Vitro, Expressing, Western Blot

    anti exportin5 antibody  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc anti exportin5 antibody
    Anti Exportin5 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti exportin5 antibody/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
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    Cell Signaling Technology Inc anti exportin 5
    Anti Exportin 5, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc xpo5
    a Diagram showing the Spearman’s correlation of top co-dependent proteins with ANKRD52 or PPP6C in CRISPR (Avana) Public 20Q3 database. Solid lines depict significant positive correlations (Correlation > 0.25, P < 0.001) and dashed lines depict weak correlation (Correlation > 0.1, P < 0.01). b , c Volcano plot showing the Spearman’s correlation and estimated significance of DICER1 ( b ) or <t>XPO5</t> ( c ) with SOCS1 mRNA levels from RNA-seq data across all TCGA cancer types. Each dot represents a cancer type in TCGA; blue dots indicate significant negative correlations ( P < 0.05, TIMER). d SOCS1 mRNA level in MC38 cells with targeted sgRNAs ( n = 3 per group). Data are representative of three independent experiments and represented as mean ± s.e.m., significance was determined using two-tailed unpaired Student’s t -test. e Killing of OVA-treated MC38 cells with targeted sgRNAs by OT-I T cells ( n = 3 per group per condition). Data are representative of two independent experiments and represented as mean ± s.d., significance was determined using two-tailed unpaired Student’s t -test. f Tumor growth curves of Ago2 -null or control MC38 tumors in WT mice treated with PD-1 antibody or not ( n = 5 for NT tumor, n = 6 for NT with anti-PD-1 and n = 7 for Ago2 -null with or without anti-PD-1). Data are represented as mean ± s.e.m., significance was determined using two-tailed unpaired Student’s t -test. g Heatmap showing the Spearman’s correlation of ANKRD52 , AGO2 , DICER1 , XPO5 , DROSHA , PPP6C , or SOCS1 mRNA levels with CD4 + and CD8 + T cell abundance in tumors across all TCGA cancer types. h Model of miRNA machinery in regulation of cancer-intrinsic evasion from T cell attack. See also Supplementary Figs. – . Source data are provided as a source data file.
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    Cell Signaling Technology Inc exportin 5
    a Immunoblotting of Dicer, Drosha, DGCR8, <t>Exportin-5,</t> and β-actin in LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer. b Clonogenic survival assays of LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer after X-ray ionizing radiation (IR) treatment. n = 3 wells per group. c Immunoblotting of DGCR8, Drosha, Exportin-5, Dicer, γH2AX, H2AX, and β-actin in LM2 cells collected at the indicated times after X-ray IR treatment. Quantification results were normalized to β-actin. d Immunoblotting of Drosha, DGCR8, and β-actin (left panel) and clonogenic survival assays (right panel) of LM2 stable cell lines overexpressing GFP, wild-type (WT) DGCR8, or Δ692-DGCR8 (the Drosha binding-deficient mutant). n = 3 wells per group. e Schematic representation of the generation of radioresistant sublines (LM2-R and MCF-7-R) from parental LM2 and MCF-7 breast cancer cell lines by three rounds of X-ray irradiation. f Clonogenic survival assays of parental LM2 and LM2-R cells after X-ray IR treatment. n = 3 wells per group. g Immunoblotting of γH2AX, H2AX, and β-actin in parental LM2 and LM2-R cells collected at the indicated times after IR. h Immunoblotting of DGCR8, Drosha, Dicer, Exportin-5, and β-actin in LM2 and LM2-R cells collected at the indicated times after IR. LE long exposure, SE short exposure. Quantification results were normalized to β-actin. i , j Immunoblotting of DGCR8 and β-actin ( i ) and clonogenic survival assays ( j ) of control or DGCR8-knockdown LM2-R cells transduced with GFP, WT DGCR8, or Δ692-DGCR8. n = 3 wells per group. k Tumor size of mice bearing xenograft tumors formed by control or DGCR8-knockdown LM2-R cells transduced with WT DGCR8 or Δ692-DGCR8, with or without fractionated doses of localized X-ray IR treatment (XRT) using an X-RAD 320 irradiator. n = 5 mice per group. l Kaplan–Meier curves of relapse-free survival of breast cancer patients (dataset: GSE2034; n = 286 patients, 87% of whom received radiotherapy), stratified by DGCR8 expression levels. Data were generated from the KM Plotter (probes: 64474_g_at in the left panel and 91617_at in the right panel). The auto-select best cutoff was used in the analysis. Statistical significance was determined by a log-rank test. HR hazard ratio. Statistical significance in b , d , f , j , and k was determined by a two-tailed unpaired t -test. Error bars are mean ± SEM. Source data are provided as a file.
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    Cell Signaling Technology Inc anti exportin5 antibody
    a Immunoblotting of Dicer, Drosha, DGCR8, <t>Exportin-5,</t> and β-actin in LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer. b Clonogenic survival assays of LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer after X-ray ionizing radiation (IR) treatment. n = 3 wells per group. c Immunoblotting of DGCR8, Drosha, Exportin-5, Dicer, γH2AX, H2AX, and β-actin in LM2 cells collected at the indicated times after X-ray IR treatment. Quantification results were normalized to β-actin. d Immunoblotting of Drosha, DGCR8, and β-actin (left panel) and clonogenic survival assays (right panel) of LM2 stable cell lines overexpressing GFP, wild-type (WT) DGCR8, or Δ692-DGCR8 (the Drosha binding-deficient mutant). n = 3 wells per group. e Schematic representation of the generation of radioresistant sublines (LM2-R and MCF-7-R) from parental LM2 and MCF-7 breast cancer cell lines by three rounds of X-ray irradiation. f Clonogenic survival assays of parental LM2 and LM2-R cells after X-ray IR treatment. n = 3 wells per group. g Immunoblotting of γH2AX, H2AX, and β-actin in parental LM2 and LM2-R cells collected at the indicated times after IR. h Immunoblotting of DGCR8, Drosha, Dicer, Exportin-5, and β-actin in LM2 and LM2-R cells collected at the indicated times after IR. LE long exposure, SE short exposure. Quantification results were normalized to β-actin. i , j Immunoblotting of DGCR8 and β-actin ( i ) and clonogenic survival assays ( j ) of control or DGCR8-knockdown LM2-R cells transduced with GFP, WT DGCR8, or Δ692-DGCR8. n = 3 wells per group. k Tumor size of mice bearing xenograft tumors formed by control or DGCR8-knockdown LM2-R cells transduced with WT DGCR8 or Δ692-DGCR8, with or without fractionated doses of localized X-ray IR treatment (XRT) using an X-RAD 320 irradiator. n = 5 mice per group. l Kaplan–Meier curves of relapse-free survival of breast cancer patients (dataset: GSE2034; n = 286 patients, 87% of whom received radiotherapy), stratified by DGCR8 expression levels. Data were generated from the KM Plotter (probes: 64474_g_at in the left panel and 91617_at in the right panel). The auto-select best cutoff was used in the analysis. Statistical significance was determined by a log-rank test. HR hazard ratio. Statistical significance in b , d , f , j , and k was determined by a two-tailed unpaired t -test. Error bars are mean ± SEM. Source data are provided as a file.
    Anti Exportin5 Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    a Diagram showing the Spearman’s correlation of top co-dependent proteins with ANKRD52 or PPP6C in CRISPR (Avana) Public 20Q3 database. Solid lines depict significant positive correlations (Correlation > 0.25, P < 0.001) and dashed lines depict weak correlation (Correlation > 0.1, P < 0.01). b , c Volcano plot showing the Spearman’s correlation and estimated significance of DICER1 ( b ) or XPO5 ( c ) with SOCS1 mRNA levels from RNA-seq data across all TCGA cancer types. Each dot represents a cancer type in TCGA; blue dots indicate significant negative correlations ( P < 0.05, TIMER). d SOCS1 mRNA level in MC38 cells with targeted sgRNAs ( n = 3 per group). Data are representative of three independent experiments and represented as mean ± s.e.m., significance was determined using two-tailed unpaired Student’s t -test. e Killing of OVA-treated MC38 cells with targeted sgRNAs by OT-I T cells ( n = 3 per group per condition). Data are representative of two independent experiments and represented as mean ± s.d., significance was determined using two-tailed unpaired Student’s t -test. f Tumor growth curves of Ago2 -null or control MC38 tumors in WT mice treated with PD-1 antibody or not ( n = 5 for NT tumor, n = 6 for NT with anti-PD-1 and n = 7 for Ago2 -null with or without anti-PD-1). Data are represented as mean ± s.e.m., significance was determined using two-tailed unpaired Student’s t -test. g Heatmap showing the Spearman’s correlation of ANKRD52 , AGO2 , DICER1 , XPO5 , DROSHA , PPP6C , or SOCS1 mRNA levels with CD4 + and CD8 + T cell abundance in tumors across all TCGA cancer types. h Model of miRNA machinery in regulation of cancer-intrinsic evasion from T cell attack. See also Supplementary Figs. – . Source data are provided as a source data file.

    Journal: Nature Communications

    Article Title: Tumor evolution selectively inactivates the core microRNA machinery for immune evasion

    doi: 10.1038/s41467-021-27331-3

    Figure Lengend Snippet: a Diagram showing the Spearman’s correlation of top co-dependent proteins with ANKRD52 or PPP6C in CRISPR (Avana) Public 20Q3 database. Solid lines depict significant positive correlations (Correlation > 0.25, P < 0.001) and dashed lines depict weak correlation (Correlation > 0.1, P < 0.01). b , c Volcano plot showing the Spearman’s correlation and estimated significance of DICER1 ( b ) or XPO5 ( c ) with SOCS1 mRNA levels from RNA-seq data across all TCGA cancer types. Each dot represents a cancer type in TCGA; blue dots indicate significant negative correlations ( P < 0.05, TIMER). d SOCS1 mRNA level in MC38 cells with targeted sgRNAs ( n = 3 per group). Data are representative of three independent experiments and represented as mean ± s.e.m., significance was determined using two-tailed unpaired Student’s t -test. e Killing of OVA-treated MC38 cells with targeted sgRNAs by OT-I T cells ( n = 3 per group per condition). Data are representative of two independent experiments and represented as mean ± s.d., significance was determined using two-tailed unpaired Student’s t -test. f Tumor growth curves of Ago2 -null or control MC38 tumors in WT mice treated with PD-1 antibody or not ( n = 5 for NT tumor, n = 6 for NT with anti-PD-1 and n = 7 for Ago2 -null with or without anti-PD-1). Data are represented as mean ± s.e.m., significance was determined using two-tailed unpaired Student’s t -test. g Heatmap showing the Spearman’s correlation of ANKRD52 , AGO2 , DICER1 , XPO5 , DROSHA , PPP6C , or SOCS1 mRNA levels with CD4 + and CD8 + T cell abundance in tumors across all TCGA cancer types. h Model of miRNA machinery in regulation of cancer-intrinsic evasion from T cell attack. See also Supplementary Figs. – . Source data are provided as a source data file.

    Article Snippet: For western blot, primary antibodies against mouse ANKRD52 (Santa Cruz, sc-398544) and CK1 a (Santa Cruz, sc-6477) were used with dilution as 1:100; human ANKRD52 (Bethyl, A302-372A), OVA (Sigma, SAB5300165), β-Actin (CST, 4967), JAK1 (CST, 3332), p-STAT1 (Tyr701) (CST, 9167), p-STAT3 (Tyr705) (CST, 9145), SOCS3 (CST, 52113), TAP1 (CST, 12341), FLAG (Sigma, F3165), Vinculin (Sigma, v9131), PPP6C (Abcam, EPR8764), AGO2 (CST, 2897 S), XPO5 (CST, 12565 S), and DGCR8 (Abcam, ab191875; Proteintech, 10996-1-AP) were used with dilution as 1:1000.

    Techniques: CRISPR, RNA Sequencing Assay, Two Tailed Test

    a Immunoblotting of Dicer, Drosha, DGCR8, Exportin-5, and β-actin in LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer. b Clonogenic survival assays of LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer after X-ray ionizing radiation (IR) treatment. n = 3 wells per group. c Immunoblotting of DGCR8, Drosha, Exportin-5, Dicer, γH2AX, H2AX, and β-actin in LM2 cells collected at the indicated times after X-ray IR treatment. Quantification results were normalized to β-actin. d Immunoblotting of Drosha, DGCR8, and β-actin (left panel) and clonogenic survival assays (right panel) of LM2 stable cell lines overexpressing GFP, wild-type (WT) DGCR8, or Δ692-DGCR8 (the Drosha binding-deficient mutant). n = 3 wells per group. e Schematic representation of the generation of radioresistant sublines (LM2-R and MCF-7-R) from parental LM2 and MCF-7 breast cancer cell lines by three rounds of X-ray irradiation. f Clonogenic survival assays of parental LM2 and LM2-R cells after X-ray IR treatment. n = 3 wells per group. g Immunoblotting of γH2AX, H2AX, and β-actin in parental LM2 and LM2-R cells collected at the indicated times after IR. h Immunoblotting of DGCR8, Drosha, Dicer, Exportin-5, and β-actin in LM2 and LM2-R cells collected at the indicated times after IR. LE long exposure, SE short exposure. Quantification results were normalized to β-actin. i , j Immunoblotting of DGCR8 and β-actin ( i ) and clonogenic survival assays ( j ) of control or DGCR8-knockdown LM2-R cells transduced with GFP, WT DGCR8, or Δ692-DGCR8. n = 3 wells per group. k Tumor size of mice bearing xenograft tumors formed by control or DGCR8-knockdown LM2-R cells transduced with WT DGCR8 or Δ692-DGCR8, with or without fractionated doses of localized X-ray IR treatment (XRT) using an X-RAD 320 irradiator. n = 5 mice per group. l Kaplan–Meier curves of relapse-free survival of breast cancer patients (dataset: GSE2034; n = 286 patients, 87% of whom received radiotherapy), stratified by DGCR8 expression levels. Data were generated from the KM Plotter (probes: 64474_g_at in the left panel and 91617_at in the right panel). The auto-select best cutoff was used in the analysis. Statistical significance was determined by a log-rank test. HR hazard ratio. Statistical significance in b , d , f , j , and k was determined by a two-tailed unpaired t -test. Error bars are mean ± SEM. Source data are provided as a file.

    Journal: Nature Communications

    Article Title: Non-canonical function of DGCR8 in DNA double-strand break repair signaling and tumor radioresistance

    doi: 10.1038/s41467-021-24298-z

    Figure Lengend Snippet: a Immunoblotting of Dicer, Drosha, DGCR8, Exportin-5, and β-actin in LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer. b Clonogenic survival assays of LM2 cells transduced with GFP, Drosha, DGCR8, Exportin-5, or Dicer after X-ray ionizing radiation (IR) treatment. n = 3 wells per group. c Immunoblotting of DGCR8, Drosha, Exportin-5, Dicer, γH2AX, H2AX, and β-actin in LM2 cells collected at the indicated times after X-ray IR treatment. Quantification results were normalized to β-actin. d Immunoblotting of Drosha, DGCR8, and β-actin (left panel) and clonogenic survival assays (right panel) of LM2 stable cell lines overexpressing GFP, wild-type (WT) DGCR8, or Δ692-DGCR8 (the Drosha binding-deficient mutant). n = 3 wells per group. e Schematic representation of the generation of radioresistant sublines (LM2-R and MCF-7-R) from parental LM2 and MCF-7 breast cancer cell lines by three rounds of X-ray irradiation. f Clonogenic survival assays of parental LM2 and LM2-R cells after X-ray IR treatment. n = 3 wells per group. g Immunoblotting of γH2AX, H2AX, and β-actin in parental LM2 and LM2-R cells collected at the indicated times after IR. h Immunoblotting of DGCR8, Drosha, Dicer, Exportin-5, and β-actin in LM2 and LM2-R cells collected at the indicated times after IR. LE long exposure, SE short exposure. Quantification results were normalized to β-actin. i , j Immunoblotting of DGCR8 and β-actin ( i ) and clonogenic survival assays ( j ) of control or DGCR8-knockdown LM2-R cells transduced with GFP, WT DGCR8, or Δ692-DGCR8. n = 3 wells per group. k Tumor size of mice bearing xenograft tumors formed by control or DGCR8-knockdown LM2-R cells transduced with WT DGCR8 or Δ692-DGCR8, with or without fractionated doses of localized X-ray IR treatment (XRT) using an X-RAD 320 irradiator. n = 5 mice per group. l Kaplan–Meier curves of relapse-free survival of breast cancer patients (dataset: GSE2034; n = 286 patients, 87% of whom received radiotherapy), stratified by DGCR8 expression levels. Data were generated from the KM Plotter (probes: 64474_g_at in the left panel and 91617_at in the right panel). The auto-select best cutoff was used in the analysis. Statistical significance was determined by a log-rank test. HR hazard ratio. Statistical significance in b , d , f , j , and k was determined by a two-tailed unpaired t -test. Error bars are mean ± SEM. Source data are provided as a file.

    Article Snippet: The following antibodies were used: antibodies against DGCR8 (1:2000, Abcam, #ab191875), Dicer (1:1000, Cell Signaling Technology, #5362S), Drosha (1:1000, Cell Signaling Technology, #3364S), Exportin-5 (1:1000, Cell Signaling Technology, #12565), γH2AX (1:1000, Cell Signaling Technology, #9718S), H2AX (1:1000, Cell Signaling Technology, #2595S), H2A (1:1000, Cell Signaling Technology, #2578S), p-CHK1 (1:1000, Cell Signaling Technology, #12302S), CHK1 (1:1000, Cell Signaling Technology, #2360S), p-CHK2 (1:1000, Cell Signaling Technology, #2661S), CHK2 (1:1000, Cell Signaling Technology, #6334S), p-ATM (1:1000, Cell Signaling Technology, #5883S), ATM (1:1000, Cell Signaling Technology, #2873S), p-ATR (1:1000, Cell Signaling Technology, #2853S), ATR (1:1000, Cell Signaling Technology, #2790S), p-S/TQ (1:1000, Cell Signaling Technology, 2851S), MBP (1:1000, Cell Signaling Technology, 2396S), GST (1:1000, Cell Signaling Technology, #2622S), MDC1 (1:1000, R&D Systems, #MAB6497), RNF8 (1:1000, Millipore, #09-813), RNF168 (1:1000, Millipore, #ABE367), USP36 (1:1000, a gift from Dr Masayuki Komada at Tokyo Institute of Technology), USP51 (1:3000, a gift from Dr Sharon Dent at MD Anderson Cancer Center), β-actin (1:1000, Santa Cruz Biotechnology, #sc-47778), FLAG (1:5000, Sigma, #F3165, clone M2), HA (1:2000, Santa Cruz Biotechnology, #sc-7392), and MYC (1:2000, Santa Cruz Biotechnology, #sc-40, clone 9E10).

    Techniques: Western Blot, Transduction, Stable Transfection, Binding Assay, Mutagenesis, Irradiation, Expressing, Generated, Two Tailed Test