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su dhl 5  (ATCC)


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    ATCC su dhl 5
    (A) Ostm1 was silenced in Ba/F3 cells using two independent sgRNAs. Successful knockout of Ostm1 was determined by genomic sequencing, which shows frame-shifting deletion, point mutations, and large-size deletion. (B) Human OSTM1-Flag was reconstituted into sg Ostm1 Ba/F3 cells, which led to the loss of IL3-independence of the sg Ostm1 cells. (C) OSTM1 was silenced in ARH-77 cells using sgRNA. Successful knockout of OSTM1 was determined by genomic sequencing. (C) Silencing OSTM1 in ARH-77 cells promoted cell proliferation. (D) OSTM1 was <t>silenced</t> <t>in</t> <t>SU-DHL-5</t> cells with two sgRNAs. Successful silencing was achieved indicated by decreased mRNA levels, which led to increased cell proliferation. Statistical analysis in panels B , D , and E was done using multiple t-test, one per row. For panel E , one way ANOVA was used. **p<0.01; ***p<0.001.
    Su Dhl 5, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 81 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    su dhl 5 - by Bioz Stars, 2026-02
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    1) Product Images from "OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway"

    Article Title: OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway

    Journal: bioRxiv

    doi: 10.64898/2026.01.23.701155

    (A) Ostm1 was silenced in Ba/F3 cells using two independent sgRNAs. Successful knockout of Ostm1 was determined by genomic sequencing, which shows frame-shifting deletion, point mutations, and large-size deletion. (B) Human OSTM1-Flag was reconstituted into sg Ostm1 Ba/F3 cells, which led to the loss of IL3-independence of the sg Ostm1 cells. (C) OSTM1 was silenced in ARH-77 cells using sgRNA. Successful knockout of OSTM1 was determined by genomic sequencing. (C) Silencing OSTM1 in ARH-77 cells promoted cell proliferation. (D) OSTM1 was silenced in SU-DHL-5 cells with two sgRNAs. Successful silencing was achieved indicated by decreased mRNA levels, which led to increased cell proliferation. Statistical analysis in panels B , D , and E was done using multiple t-test, one per row. For panel E , one way ANOVA was used. **p<0.01; ***p<0.001.
    Figure Legend Snippet: (A) Ostm1 was silenced in Ba/F3 cells using two independent sgRNAs. Successful knockout of Ostm1 was determined by genomic sequencing, which shows frame-shifting deletion, point mutations, and large-size deletion. (B) Human OSTM1-Flag was reconstituted into sg Ostm1 Ba/F3 cells, which led to the loss of IL3-independence of the sg Ostm1 cells. (C) OSTM1 was silenced in ARH-77 cells using sgRNA. Successful knockout of OSTM1 was determined by genomic sequencing. (C) Silencing OSTM1 in ARH-77 cells promoted cell proliferation. (D) OSTM1 was silenced in SU-DHL-5 cells with two sgRNAs. Successful silencing was achieved indicated by decreased mRNA levels, which led to increased cell proliferation. Statistical analysis in panels B , D , and E was done using multiple t-test, one per row. For panel E , one way ANOVA was used. **p<0.01; ***p<0.001.

    Techniques Used: Knock-Out, Genomic Sequencing

    (A) sg Ostm1 and sgControl Ba/F3 cells were subjected to TMT-MS. Volcano plot (log₂ fold change vs. –log₁₀ p-value) was generated using VolcaNoseR. Dashed lines indicate significance cutoffs. Selected proteins involved in hematopoeitic function and differentiation are highlighted in red. (B) KEGG pathway enrichment analysis of proteins involved in sg Ostm1 Ba/F3 cells with-log10(FDR) used as the significance metric. (C) Venn diagram depicting the overlap between proteins enriched in sg Ostm1 cells identified by TMT-MS and OSTM1-interacting partners identified by BioID in Ba/F3 cells. The table shows BioID enrichment scores for Pde3b. (D and E) His-tagged PDE3B and Flag-tagged OSTM1 were co-transfected into HEK293T cells, in the presence or absence of MG132 (10 µM). Co-immunoprecipitation (Co-IP) was performed using anti-His (D) or anti-Flag (E) antibodies, followed by IB. (F) Ostm1 was silenced in Ba/F3 cells, and three independent cell clones were probed for Pde3b by IB. (G) qRT-PCR analysis of sg Ostm1 cell clones showing that Pde3b mRNA levels were not affected by Ostm1 silencing. (H) OSTM1-Flag was stably reconstituted in sg Ostm1 Ba/F3 cell clone #3, and Pde3b was probed by IB. (I) sgControl and sg Ostm1 Ba/F3 cells were treated with cycloheximide (CHX, 100 µg/ml) for the indicated hours. Pde3b was probled by IB and quantified using ImageJ. Pde3b half-life was calculated based on densitometry. Total ubiquitylated proteins were probed as an indicator of global protein turnover following CHX tratment. (J) sgControl and sg Ostm1 Ba/F3 cells were treated with MG132 (10 µM) or chloroquine (100 µM) for indicated hours, in the presence of CHX (100 µg/ml). Pde3b stability was determined by IB. Ubiquitin and Lc3b were probed to confirm the effectiveness of MG132 and CQ treatment. The Pde3b/Gapdh ratio is shown below the blots. (K) sgControl and sg Ostm1 Ba/F3 cells were treated with indicated concenrations of MG132 for 8 h, and Pde3b was detected by IB. (L) PDE3B-His was expressed in sgControl or sg Ostm1 Ba/F3 cells. IP with PDE3B antibody was performed, followed by IB with indicated antibodies. PDE3B-His ubiquitination was detected in sgControl cells and reduced in sg Ostm1 cells. (M) OSTM1-Flag and PDE3B-His were transfected into HEK293T cells, individually or together, along with His-ubiquitin. Cells were treated with MG132 (10 µM) for 8 h prior to IP with PDE3B antibody and IB. (N) OSTM1-Flag and PDE3B-His were expressed separately in HEK293T cells. Cell lysates were used individually or combined for in vitro ubiquitylation assays. OSTM1-Flag promoted both its auto-ubiquitylation and PDE3B ubiquitylation. (O) Spearman correlation analysis of OSTM1 and PDE3B protein abundance across BCL cell lines from different subtypes using CCLE proteomic data. (P) OSTM1-Flag was stably expressed in indicated BCL cell lines. Flag pull-down assays were performed, and interacting proteins were analyzed by IB. (Q and R) OSTM1 was silenced in SU-DHL-5 ( Q ) and ARH-77 ( R ) cell lines. Two clones per cell line were probed for PDE3B by IB. (S) sgControl and sg OSTM1 ARH-77 cells were treated with CHX (100 µg/ml). PDE3B was probed by IB, and its half-life was calculated based on ImageJ densitometric quantification.
    Figure Legend Snippet: (A) sg Ostm1 and sgControl Ba/F3 cells were subjected to TMT-MS. Volcano plot (log₂ fold change vs. –log₁₀ p-value) was generated using VolcaNoseR. Dashed lines indicate significance cutoffs. Selected proteins involved in hematopoeitic function and differentiation are highlighted in red. (B) KEGG pathway enrichment analysis of proteins involved in sg Ostm1 Ba/F3 cells with-log10(FDR) used as the significance metric. (C) Venn diagram depicting the overlap between proteins enriched in sg Ostm1 cells identified by TMT-MS and OSTM1-interacting partners identified by BioID in Ba/F3 cells. The table shows BioID enrichment scores for Pde3b. (D and E) His-tagged PDE3B and Flag-tagged OSTM1 were co-transfected into HEK293T cells, in the presence or absence of MG132 (10 µM). Co-immunoprecipitation (Co-IP) was performed using anti-His (D) or anti-Flag (E) antibodies, followed by IB. (F) Ostm1 was silenced in Ba/F3 cells, and three independent cell clones were probed for Pde3b by IB. (G) qRT-PCR analysis of sg Ostm1 cell clones showing that Pde3b mRNA levels were not affected by Ostm1 silencing. (H) OSTM1-Flag was stably reconstituted in sg Ostm1 Ba/F3 cell clone #3, and Pde3b was probed by IB. (I) sgControl and sg Ostm1 Ba/F3 cells were treated with cycloheximide (CHX, 100 µg/ml) for the indicated hours. Pde3b was probled by IB and quantified using ImageJ. Pde3b half-life was calculated based on densitometry. Total ubiquitylated proteins were probed as an indicator of global protein turnover following CHX tratment. (J) sgControl and sg Ostm1 Ba/F3 cells were treated with MG132 (10 µM) or chloroquine (100 µM) for indicated hours, in the presence of CHX (100 µg/ml). Pde3b stability was determined by IB. Ubiquitin and Lc3b were probed to confirm the effectiveness of MG132 and CQ treatment. The Pde3b/Gapdh ratio is shown below the blots. (K) sgControl and sg Ostm1 Ba/F3 cells were treated with indicated concenrations of MG132 for 8 h, and Pde3b was detected by IB. (L) PDE3B-His was expressed in sgControl or sg Ostm1 Ba/F3 cells. IP with PDE3B antibody was performed, followed by IB with indicated antibodies. PDE3B-His ubiquitination was detected in sgControl cells and reduced in sg Ostm1 cells. (M) OSTM1-Flag and PDE3B-His were transfected into HEK293T cells, individually or together, along with His-ubiquitin. Cells were treated with MG132 (10 µM) for 8 h prior to IP with PDE3B antibody and IB. (N) OSTM1-Flag and PDE3B-His were expressed separately in HEK293T cells. Cell lysates were used individually or combined for in vitro ubiquitylation assays. OSTM1-Flag promoted both its auto-ubiquitylation and PDE3B ubiquitylation. (O) Spearman correlation analysis of OSTM1 and PDE3B protein abundance across BCL cell lines from different subtypes using CCLE proteomic data. (P) OSTM1-Flag was stably expressed in indicated BCL cell lines. Flag pull-down assays were performed, and interacting proteins were analyzed by IB. (Q and R) OSTM1 was silenced in SU-DHL-5 ( Q ) and ARH-77 ( R ) cell lines. Two clones per cell line were probed for PDE3B by IB. (S) sgControl and sg OSTM1 ARH-77 cells were treated with CHX (100 µg/ml). PDE3B was probed by IB, and its half-life was calculated based on ImageJ densitometric quantification.

    Techniques Used: Generated, Transfection, Immunoprecipitation, Co-Immunoprecipitation Assay, Clone Assay, Quantitative RT-PCR, Stable Transfection, Ubiquitin Proteomics, In Vitro, Quantitative Proteomics

    (A) Venn diagram showing overlap of B cell-specific CREB1 and CREBBP ChIP-seq targets. All targets identified in each dataset were used to determine overlap, and the top 1,500 common targets were selected for downstream analyses. (B) RNA expression data from the TCGA MDACC B-cell malignancies cohort. Heatmaps showing correlations between OSTM1, CREB1, or PDE3B mRNA levels and the top 1,500 CREB1/CREBBP co-occupied target genes identified in ( A ). (C) Venn diagrams showing overlap among genes significantly correlated with OSTM1, CREB1, or PDE3B within the top 1,500 CREB1/CREBBP targets. As OSTM1 negatively regulates PDE3B, genes positively correlated with OSTM1 and CREB1 expression and negatively correlated with PDE3B expression showed substantial overlap (78.2%). Conversely, genes negatively correlated with OSTM1 and CREB1 expression and positively correlated with PDE3B expression also overlapped significantly (66.8%). (D) CRISPR gene-effect scores from the CCLE database for OSTM1 and PDE3B across BCL lines, showing generally negative effects upon PDE3B silencing and positive effects upon OSTM1 silencing. (E) Pde3b was silenced by sgRNA in sg Ostm1 clone #3 Ba/F3 cells. PDE3B protein levels were determined by IB, and sg Ostm1/Pde3b double knockout (DKO) Ba/F3 cells were selected for subsequent experiments. (F) sgControl, sg Ostm1 , and DKO Ba/F3 cells were cutured in the presense or absence of IL3. Pde3b silencing reversed IL3-independence in sg Ostm1 cells. (G) GFP-expressing sg Ostm1 or DKO Ba/F3 cells were transplanted into nude mice via i.p. injection. Mice were harvested at the endpoint of the sg Ostm1 cohort. Spleens and livers were photographed and weighed. P values were calculated using Student’s t-test. GFP-positive tumor cells were detected only in sg Ostm1 recipients, but not in DKO recipients. (H) qRT-PCR in sgControl and sg Ostm1 Ba/F3 cells showing that Ostm1 silencing reduced expression of PKA/CREB/CREBBP target genes. (I) sgCtrl, sg Ostm1 , and DKO Ba/F3 cells were probed for phospho-PKA substrates and phospho-CREB (Ser133). (J) OSTM1 was silenced using two independent sgRNAs in SU-DHL-5 cells. Left: qPCR validation of OSTM1 knockout using on-target primers. Right: IB showing stablization of PDE3B and downregulation of cAMP/PKA signaling upon OSTM1 deletion. (K) OSTM1 was silenced in ARH-77 cells. IB of two clones shows increased PDE3B protein levles and decreased cAMP/PKA signaling upon OSTM1 silencing. (L) PDE3B-His was stably expressed in SU-DHL-10 cell line, which suppressed cAMP/PKA signaling. (M) OSTM1-Flag or OSTM1Δ31-Flag was stably expressed in OPM2 and RPMI-8226 cells. IB shows that OSTM1Δ31, but not the full-length OSTM1, promoted PDE3B degradation and enhanced cAMP/PKA signaling. (N) IB of whole-spleen lysates from indicated age-matched mice collected at the endpoints of O +/- ;C -/- or DKO cohorts. Phosphorylation levels of CREB and PKA substrates were generally reduced in the O -/- , O +/- C -/- , and DKO mice. (O) Bulk RNA-seq of purified splenic B cells from the indicated genotypes (as in ). Genes up-or down-regulated in DKO versus C -/- mice were intersected with the CREB1/CREBBP ChIP-seq targets identified in (A) . (P) Spleens from two-month-old C -/- and DKO mice were harvested, and 10,000 cells per mouse were analyzed by scRNA-seq. UMAP plots of B-cell subpopulations are shown by genotype. Bar graphs show the relative proportions of B-cell subsets. (Q) Genes down-regulated in DKO vs C -/- B cells, as identified by both bulk RNA-seq of splenic B cells and scRNA-seq of follicular B cells, were intersected with CREB1/CREBBP targets. Eight genes were commonly identified across all 4 datasets.
    Figure Legend Snippet: (A) Venn diagram showing overlap of B cell-specific CREB1 and CREBBP ChIP-seq targets. All targets identified in each dataset were used to determine overlap, and the top 1,500 common targets were selected for downstream analyses. (B) RNA expression data from the TCGA MDACC B-cell malignancies cohort. Heatmaps showing correlations between OSTM1, CREB1, or PDE3B mRNA levels and the top 1,500 CREB1/CREBBP co-occupied target genes identified in ( A ). (C) Venn diagrams showing overlap among genes significantly correlated with OSTM1, CREB1, or PDE3B within the top 1,500 CREB1/CREBBP targets. As OSTM1 negatively regulates PDE3B, genes positively correlated with OSTM1 and CREB1 expression and negatively correlated with PDE3B expression showed substantial overlap (78.2%). Conversely, genes negatively correlated with OSTM1 and CREB1 expression and positively correlated with PDE3B expression also overlapped significantly (66.8%). (D) CRISPR gene-effect scores from the CCLE database for OSTM1 and PDE3B across BCL lines, showing generally negative effects upon PDE3B silencing and positive effects upon OSTM1 silencing. (E) Pde3b was silenced by sgRNA in sg Ostm1 clone #3 Ba/F3 cells. PDE3B protein levels were determined by IB, and sg Ostm1/Pde3b double knockout (DKO) Ba/F3 cells were selected for subsequent experiments. (F) sgControl, sg Ostm1 , and DKO Ba/F3 cells were cutured in the presense or absence of IL3. Pde3b silencing reversed IL3-independence in sg Ostm1 cells. (G) GFP-expressing sg Ostm1 or DKO Ba/F3 cells were transplanted into nude mice via i.p. injection. Mice were harvested at the endpoint of the sg Ostm1 cohort. Spleens and livers were photographed and weighed. P values were calculated using Student’s t-test. GFP-positive tumor cells were detected only in sg Ostm1 recipients, but not in DKO recipients. (H) qRT-PCR in sgControl and sg Ostm1 Ba/F3 cells showing that Ostm1 silencing reduced expression of PKA/CREB/CREBBP target genes. (I) sgCtrl, sg Ostm1 , and DKO Ba/F3 cells were probed for phospho-PKA substrates and phospho-CREB (Ser133). (J) OSTM1 was silenced using two independent sgRNAs in SU-DHL-5 cells. Left: qPCR validation of OSTM1 knockout using on-target primers. Right: IB showing stablization of PDE3B and downregulation of cAMP/PKA signaling upon OSTM1 deletion. (K) OSTM1 was silenced in ARH-77 cells. IB of two clones shows increased PDE3B protein levles and decreased cAMP/PKA signaling upon OSTM1 silencing. (L) PDE3B-His was stably expressed in SU-DHL-10 cell line, which suppressed cAMP/PKA signaling. (M) OSTM1-Flag or OSTM1Δ31-Flag was stably expressed in OPM2 and RPMI-8226 cells. IB shows that OSTM1Δ31, but not the full-length OSTM1, promoted PDE3B degradation and enhanced cAMP/PKA signaling. (N) IB of whole-spleen lysates from indicated age-matched mice collected at the endpoints of O +/- ;C -/- or DKO cohorts. Phosphorylation levels of CREB and PKA substrates were generally reduced in the O -/- , O +/- C -/- , and DKO mice. (O) Bulk RNA-seq of purified splenic B cells from the indicated genotypes (as in ). Genes up-or down-regulated in DKO versus C -/- mice were intersected with the CREB1/CREBBP ChIP-seq targets identified in (A) . (P) Spleens from two-month-old C -/- and DKO mice were harvested, and 10,000 cells per mouse were analyzed by scRNA-seq. UMAP plots of B-cell subpopulations are shown by genotype. Bar graphs show the relative proportions of B-cell subsets. (Q) Genes down-regulated in DKO vs C -/- B cells, as identified by both bulk RNA-seq of splenic B cells and scRNA-seq of follicular B cells, were intersected with CREB1/CREBBP targets. Eight genes were commonly identified across all 4 datasets.

    Techniques Used: ChIP-sequencing, RNA Expression, Expressing, CRISPR, Double Knockout, Injection, Quantitative RT-PCR, Biomarker Discovery, Knock-Out, Clone Assay, Stable Transfection, Phospho-proteomics, RNA Sequencing, Purification



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    (A) Ostm1 was silenced in Ba/F3 cells using two independent sgRNAs. Successful knockout of Ostm1 was determined by genomic sequencing, which shows frame-shifting deletion, point mutations, and large-size deletion. (B) Human OSTM1-Flag was reconstituted into sg Ostm1 Ba/F3 cells, which led to the loss of IL3-independence of the sg Ostm1 cells. (C) OSTM1 was silenced in ARH-77 cells using sgRNA. Successful knockout of OSTM1 was determined by genomic sequencing. (C) Silencing OSTM1 in ARH-77 cells promoted cell proliferation. (D) OSTM1 was <t>silenced</t> <t>in</t> <t>SU-DHL-5</t> cells with two sgRNAs. Successful silencing was achieved indicated by decreased mRNA levels, which led to increased cell proliferation. Statistical analysis in panels B , D , and E was done using multiple t-test, one per row. For panel E , one way ANOVA was used. **p<0.01; ***p<0.001.
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    Image Search Results


    (A) Ostm1 was silenced in Ba/F3 cells using two independent sgRNAs. Successful knockout of Ostm1 was determined by genomic sequencing, which shows frame-shifting deletion, point mutations, and large-size deletion. (B) Human OSTM1-Flag was reconstituted into sg Ostm1 Ba/F3 cells, which led to the loss of IL3-independence of the sg Ostm1 cells. (C) OSTM1 was silenced in ARH-77 cells using sgRNA. Successful knockout of OSTM1 was determined by genomic sequencing. (C) Silencing OSTM1 in ARH-77 cells promoted cell proliferation. (D) OSTM1 was silenced in SU-DHL-5 cells with two sgRNAs. Successful silencing was achieved indicated by decreased mRNA levels, which led to increased cell proliferation. Statistical analysis in panels B , D , and E was done using multiple t-test, one per row. For panel E , one way ANOVA was used. **p<0.01; ***p<0.001.

    Journal: bioRxiv

    Article Title: OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway

    doi: 10.64898/2026.01.23.701155

    Figure Lengend Snippet: (A) Ostm1 was silenced in Ba/F3 cells using two independent sgRNAs. Successful knockout of Ostm1 was determined by genomic sequencing, which shows frame-shifting deletion, point mutations, and large-size deletion. (B) Human OSTM1-Flag was reconstituted into sg Ostm1 Ba/F3 cells, which led to the loss of IL3-independence of the sg Ostm1 cells. (C) OSTM1 was silenced in ARH-77 cells using sgRNA. Successful knockout of OSTM1 was determined by genomic sequencing. (C) Silencing OSTM1 in ARH-77 cells promoted cell proliferation. (D) OSTM1 was silenced in SU-DHL-5 cells with two sgRNAs. Successful silencing was achieved indicated by decreased mRNA levels, which led to increased cell proliferation. Statistical analysis in panels B , D , and E was done using multiple t-test, one per row. For panel E , one way ANOVA was used. **p<0.01; ***p<0.001.

    Article Snippet: Human DLBCL cell lines SU-DHL-4 (CRL-2957), SU-DHL-5 (CRL-2958), and SU-DHL-10 (CRL-2963), Burkitt’s lymphoma cell lines Daudi and Ramos, as well as mantle cell lymphoma cell lines Z-138 and JeKo-1 were obtained from American Type Culture Collection (ATCC, Manassas, VA).

    Techniques: Knock-Out, Genomic Sequencing

    (A) sg Ostm1 and sgControl Ba/F3 cells were subjected to TMT-MS. Volcano plot (log₂ fold change vs. –log₁₀ p-value) was generated using VolcaNoseR. Dashed lines indicate significance cutoffs. Selected proteins involved in hematopoeitic function and differentiation are highlighted in red. (B) KEGG pathway enrichment analysis of proteins involved in sg Ostm1 Ba/F3 cells with-log10(FDR) used as the significance metric. (C) Venn diagram depicting the overlap between proteins enriched in sg Ostm1 cells identified by TMT-MS and OSTM1-interacting partners identified by BioID in Ba/F3 cells. The table shows BioID enrichment scores for Pde3b. (D and E) His-tagged PDE3B and Flag-tagged OSTM1 were co-transfected into HEK293T cells, in the presence or absence of MG132 (10 µM). Co-immunoprecipitation (Co-IP) was performed using anti-His (D) or anti-Flag (E) antibodies, followed by IB. (F) Ostm1 was silenced in Ba/F3 cells, and three independent cell clones were probed for Pde3b by IB. (G) qRT-PCR analysis of sg Ostm1 cell clones showing that Pde3b mRNA levels were not affected by Ostm1 silencing. (H) OSTM1-Flag was stably reconstituted in sg Ostm1 Ba/F3 cell clone #3, and Pde3b was probed by IB. (I) sgControl and sg Ostm1 Ba/F3 cells were treated with cycloheximide (CHX, 100 µg/ml) for the indicated hours. Pde3b was probled by IB and quantified using ImageJ. Pde3b half-life was calculated based on densitometry. Total ubiquitylated proteins were probed as an indicator of global protein turnover following CHX tratment. (J) sgControl and sg Ostm1 Ba/F3 cells were treated with MG132 (10 µM) or chloroquine (100 µM) for indicated hours, in the presence of CHX (100 µg/ml). Pde3b stability was determined by IB. Ubiquitin and Lc3b were probed to confirm the effectiveness of MG132 and CQ treatment. The Pde3b/Gapdh ratio is shown below the blots. (K) sgControl and sg Ostm1 Ba/F3 cells were treated with indicated concenrations of MG132 for 8 h, and Pde3b was detected by IB. (L) PDE3B-His was expressed in sgControl or sg Ostm1 Ba/F3 cells. IP with PDE3B antibody was performed, followed by IB with indicated antibodies. PDE3B-His ubiquitination was detected in sgControl cells and reduced in sg Ostm1 cells. (M) OSTM1-Flag and PDE3B-His were transfected into HEK293T cells, individually or together, along with His-ubiquitin. Cells were treated with MG132 (10 µM) for 8 h prior to IP with PDE3B antibody and IB. (N) OSTM1-Flag and PDE3B-His were expressed separately in HEK293T cells. Cell lysates were used individually or combined for in vitro ubiquitylation assays. OSTM1-Flag promoted both its auto-ubiquitylation and PDE3B ubiquitylation. (O) Spearman correlation analysis of OSTM1 and PDE3B protein abundance across BCL cell lines from different subtypes using CCLE proteomic data. (P) OSTM1-Flag was stably expressed in indicated BCL cell lines. Flag pull-down assays were performed, and interacting proteins were analyzed by IB. (Q and R) OSTM1 was silenced in SU-DHL-5 ( Q ) and ARH-77 ( R ) cell lines. Two clones per cell line were probed for PDE3B by IB. (S) sgControl and sg OSTM1 ARH-77 cells were treated with CHX (100 µg/ml). PDE3B was probed by IB, and its half-life was calculated based on ImageJ densitometric quantification.

    Journal: bioRxiv

    Article Title: OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway

    doi: 10.64898/2026.01.23.701155

    Figure Lengend Snippet: (A) sg Ostm1 and sgControl Ba/F3 cells were subjected to TMT-MS. Volcano plot (log₂ fold change vs. –log₁₀ p-value) was generated using VolcaNoseR. Dashed lines indicate significance cutoffs. Selected proteins involved in hematopoeitic function and differentiation are highlighted in red. (B) KEGG pathway enrichment analysis of proteins involved in sg Ostm1 Ba/F3 cells with-log10(FDR) used as the significance metric. (C) Venn diagram depicting the overlap between proteins enriched in sg Ostm1 cells identified by TMT-MS and OSTM1-interacting partners identified by BioID in Ba/F3 cells. The table shows BioID enrichment scores for Pde3b. (D and E) His-tagged PDE3B and Flag-tagged OSTM1 were co-transfected into HEK293T cells, in the presence or absence of MG132 (10 µM). Co-immunoprecipitation (Co-IP) was performed using anti-His (D) or anti-Flag (E) antibodies, followed by IB. (F) Ostm1 was silenced in Ba/F3 cells, and three independent cell clones were probed for Pde3b by IB. (G) qRT-PCR analysis of sg Ostm1 cell clones showing that Pde3b mRNA levels were not affected by Ostm1 silencing. (H) OSTM1-Flag was stably reconstituted in sg Ostm1 Ba/F3 cell clone #3, and Pde3b was probed by IB. (I) sgControl and sg Ostm1 Ba/F3 cells were treated with cycloheximide (CHX, 100 µg/ml) for the indicated hours. Pde3b was probled by IB and quantified using ImageJ. Pde3b half-life was calculated based on densitometry. Total ubiquitylated proteins were probed as an indicator of global protein turnover following CHX tratment. (J) sgControl and sg Ostm1 Ba/F3 cells were treated with MG132 (10 µM) or chloroquine (100 µM) for indicated hours, in the presence of CHX (100 µg/ml). Pde3b stability was determined by IB. Ubiquitin and Lc3b were probed to confirm the effectiveness of MG132 and CQ treatment. The Pde3b/Gapdh ratio is shown below the blots. (K) sgControl and sg Ostm1 Ba/F3 cells were treated with indicated concenrations of MG132 for 8 h, and Pde3b was detected by IB. (L) PDE3B-His was expressed in sgControl or sg Ostm1 Ba/F3 cells. IP with PDE3B antibody was performed, followed by IB with indicated antibodies. PDE3B-His ubiquitination was detected in sgControl cells and reduced in sg Ostm1 cells. (M) OSTM1-Flag and PDE3B-His were transfected into HEK293T cells, individually or together, along with His-ubiquitin. Cells were treated with MG132 (10 µM) for 8 h prior to IP with PDE3B antibody and IB. (N) OSTM1-Flag and PDE3B-His were expressed separately in HEK293T cells. Cell lysates were used individually or combined for in vitro ubiquitylation assays. OSTM1-Flag promoted both its auto-ubiquitylation and PDE3B ubiquitylation. (O) Spearman correlation analysis of OSTM1 and PDE3B protein abundance across BCL cell lines from different subtypes using CCLE proteomic data. (P) OSTM1-Flag was stably expressed in indicated BCL cell lines. Flag pull-down assays were performed, and interacting proteins were analyzed by IB. (Q and R) OSTM1 was silenced in SU-DHL-5 ( Q ) and ARH-77 ( R ) cell lines. Two clones per cell line were probed for PDE3B by IB. (S) sgControl and sg OSTM1 ARH-77 cells were treated with CHX (100 µg/ml). PDE3B was probed by IB, and its half-life was calculated based on ImageJ densitometric quantification.

    Article Snippet: Human DLBCL cell lines SU-DHL-4 (CRL-2957), SU-DHL-5 (CRL-2958), and SU-DHL-10 (CRL-2963), Burkitt’s lymphoma cell lines Daudi and Ramos, as well as mantle cell lymphoma cell lines Z-138 and JeKo-1 were obtained from American Type Culture Collection (ATCC, Manassas, VA).

    Techniques: Generated, Transfection, Immunoprecipitation, Co-Immunoprecipitation Assay, Clone Assay, Quantitative RT-PCR, Stable Transfection, Ubiquitin Proteomics, In Vitro, Quantitative Proteomics

    (A) Venn diagram showing overlap of B cell-specific CREB1 and CREBBP ChIP-seq targets. All targets identified in each dataset were used to determine overlap, and the top 1,500 common targets were selected for downstream analyses. (B) RNA expression data from the TCGA MDACC B-cell malignancies cohort. Heatmaps showing correlations between OSTM1, CREB1, or PDE3B mRNA levels and the top 1,500 CREB1/CREBBP co-occupied target genes identified in ( A ). (C) Venn diagrams showing overlap among genes significantly correlated with OSTM1, CREB1, or PDE3B within the top 1,500 CREB1/CREBBP targets. As OSTM1 negatively regulates PDE3B, genes positively correlated with OSTM1 and CREB1 expression and negatively correlated with PDE3B expression showed substantial overlap (78.2%). Conversely, genes negatively correlated with OSTM1 and CREB1 expression and positively correlated with PDE3B expression also overlapped significantly (66.8%). (D) CRISPR gene-effect scores from the CCLE database for OSTM1 and PDE3B across BCL lines, showing generally negative effects upon PDE3B silencing and positive effects upon OSTM1 silencing. (E) Pde3b was silenced by sgRNA in sg Ostm1 clone #3 Ba/F3 cells. PDE3B protein levels were determined by IB, and sg Ostm1/Pde3b double knockout (DKO) Ba/F3 cells were selected for subsequent experiments. (F) sgControl, sg Ostm1 , and DKO Ba/F3 cells were cutured in the presense or absence of IL3. Pde3b silencing reversed IL3-independence in sg Ostm1 cells. (G) GFP-expressing sg Ostm1 or DKO Ba/F3 cells were transplanted into nude mice via i.p. injection. Mice were harvested at the endpoint of the sg Ostm1 cohort. Spleens and livers were photographed and weighed. P values were calculated using Student’s t-test. GFP-positive tumor cells were detected only in sg Ostm1 recipients, but not in DKO recipients. (H) qRT-PCR in sgControl and sg Ostm1 Ba/F3 cells showing that Ostm1 silencing reduced expression of PKA/CREB/CREBBP target genes. (I) sgCtrl, sg Ostm1 , and DKO Ba/F3 cells were probed for phospho-PKA substrates and phospho-CREB (Ser133). (J) OSTM1 was silenced using two independent sgRNAs in SU-DHL-5 cells. Left: qPCR validation of OSTM1 knockout using on-target primers. Right: IB showing stablization of PDE3B and downregulation of cAMP/PKA signaling upon OSTM1 deletion. (K) OSTM1 was silenced in ARH-77 cells. IB of two clones shows increased PDE3B protein levles and decreased cAMP/PKA signaling upon OSTM1 silencing. (L) PDE3B-His was stably expressed in SU-DHL-10 cell line, which suppressed cAMP/PKA signaling. (M) OSTM1-Flag or OSTM1Δ31-Flag was stably expressed in OPM2 and RPMI-8226 cells. IB shows that OSTM1Δ31, but not the full-length OSTM1, promoted PDE3B degradation and enhanced cAMP/PKA signaling. (N) IB of whole-spleen lysates from indicated age-matched mice collected at the endpoints of O +/- ;C -/- or DKO cohorts. Phosphorylation levels of CREB and PKA substrates were generally reduced in the O -/- , O +/- C -/- , and DKO mice. (O) Bulk RNA-seq of purified splenic B cells from the indicated genotypes (as in ). Genes up-or down-regulated in DKO versus C -/- mice were intersected with the CREB1/CREBBP ChIP-seq targets identified in (A) . (P) Spleens from two-month-old C -/- and DKO mice were harvested, and 10,000 cells per mouse were analyzed by scRNA-seq. UMAP plots of B-cell subpopulations are shown by genotype. Bar graphs show the relative proportions of B-cell subsets. (Q) Genes down-regulated in DKO vs C -/- B cells, as identified by both bulk RNA-seq of splenic B cells and scRNA-seq of follicular B cells, were intersected with CREB1/CREBBP targets. Eight genes were commonly identified across all 4 datasets.

    Journal: bioRxiv

    Article Title: OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway

    doi: 10.64898/2026.01.23.701155

    Figure Lengend Snippet: (A) Venn diagram showing overlap of B cell-specific CREB1 and CREBBP ChIP-seq targets. All targets identified in each dataset were used to determine overlap, and the top 1,500 common targets were selected for downstream analyses. (B) RNA expression data from the TCGA MDACC B-cell malignancies cohort. Heatmaps showing correlations between OSTM1, CREB1, or PDE3B mRNA levels and the top 1,500 CREB1/CREBBP co-occupied target genes identified in ( A ). (C) Venn diagrams showing overlap among genes significantly correlated with OSTM1, CREB1, or PDE3B within the top 1,500 CREB1/CREBBP targets. As OSTM1 negatively regulates PDE3B, genes positively correlated with OSTM1 and CREB1 expression and negatively correlated with PDE3B expression showed substantial overlap (78.2%). Conversely, genes negatively correlated with OSTM1 and CREB1 expression and positively correlated with PDE3B expression also overlapped significantly (66.8%). (D) CRISPR gene-effect scores from the CCLE database for OSTM1 and PDE3B across BCL lines, showing generally negative effects upon PDE3B silencing and positive effects upon OSTM1 silencing. (E) Pde3b was silenced by sgRNA in sg Ostm1 clone #3 Ba/F3 cells. PDE3B protein levels were determined by IB, and sg Ostm1/Pde3b double knockout (DKO) Ba/F3 cells were selected for subsequent experiments. (F) sgControl, sg Ostm1 , and DKO Ba/F3 cells were cutured in the presense or absence of IL3. Pde3b silencing reversed IL3-independence in sg Ostm1 cells. (G) GFP-expressing sg Ostm1 or DKO Ba/F3 cells were transplanted into nude mice via i.p. injection. Mice were harvested at the endpoint of the sg Ostm1 cohort. Spleens and livers were photographed and weighed. P values were calculated using Student’s t-test. GFP-positive tumor cells were detected only in sg Ostm1 recipients, but not in DKO recipients. (H) qRT-PCR in sgControl and sg Ostm1 Ba/F3 cells showing that Ostm1 silencing reduced expression of PKA/CREB/CREBBP target genes. (I) sgCtrl, sg Ostm1 , and DKO Ba/F3 cells were probed for phospho-PKA substrates and phospho-CREB (Ser133). (J) OSTM1 was silenced using two independent sgRNAs in SU-DHL-5 cells. Left: qPCR validation of OSTM1 knockout using on-target primers. Right: IB showing stablization of PDE3B and downregulation of cAMP/PKA signaling upon OSTM1 deletion. (K) OSTM1 was silenced in ARH-77 cells. IB of two clones shows increased PDE3B protein levles and decreased cAMP/PKA signaling upon OSTM1 silencing. (L) PDE3B-His was stably expressed in SU-DHL-10 cell line, which suppressed cAMP/PKA signaling. (M) OSTM1-Flag or OSTM1Δ31-Flag was stably expressed in OPM2 and RPMI-8226 cells. IB shows that OSTM1Δ31, but not the full-length OSTM1, promoted PDE3B degradation and enhanced cAMP/PKA signaling. (N) IB of whole-spleen lysates from indicated age-matched mice collected at the endpoints of O +/- ;C -/- or DKO cohorts. Phosphorylation levels of CREB and PKA substrates were generally reduced in the O -/- , O +/- C -/- , and DKO mice. (O) Bulk RNA-seq of purified splenic B cells from the indicated genotypes (as in ). Genes up-or down-regulated in DKO versus C -/- mice were intersected with the CREB1/CREBBP ChIP-seq targets identified in (A) . (P) Spleens from two-month-old C -/- and DKO mice were harvested, and 10,000 cells per mouse were analyzed by scRNA-seq. UMAP plots of B-cell subpopulations are shown by genotype. Bar graphs show the relative proportions of B-cell subsets. (Q) Genes down-regulated in DKO vs C -/- B cells, as identified by both bulk RNA-seq of splenic B cells and scRNA-seq of follicular B cells, were intersected with CREB1/CREBBP targets. Eight genes were commonly identified across all 4 datasets.

    Article Snippet: Human DLBCL cell lines SU-DHL-4 (CRL-2957), SU-DHL-5 (CRL-2958), and SU-DHL-10 (CRL-2963), Burkitt’s lymphoma cell lines Daudi and Ramos, as well as mantle cell lymphoma cell lines Z-138 and JeKo-1 were obtained from American Type Culture Collection (ATCC, Manassas, VA).

    Techniques: ChIP-sequencing, RNA Expression, Expressing, CRISPR, Double Knockout, Injection, Quantitative RT-PCR, Biomarker Discovery, Knock-Out, Clone Assay, Stable Transfection, Phospho-proteomics, RNA Sequencing, Purification