kasumi 1  (ATCC)


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    ATCC kasumi 1
    a Western blot of WT, PLK2 − / − , USP18 − / − , and USP18 − / − PLK2 − / − THP-1 cells treated with or without IFNα (1000 U/ml) for 48 h with indicated antibodies. b Percentage of live cells in ( a ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. c Analysis of ICD markers (LDH release and ecto-CRT) in ( b ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. d Western blot of PLK2 − / − THP-1 cells infected with Mock or PLK2 after two days of blasticidin selection using the indicated antibodies. e; Percentage of live cells in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. f Analysis of ICD markers (LDH release and ecto-CRT) and IL-1β secretions in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. g ; THP-1 and <t>Kasumi-1</t> cells were transduced with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, cell lysates were analyzed by western blot with indicated antibodies. h Ectopic PLK2 expression induces cell death in several AML cell lines independent of its kinase activity. THP-1, Kasumi-1, and MV4-11 cells were infected with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, live cells were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. i THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 (final 10 µM) for 48 h, then cell lysates were analyzed. j THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 for indicated times, then PI (%) and Annexin V + (%) were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. k Two different PDX AML cells were cultured with different dose of TC-S7005, and analyzed cell growth ( n = 3 independent samples each conditions). All data represent mean ± s.d, except where indicated. n.s. not statistically significant. p -value was determined by one-way ANOVA test. Source data are provided as a Source Data file.
    Kasumi 1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Expansion of interferon inducible gene pool via USP18 inhibition promotes cancer cell pyroptosis"

    Article Title: Expansion of interferon inducible gene pool via USP18 inhibition promotes cancer cell pyroptosis

    Journal: Nature Communications

    doi: 10.1038/s41467-022-35348-5

    a Western blot of WT, PLK2 − / − , USP18 − / − , and USP18 − / − PLK2 − / − THP-1 cells treated with or without IFNα (1000 U/ml) for 48 h with indicated antibodies. b Percentage of live cells in ( a ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. c Analysis of ICD markers (LDH release and ecto-CRT) in ( b ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. d Western blot of PLK2 − / − THP-1 cells infected with Mock or PLK2 after two days of blasticidin selection using the indicated antibodies. e; Percentage of live cells in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. f Analysis of ICD markers (LDH release and ecto-CRT) and IL-1β secretions in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. g ; THP-1 and Kasumi-1 cells were transduced with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, cell lysates were analyzed by western blot with indicated antibodies. h Ectopic PLK2 expression induces cell death in several AML cell lines independent of its kinase activity. THP-1, Kasumi-1, and MV4-11 cells were infected with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, live cells were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. i THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 (final 10 µM) for 48 h, then cell lysates were analyzed. j THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 for indicated times, then PI (%) and Annexin V + (%) were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. k Two different PDX AML cells were cultured with different dose of TC-S7005, and analyzed cell growth ( n = 3 independent samples each conditions). All data represent mean ± s.d, except where indicated. n.s. not statistically significant. p -value was determined by one-way ANOVA test. Source data are provided as a Source Data file.
    Figure Legend Snippet: a Western blot of WT, PLK2 − / − , USP18 − / − , and USP18 − / − PLK2 − / − THP-1 cells treated with or without IFNα (1000 U/ml) for 48 h with indicated antibodies. b Percentage of live cells in ( a ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. c Analysis of ICD markers (LDH release and ecto-CRT) in ( b ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. d Western blot of PLK2 − / − THP-1 cells infected with Mock or PLK2 after two days of blasticidin selection using the indicated antibodies. e; Percentage of live cells in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. f Analysis of ICD markers (LDH release and ecto-CRT) and IL-1β secretions in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. g ; THP-1 and Kasumi-1 cells were transduced with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, cell lysates were analyzed by western blot with indicated antibodies. h Ectopic PLK2 expression induces cell death in several AML cell lines independent of its kinase activity. THP-1, Kasumi-1, and MV4-11 cells were infected with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, live cells were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. i THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 (final 10 µM) for 48 h, then cell lysates were analyzed. j THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 for indicated times, then PI (%) and Annexin V + (%) were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. k Two different PDX AML cells were cultured with different dose of TC-S7005, and analyzed cell growth ( n = 3 independent samples each conditions). All data represent mean ± s.d, except where indicated. n.s. not statistically significant. p -value was determined by one-way ANOVA test. Source data are provided as a Source Data file.

    Techniques Used: Western Blot, Infection, Selection, Two Tailed Test, Transduction, Activity Assay, Expressing, Cell Culture

    kasumi 1  (ATCC)


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    ATCC kasumi 1
    a Western blot of WT, PLK2 − / − , USP18 − / − , and USP18 − / − PLK2 − / − THP-1 cells treated with or without IFNα (1000 U/ml) for 48 h with indicated antibodies. b Percentage of live cells in ( a ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. c Analysis of ICD markers (LDH release and ecto-CRT) in ( b ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. d Western blot of PLK2 − / − THP-1 cells infected with Mock or PLK2 after two days of blasticidin selection using the indicated antibodies. e; Percentage of live cells in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. f Analysis of ICD markers (LDH release and ecto-CRT) and IL-1β secretions in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. g ; THP-1 and <t>Kasumi-1</t> cells were transduced with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, cell lysates were analyzed by western blot with indicated antibodies. h Ectopic PLK2 expression induces cell death in several AML cell lines independent of its kinase activity. THP-1, Kasumi-1, and MV4-11 cells were infected with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, live cells were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. i THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 (final 10 µM) for 48 h, then cell lysates were analyzed. j THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 for indicated times, then PI (%) and Annexin V + (%) were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. k Two different PDX AML cells were cultured with different dose of TC-S7005, and analyzed cell growth ( n = 3 independent samples each conditions). All data represent mean ± s.d, except where indicated. n.s. not statistically significant. p -value was determined by one-way ANOVA test. Source data are provided as a Source Data file.
    Kasumi 1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/kasumi 1/product/ATCC
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    kasumi 1 - by Bioz Stars, 2024-06
    99/100 stars

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    1) Product Images from "Expansion of interferon inducible gene pool via USP18 inhibition promotes cancer cell pyroptosis"

    Article Title: Expansion of interferon inducible gene pool via USP18 inhibition promotes cancer cell pyroptosis

    Journal: Nature Communications

    doi: 10.1038/s41467-022-35348-5

    a Western blot of WT, PLK2 − / − , USP18 − / − , and USP18 − / − PLK2 − / − THP-1 cells treated with or without IFNα (1000 U/ml) for 48 h with indicated antibodies. b Percentage of live cells in ( a ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. c Analysis of ICD markers (LDH release and ecto-CRT) in ( b ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. d Western blot of PLK2 − / − THP-1 cells infected with Mock or PLK2 after two days of blasticidin selection using the indicated antibodies. e; Percentage of live cells in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. f Analysis of ICD markers (LDH release and ecto-CRT) and IL-1β secretions in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. g ; THP-1 and Kasumi-1 cells were transduced with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, cell lysates were analyzed by western blot with indicated antibodies. h Ectopic PLK2 expression induces cell death in several AML cell lines independent of its kinase activity. THP-1, Kasumi-1, and MV4-11 cells were infected with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, live cells were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. i THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 (final 10 µM) for 48 h, then cell lysates were analyzed. j THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 for indicated times, then PI (%) and Annexin V + (%) were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. k Two different PDX AML cells were cultured with different dose of TC-S7005, and analyzed cell growth ( n = 3 independent samples each conditions). All data represent mean ± s.d, except where indicated. n.s. not statistically significant. p -value was determined by one-way ANOVA test. Source data are provided as a Source Data file.
    Figure Legend Snippet: a Western blot of WT, PLK2 − / − , USP18 − / − , and USP18 − / − PLK2 − / − THP-1 cells treated with or without IFNα (1000 U/ml) for 48 h with indicated antibodies. b Percentage of live cells in ( a ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. c Analysis of ICD markers (LDH release and ecto-CRT) in ( b ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. d Western blot of PLK2 − / − THP-1 cells infected with Mock or PLK2 after two days of blasticidin selection using the indicated antibodies. e; Percentage of live cells in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. f Analysis of ICD markers (LDH release and ecto-CRT) and IL-1β secretions in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. g ; THP-1 and Kasumi-1 cells were transduced with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, cell lysates were analyzed by western blot with indicated antibodies. h Ectopic PLK2 expression induces cell death in several AML cell lines independent of its kinase activity. THP-1, Kasumi-1, and MV4-11 cells were infected with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, live cells were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. i THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 (final 10 µM) for 48 h, then cell lysates were analyzed. j THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 for indicated times, then PI (%) and Annexin V + (%) were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. k Two different PDX AML cells were cultured with different dose of TC-S7005, and analyzed cell growth ( n = 3 independent samples each conditions). All data represent mean ± s.d, except where indicated. n.s. not statistically significant. p -value was determined by one-way ANOVA test. Source data are provided as a Source Data file.

    Techniques Used: Western Blot, Infection, Selection, Two Tailed Test, Transduction, Activity Assay, Expressing, Cell Culture

    kasumi1  (ATCC)


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    ATCC kasumi1
    Kasumi1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    nomo 1  (ATCC)


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    ATCC nomo 1
    Nomo 1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    human aml cell line kasumi  (ATCC)


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    ATCC human aml cell line kasumi
    Downregulation of SMIM3 inhibited cell proliferation and colony formation in AML cells. The efficiency of SMIM3 knockdown in the <t>Kasumi-1</t> and THP-1 cell lines was verified by A , B reverse transcription-quantitative polymerase chain reaction and E , F immune fluorescence, respectively. C , D Cell proliferation was detected by the CCK-8 assay in Kasumi-1 and THP-1. G , H The colony formation of SMIM3 -CTRL and SMIM3 -KD in Kasumi-1 and THP-1. CTRL, control; KD, knockdown; *P < 0.05 compared with CTRL cells; **P < 0.01 compared with CTRL cells; ***P < 0.001 compared with CTRL cells; Error bars indicate the standard deviation
    Human Aml Cell Line Kasumi, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Downregulation of SMIM3 inhibits growth of leukemia via PI3K-AKT signaling pathway and correlates with prognosis of adult acute myeloid leukemia with normal karyotype"

    Article Title: Downregulation of SMIM3 inhibits growth of leukemia via PI3K-AKT signaling pathway and correlates with prognosis of adult acute myeloid leukemia with normal karyotype

    Journal: Journal of Translational Medicine

    doi: 10.1186/s12967-022-03831-8

    Downregulation of SMIM3 inhibited cell proliferation and colony formation in AML cells. The efficiency of SMIM3 knockdown in the Kasumi-1 and THP-1 cell lines was verified by A , B reverse transcription-quantitative polymerase chain reaction and E , F immune fluorescence, respectively. C , D Cell proliferation was detected by the CCK-8 assay in Kasumi-1 and THP-1. G , H The colony formation of SMIM3 -CTRL and SMIM3 -KD in Kasumi-1 and THP-1. CTRL, control; KD, knockdown; *P < 0.05 compared with CTRL cells; **P < 0.01 compared with CTRL cells; ***P < 0.001 compared with CTRL cells; Error bars indicate the standard deviation
    Figure Legend Snippet: Downregulation of SMIM3 inhibited cell proliferation and colony formation in AML cells. The efficiency of SMIM3 knockdown in the Kasumi-1 and THP-1 cell lines was verified by A , B reverse transcription-quantitative polymerase chain reaction and E , F immune fluorescence, respectively. C , D Cell proliferation was detected by the CCK-8 assay in Kasumi-1 and THP-1. G , H The colony formation of SMIM3 -CTRL and SMIM3 -KD in Kasumi-1 and THP-1. CTRL, control; KD, knockdown; *P < 0.05 compared with CTRL cells; **P < 0.01 compared with CTRL cells; ***P < 0.001 compared with CTRL cells; Error bars indicate the standard deviation

    Techniques Used: Real-time Polymerase Chain Reaction, Fluorescence, CCK-8 Assay, Standard Deviation

    Apoptosis and cell cycle analysis in AML cell lines. A , B The flow cytometry was applied to analyze apoptosis in SMIM3 knockdown cells compared with control. C – E Propidium iodide (PI) staining was applied to analyze the cell cycle of SMIM3 knockdown cells compared with control. F Alterations in apoptosis and cell cycle-related protein assay in SMIM3 knockdown cells compared with control. G , H Densitometric analysis of the WB signals. CTRL, control; KD, knockdown; *P < 0.05 compared with CTRL cells; **P < 0.01 compared with CTRL cells; ***P < 0.001 compared with CTRL cells
    Figure Legend Snippet: Apoptosis and cell cycle analysis in AML cell lines. A , B The flow cytometry was applied to analyze apoptosis in SMIM3 knockdown cells compared with control. C – E Propidium iodide (PI) staining was applied to analyze the cell cycle of SMIM3 knockdown cells compared with control. F Alterations in apoptosis and cell cycle-related protein assay in SMIM3 knockdown cells compared with control. G , H Densitometric analysis of the WB signals. CTRL, control; KD, knockdown; *P < 0.05 compared with CTRL cells; **P < 0.01 compared with CTRL cells; ***P < 0.001 compared with CTRL cells

    Techniques Used: Cell Cycle Assay, Flow Cytometry, Staining

    GO/KEGG enrichment analysis of subjects with high or low SMIM3 expression in the TCGA-LAML dataset. A Volcano map of the DEGs, including 231up-regulated genes and 1889 down-regulated genes. B Heat map showing the top ten up-regulated and the top ten down-regulated genes. The samples are shown on the X-axis, and the DEGs are shown on the Y-axis. D Venn diagram of the overlap among the DEGs and correlated genes. C GO and KEGG enrichment analysis of the co-expressed genes of DEGs and correlated genes. MF, molecular function. CC, cellular component. BP, biological process. Different categories were shown on the Y-axis, and the X-axis reflected the percentage of DEGs. PI3K-AKT signaling pathway is critical for SMIM3 -mediated changes. G Western blot analysis of PI3K-AKT signaling pathway in SMIM3 -KD cells and controls. H , I Densitometric analysis of the WB signals. E SC79 (10 mM) reversed the inhibitory effect of SMIM3 knockdown on the proliferation of Kasumi-1, F at 24 h. CTRL, control; KD, knockdown; ***P < 0.001 compared with CTRL cells; Error bars indicate the standard deviation
    Figure Legend Snippet: GO/KEGG enrichment analysis of subjects with high or low SMIM3 expression in the TCGA-LAML dataset. A Volcano map of the DEGs, including 231up-regulated genes and 1889 down-regulated genes. B Heat map showing the top ten up-regulated and the top ten down-regulated genes. The samples are shown on the X-axis, and the DEGs are shown on the Y-axis. D Venn diagram of the overlap among the DEGs and correlated genes. C GO and KEGG enrichment analysis of the co-expressed genes of DEGs and correlated genes. MF, molecular function. CC, cellular component. BP, biological process. Different categories were shown on the Y-axis, and the X-axis reflected the percentage of DEGs. PI3K-AKT signaling pathway is critical for SMIM3 -mediated changes. G Western blot analysis of PI3K-AKT signaling pathway in SMIM3 -KD cells and controls. H , I Densitometric analysis of the WB signals. E SC79 (10 mM) reversed the inhibitory effect of SMIM3 knockdown on the proliferation of Kasumi-1, F at 24 h. CTRL, control; KD, knockdown; ***P < 0.001 compared with CTRL cells; Error bars indicate the standard deviation

    Techniques Used: Expressing, Western Blot, Standard Deviation

    SMIM3 knockdown reduced the proliferation of AML cells in nude mice by inhibiting PI3K-AKT signaling pathway. A – D , F – I SMIM3 -KD inhibits tumor growth in Kasumi-1 and THP-1 cells. E , J The expression of PI3K-AKT signaling pathway proteins in tumor tissues by Western blot. CTRL, control; KD, knockdown; ***P < 0.001 compared with CTRL cells
    Figure Legend Snippet: SMIM3 knockdown reduced the proliferation of AML cells in nude mice by inhibiting PI3K-AKT signaling pathway. A – D , F – I SMIM3 -KD inhibits tumor growth in Kasumi-1 and THP-1 cells. E , J The expression of PI3K-AKT signaling pathway proteins in tumor tissues by Western blot. CTRL, control; KD, knockdown; ***P < 0.001 compared with CTRL cells

    Techniques Used: Expressing, Western Blot

    kasumi 1  (ATCC)


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    ATCC kasumi 1
    Kasumi 1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    kasumi 1  (ATCC)


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    ATCC kasumi 1
    The cultured AE-positive AML cell lines <t>Kasumi-1</t> and SKNO-1 cells were treated with given doses of C646 or 0.1% DMSO for 24 h before being subjected to the following assays. (A) C646-induced growth inhibition in both cell lines was detected by Cell Counting Kit-8 at the indicated times; means ± SD of 3 independent experiments. (B) C646-evoked ablation of leukemia colony-forming units in both cell lines was performed by colony formation assay. (C) Dose-dependent retardance of C646 on cell cycle distribution in both cell lines. The cells were stained with propidium iodide and measured by flow cytometry. (D) Dose- and time-dependent effects of C646 on apoptosis in both cell lines. The cells were stained with Annexin V-FITC and measured by flow cytometry. Histograms showed means ± SD of 3 independent experiments. * P <0.05. (E) C646 triggered caspase cleavage in Kasumi-1 cells. The Kasumi-1 cells treated with given doses of C646 in the presence or absence of 50 µM pan-caspase inhibitor Q-VD-OPH were collected and lysed at the indicated time points, and western blotting performed with the indicated antibodies. Equalization of protein loading was verified on the same membrane by reprobing after stripping. Data shown were representative of 2 independent experiments.
    Kasumi 1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "A Histone Acetyltransferase p300 Inhibitor C646 Induces Cell Cycle Arrest and Apoptosis Selectively in AML1-ETO-Positive AML Cells"

    Article Title: A Histone Acetyltransferase p300 Inhibitor C646 Induces Cell Cycle Arrest and Apoptosis Selectively in AML1-ETO-Positive AML Cells

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0055481

    The cultured AE-positive AML cell lines Kasumi-1 and SKNO-1 cells were treated with given doses of C646 or 0.1% DMSO for 24 h before being subjected to the following assays. (A) C646-induced growth inhibition in both cell lines was detected by Cell Counting Kit-8 at the indicated times; means ± SD of 3 independent experiments. (B) C646-evoked ablation of leukemia colony-forming units in both cell lines was performed by colony formation assay. (C) Dose-dependent retardance of C646 on cell cycle distribution in both cell lines. The cells were stained with propidium iodide and measured by flow cytometry. (D) Dose- and time-dependent effects of C646 on apoptosis in both cell lines. The cells were stained with Annexin V-FITC and measured by flow cytometry. Histograms showed means ± SD of 3 independent experiments. * P <0.05. (E) C646 triggered caspase cleavage in Kasumi-1 cells. The Kasumi-1 cells treated with given doses of C646 in the presence or absence of 50 µM pan-caspase inhibitor Q-VD-OPH were collected and lysed at the indicated time points, and western blotting performed with the indicated antibodies. Equalization of protein loading was verified on the same membrane by reprobing after stripping. Data shown were representative of 2 independent experiments.
    Figure Legend Snippet: The cultured AE-positive AML cell lines Kasumi-1 and SKNO-1 cells were treated with given doses of C646 or 0.1% DMSO for 24 h before being subjected to the following assays. (A) C646-induced growth inhibition in both cell lines was detected by Cell Counting Kit-8 at the indicated times; means ± SD of 3 independent experiments. (B) C646-evoked ablation of leukemia colony-forming units in both cell lines was performed by colony formation assay. (C) Dose-dependent retardance of C646 on cell cycle distribution in both cell lines. The cells were stained with propidium iodide and measured by flow cytometry. (D) Dose- and time-dependent effects of C646 on apoptosis in both cell lines. The cells were stained with Annexin V-FITC and measured by flow cytometry. Histograms showed means ± SD of 3 independent experiments. * P <0.05. (E) C646 triggered caspase cleavage in Kasumi-1 cells. The Kasumi-1 cells treated with given doses of C646 in the presence or absence of 50 µM pan-caspase inhibitor Q-VD-OPH were collected and lysed at the indicated time points, and western blotting performed with the indicated antibodies. Equalization of protein loading was verified on the same membrane by reprobing after stripping. Data shown were representative of 2 independent experiments.

    Techniques Used: Cell Culture, Inhibition, Cell Counting, Colony Assay, Staining, Flow Cytometry, Western Blot, Stripping Membranes

    Western blot analysis of (A) acetylated H3, total histone H3, (B) c-kit and bcl-2 proteins in Kasumi-1 and SKNO-1 cells after 24 h treatment with C646 or DMSO. The cells were lysed and western blotting performed with the indicated antibodies. Equalization of protein loading was verified on the same membrane by reprobing after stripping. Data shown were representative of 2 independent experiments. (C) qRT-PCR analysis of c-kit and bcl-2 mRNA levels in the cells after 24 h treatment with C646 or DMSO. Histograms show relative mRNA levels normalized to control ABL gene; means ± SD of 3 independent experiments. * P <0.05.
    Figure Legend Snippet: Western blot analysis of (A) acetylated H3, total histone H3, (B) c-kit and bcl-2 proteins in Kasumi-1 and SKNO-1 cells after 24 h treatment with C646 or DMSO. The cells were lysed and western blotting performed with the indicated antibodies. Equalization of protein loading was verified on the same membrane by reprobing after stripping. Data shown were representative of 2 independent experiments. (C) qRT-PCR analysis of c-kit and bcl-2 mRNA levels in the cells after 24 h treatment with C646 or DMSO. Histograms show relative mRNA levels normalized to control ABL gene; means ± SD of 3 independent experiments. * P <0.05.

    Techniques Used: Western Blot, Stripping Membranes, Quantitative RT-PCR

    kasumi 1  (ATCC)


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    ATCC kasumi 1
    A. RT-PCR was performed to analyze IER5 mRNA expression in AML cell lines (KG-1, <t>Kasumi-1,</t> U937, and YRK2) treated with or without TMPP (5 and 10 µM) or Ara-C (1 µM) for 24 h. GAPDH mRNA expression is shown as an internal control. RT-PCR results representative of three independent experiments are shown. Relative levels of IER5 mRNA expression in AMLs were measured using QRT-PCR. B. IER5 mRNA and protein expression in U937 cells that were transfected with IER5 cDNA, shRNA-#1, or -#2, or were treated with TMPP (5 µM), were assessed using RT-PCR and QRT-PCR, and Western blotting, respectively. Actin was immunoblotted as a loading control. The expression levels of the target mRNAs were normalized to the expression of GAPDH mRNA. The results are expressed relative to the untreated control which was set at 1. Each RT-PCR assay was performed at least three times, and the results are expressed as means ± SD. * P <0.01. Western blotting results representative of three independent experiments are shown.
    Kasumi 1, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Transcriptional Repression of Cdc25B by IER5 Inhibits the Proliferation of Leukemic Progenitor Cells through NF-YB and p300 in Acute Myeloid Leukemia"

    Article Title: Transcriptional Repression of Cdc25B by IER5 Inhibits the Proliferation of Leukemic Progenitor Cells through NF-YB and p300 in Acute Myeloid Leukemia

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0028011

    A. RT-PCR was performed to analyze IER5 mRNA expression in AML cell lines (KG-1, Kasumi-1, U937, and YRK2) treated with or without TMPP (5 and 10 µM) or Ara-C (1 µM) for 24 h. GAPDH mRNA expression is shown as an internal control. RT-PCR results representative of three independent experiments are shown. Relative levels of IER5 mRNA expression in AMLs were measured using QRT-PCR. B. IER5 mRNA and protein expression in U937 cells that were transfected with IER5 cDNA, shRNA-#1, or -#2, or were treated with TMPP (5 µM), were assessed using RT-PCR and QRT-PCR, and Western blotting, respectively. Actin was immunoblotted as a loading control. The expression levels of the target mRNAs were normalized to the expression of GAPDH mRNA. The results are expressed relative to the untreated control which was set at 1. Each RT-PCR assay was performed at least three times, and the results are expressed as means ± SD. * P <0.01. Western blotting results representative of three independent experiments are shown.
    Figure Legend Snippet: A. RT-PCR was performed to analyze IER5 mRNA expression in AML cell lines (KG-1, Kasumi-1, U937, and YRK2) treated with or without TMPP (5 and 10 µM) or Ara-C (1 µM) for 24 h. GAPDH mRNA expression is shown as an internal control. RT-PCR results representative of three independent experiments are shown. Relative levels of IER5 mRNA expression in AMLs were measured using QRT-PCR. B. IER5 mRNA and protein expression in U937 cells that were transfected with IER5 cDNA, shRNA-#1, or -#2, or were treated with TMPP (5 µM), were assessed using RT-PCR and QRT-PCR, and Western blotting, respectively. Actin was immunoblotted as a loading control. The expression levels of the target mRNAs were normalized to the expression of GAPDH mRNA. The results are expressed relative to the untreated control which was set at 1. Each RT-PCR assay was performed at least three times, and the results are expressed as means ± SD. * P <0.01. Western blotting results representative of three independent experiments are shown.

    Techniques Used: Reverse Transcription Polymerase Chain Reaction, Expressing, Quantitative RT-PCR, Transfection, shRNA, Western Blot

    kasumi 1  (ATCC)


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    ATCC kasumi 1
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    myeloid  (ATCC)


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    kasumi 1  (ATCC)


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    ATCC kasumi 1
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    ATCC kasumi 1
    a Western blot of WT, PLK2 − / − , USP18 − / − , and USP18 − / − PLK2 − / − THP-1 cells treated with or without IFNα (1000 U/ml) for 48 h with indicated antibodies. b Percentage of live cells in ( a ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. c Analysis of ICD markers (LDH release and ecto-CRT) in ( b ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. d Western blot of PLK2 − / − THP-1 cells infected with Mock or PLK2 after two days of blasticidin selection using the indicated antibodies. e; Percentage of live cells in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. f Analysis of ICD markers (LDH release and ecto-CRT) and IL-1β secretions in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. g ; THP-1 and <t>Kasumi-1</t> cells were transduced with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, cell lysates were analyzed by western blot with indicated antibodies. h Ectopic PLK2 expression induces cell death in several AML cell lines independent of its kinase activity. THP-1, Kasumi-1, and MV4-11 cells were infected with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, live cells were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. i THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 (final 10 µM) for 48 h, then cell lysates were analyzed. j THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 for indicated times, then PI (%) and Annexin V + (%) were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. k Two different PDX AML cells were cultured with different dose of TC-S7005, and analyzed cell growth ( n = 3 independent samples each conditions). All data represent mean ± s.d, except where indicated. n.s. not statistically significant. p -value was determined by one-way ANOVA test. Source data are provided as a Source Data file.
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    ATCC kasumi1
    a Western blot of WT, PLK2 − / − , USP18 − / − , and USP18 − / − PLK2 − / − THP-1 cells treated with or without IFNα (1000 U/ml) for 48 h with indicated antibodies. b Percentage of live cells in ( a ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. c Analysis of ICD markers (LDH release and ecto-CRT) in ( b ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. d Western blot of PLK2 − / − THP-1 cells infected with Mock or PLK2 after two days of blasticidin selection using the indicated antibodies. e; Percentage of live cells in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. f Analysis of ICD markers (LDH release and ecto-CRT) and IL-1β secretions in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. g ; THP-1 and <t>Kasumi-1</t> cells were transduced with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, cell lysates were analyzed by western blot with indicated antibodies. h Ectopic PLK2 expression induces cell death in several AML cell lines independent of its kinase activity. THP-1, Kasumi-1, and MV4-11 cells were infected with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, live cells were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. i THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 (final 10 µM) for 48 h, then cell lysates were analyzed. j THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 for indicated times, then PI (%) and Annexin V + (%) were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. k Two different PDX AML cells were cultured with different dose of TC-S7005, and analyzed cell growth ( n = 3 independent samples each conditions). All data represent mean ± s.d, except where indicated. n.s. not statistically significant. p -value was determined by one-way ANOVA test. Source data are provided as a Source Data file.
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    nomo 1  (ATCC)
    99
    ATCC nomo 1
    a Western blot of WT, PLK2 − / − , USP18 − / − , and USP18 − / − PLK2 − / − THP-1 cells treated with or without IFNα (1000 U/ml) for 48 h with indicated antibodies. b Percentage of live cells in ( a ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. c Analysis of ICD markers (LDH release and ecto-CRT) in ( b ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. d Western blot of PLK2 − / − THP-1 cells infected with Mock or PLK2 after two days of blasticidin selection using the indicated antibodies. e; Percentage of live cells in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. f Analysis of ICD markers (LDH release and ecto-CRT) and IL-1β secretions in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. g ; THP-1 and <t>Kasumi-1</t> cells were transduced with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, cell lysates were analyzed by western blot with indicated antibodies. h Ectopic PLK2 expression induces cell death in several AML cell lines independent of its kinase activity. THP-1, Kasumi-1, and MV4-11 cells were infected with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, live cells were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. i THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 (final 10 µM) for 48 h, then cell lysates were analyzed. j THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 for indicated times, then PI (%) and Annexin V + (%) were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. k Two different PDX AML cells were cultured with different dose of TC-S7005, and analyzed cell growth ( n = 3 independent samples each conditions). All data represent mean ± s.d, except where indicated. n.s. not statistically significant. p -value was determined by one-way ANOVA test. Source data are provided as a Source Data file.
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    ATCC human aml cell line kasumi
    Downregulation of SMIM3 inhibited cell proliferation and colony formation in AML cells. The efficiency of SMIM3 knockdown in the <t>Kasumi-1</t> and THP-1 cell lines was verified by A , B reverse transcription-quantitative polymerase chain reaction and E , F immune fluorescence, respectively. C , D Cell proliferation was detected by the CCK-8 assay in Kasumi-1 and THP-1. G , H The colony formation of SMIM3 -CTRL and SMIM3 -KD in Kasumi-1 and THP-1. CTRL, control; KD, knockdown; *P < 0.05 compared with CTRL cells; **P < 0.01 compared with CTRL cells; ***P < 0.001 compared with CTRL cells; Error bars indicate the standard deviation
    Human Aml Cell Line Kasumi, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC myeloid
    Downregulation of SMIM3 inhibited cell proliferation and colony formation in AML cells. The efficiency of SMIM3 knockdown in the <t>Kasumi-1</t> and THP-1 cell lines was verified by A , B reverse transcription-quantitative polymerase chain reaction and E , F immune fluorescence, respectively. C , D Cell proliferation was detected by the CCK-8 assay in Kasumi-1 and THP-1. G , H The colony formation of SMIM3 -CTRL and SMIM3 -KD in Kasumi-1 and THP-1. CTRL, control; KD, knockdown; *P < 0.05 compared with CTRL cells; **P < 0.01 compared with CTRL cells; ***P < 0.001 compared with CTRL cells; Error bars indicate the standard deviation
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    a Western blot of WT, PLK2 − / − , USP18 − / − , and USP18 − / − PLK2 − / − THP-1 cells treated with or without IFNα (1000 U/ml) for 48 h with indicated antibodies. b Percentage of live cells in ( a ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. c Analysis of ICD markers (LDH release and ecto-CRT) in ( b ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. d Western blot of PLK2 − / − THP-1 cells infected with Mock or PLK2 after two days of blasticidin selection using the indicated antibodies. e; Percentage of live cells in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. f Analysis of ICD markers (LDH release and ecto-CRT) and IL-1β secretions in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. g ; THP-1 and Kasumi-1 cells were transduced with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, cell lysates were analyzed by western blot with indicated antibodies. h Ectopic PLK2 expression induces cell death in several AML cell lines independent of its kinase activity. THP-1, Kasumi-1, and MV4-11 cells were infected with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, live cells were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. i THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 (final 10 µM) for 48 h, then cell lysates were analyzed. j THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 for indicated times, then PI (%) and Annexin V + (%) were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. k Two different PDX AML cells were cultured with different dose of TC-S7005, and analyzed cell growth ( n = 3 independent samples each conditions). All data represent mean ± s.d, except where indicated. n.s. not statistically significant. p -value was determined by one-way ANOVA test. Source data are provided as a Source Data file.

    Journal: Nature Communications

    Article Title: Expansion of interferon inducible gene pool via USP18 inhibition promotes cancer cell pyroptosis

    doi: 10.1038/s41467-022-35348-5

    Figure Lengend Snippet: a Western blot of WT, PLK2 − / − , USP18 − / − , and USP18 − / − PLK2 − / − THP-1 cells treated with or without IFNα (1000 U/ml) for 48 h with indicated antibodies. b Percentage of live cells in ( a ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. c Analysis of ICD markers (LDH release and ecto-CRT) in ( b ) ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. d Western blot of PLK2 − / − THP-1 cells infected with Mock or PLK2 after two days of blasticidin selection using the indicated antibodies. e; Percentage of live cells in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. f Analysis of ICD markers (LDH release and ecto-CRT) and IL-1β secretions in ( d ) ( n = 3 independent samples each). p -value was determined by two-tailed Student t -test. g ; THP-1 and Kasumi-1 cells were transduced with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, cell lysates were analyzed by western blot with indicated antibodies. h Ectopic PLK2 expression induces cell death in several AML cell lines independent of its kinase activity. THP-1, Kasumi-1, and MV4-11 cells were infected with MIP, MIP-PLK2 WT, or MIP-PLK2 enzyme activity mutants. Two days after puromycin selection, live cells were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. i THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 (final 10 µM) for 48 h, then cell lysates were analyzed. j THP-1 or OCI-AML3 cells were treated with DMSO or TC-S7005 for indicated times, then PI (%) and Annexin V + (%) were analyzed by FACS ( n = 3 independent samples each). p -value was determined by one-way ANOVA test. k Two different PDX AML cells were cultured with different dose of TC-S7005, and analyzed cell growth ( n = 3 independent samples each conditions). All data represent mean ± s.d, except where indicated. n.s. not statistically significant. p -value was determined by one-way ANOVA test. Source data are provided as a Source Data file.

    Article Snippet: THP-1 (ATCC), MV4-11 (ATCC), MOLM13 (ATCC), OCI-AML3 (ATCC), Kasumi-1 (ATCC), B16F10 (ATCC) and MC38 (NCI) cells were grown in RPMI media supplemented with glutamine, penicillin/streptomycin, and 10% FBS.

    Techniques: Western Blot, Infection, Selection, Two Tailed Test, Transduction, Activity Assay, Expressing, Cell Culture

    Downregulation of SMIM3 inhibited cell proliferation and colony formation in AML cells. The efficiency of SMIM3 knockdown in the Kasumi-1 and THP-1 cell lines was verified by A , B reverse transcription-quantitative polymerase chain reaction and E , F immune fluorescence, respectively. C , D Cell proliferation was detected by the CCK-8 assay in Kasumi-1 and THP-1. G , H The colony formation of SMIM3 -CTRL and SMIM3 -KD in Kasumi-1 and THP-1. CTRL, control; KD, knockdown; *P < 0.05 compared with CTRL cells; **P < 0.01 compared with CTRL cells; ***P < 0.001 compared with CTRL cells; Error bars indicate the standard deviation

    Journal: Journal of Translational Medicine

    Article Title: Downregulation of SMIM3 inhibits growth of leukemia via PI3K-AKT signaling pathway and correlates with prognosis of adult acute myeloid leukemia with normal karyotype

    doi: 10.1186/s12967-022-03831-8

    Figure Lengend Snippet: Downregulation of SMIM3 inhibited cell proliferation and colony formation in AML cells. The efficiency of SMIM3 knockdown in the Kasumi-1 and THP-1 cell lines was verified by A , B reverse transcription-quantitative polymerase chain reaction and E , F immune fluorescence, respectively. C , D Cell proliferation was detected by the CCK-8 assay in Kasumi-1 and THP-1. G , H The colony formation of SMIM3 -CTRL and SMIM3 -KD in Kasumi-1 and THP-1. CTRL, control; KD, knockdown; *P < 0.05 compared with CTRL cells; **P < 0.01 compared with CTRL cells; ***P < 0.001 compared with CTRL cells; Error bars indicate the standard deviation

    Article Snippet: The human AML cell line Kasumi-1 was purchased from American Type Culture Collection (Manassas, VA, USA).

    Techniques: Real-time Polymerase Chain Reaction, Fluorescence, CCK-8 Assay, Standard Deviation

    Apoptosis and cell cycle analysis in AML cell lines. A , B The flow cytometry was applied to analyze apoptosis in SMIM3 knockdown cells compared with control. C – E Propidium iodide (PI) staining was applied to analyze the cell cycle of SMIM3 knockdown cells compared with control. F Alterations in apoptosis and cell cycle-related protein assay in SMIM3 knockdown cells compared with control. G , H Densitometric analysis of the WB signals. CTRL, control; KD, knockdown; *P < 0.05 compared with CTRL cells; **P < 0.01 compared with CTRL cells; ***P < 0.001 compared with CTRL cells

    Journal: Journal of Translational Medicine

    Article Title: Downregulation of SMIM3 inhibits growth of leukemia via PI3K-AKT signaling pathway and correlates with prognosis of adult acute myeloid leukemia with normal karyotype

    doi: 10.1186/s12967-022-03831-8

    Figure Lengend Snippet: Apoptosis and cell cycle analysis in AML cell lines. A , B The flow cytometry was applied to analyze apoptosis in SMIM3 knockdown cells compared with control. C – E Propidium iodide (PI) staining was applied to analyze the cell cycle of SMIM3 knockdown cells compared with control. F Alterations in apoptosis and cell cycle-related protein assay in SMIM3 knockdown cells compared with control. G , H Densitometric analysis of the WB signals. CTRL, control; KD, knockdown; *P < 0.05 compared with CTRL cells; **P < 0.01 compared with CTRL cells; ***P < 0.001 compared with CTRL cells

    Article Snippet: The human AML cell line Kasumi-1 was purchased from American Type Culture Collection (Manassas, VA, USA).

    Techniques: Cell Cycle Assay, Flow Cytometry, Staining

    GO/KEGG enrichment analysis of subjects with high or low SMIM3 expression in the TCGA-LAML dataset. A Volcano map of the DEGs, including 231up-regulated genes and 1889 down-regulated genes. B Heat map showing the top ten up-regulated and the top ten down-regulated genes. The samples are shown on the X-axis, and the DEGs are shown on the Y-axis. D Venn diagram of the overlap among the DEGs and correlated genes. C GO and KEGG enrichment analysis of the co-expressed genes of DEGs and correlated genes. MF, molecular function. CC, cellular component. BP, biological process. Different categories were shown on the Y-axis, and the X-axis reflected the percentage of DEGs. PI3K-AKT signaling pathway is critical for SMIM3 -mediated changes. G Western blot analysis of PI3K-AKT signaling pathway in SMIM3 -KD cells and controls. H , I Densitometric analysis of the WB signals. E SC79 (10 mM) reversed the inhibitory effect of SMIM3 knockdown on the proliferation of Kasumi-1, F at 24 h. CTRL, control; KD, knockdown; ***P < 0.001 compared with CTRL cells; Error bars indicate the standard deviation

    Journal: Journal of Translational Medicine

    Article Title: Downregulation of SMIM3 inhibits growth of leukemia via PI3K-AKT signaling pathway and correlates with prognosis of adult acute myeloid leukemia with normal karyotype

    doi: 10.1186/s12967-022-03831-8

    Figure Lengend Snippet: GO/KEGG enrichment analysis of subjects with high or low SMIM3 expression in the TCGA-LAML dataset. A Volcano map of the DEGs, including 231up-regulated genes and 1889 down-regulated genes. B Heat map showing the top ten up-regulated and the top ten down-regulated genes. The samples are shown on the X-axis, and the DEGs are shown on the Y-axis. D Venn diagram of the overlap among the DEGs and correlated genes. C GO and KEGG enrichment analysis of the co-expressed genes of DEGs and correlated genes. MF, molecular function. CC, cellular component. BP, biological process. Different categories were shown on the Y-axis, and the X-axis reflected the percentage of DEGs. PI3K-AKT signaling pathway is critical for SMIM3 -mediated changes. G Western blot analysis of PI3K-AKT signaling pathway in SMIM3 -KD cells and controls. H , I Densitometric analysis of the WB signals. E SC79 (10 mM) reversed the inhibitory effect of SMIM3 knockdown on the proliferation of Kasumi-1, F at 24 h. CTRL, control; KD, knockdown; ***P < 0.001 compared with CTRL cells; Error bars indicate the standard deviation

    Article Snippet: The human AML cell line Kasumi-1 was purchased from American Type Culture Collection (Manassas, VA, USA).

    Techniques: Expressing, Western Blot, Standard Deviation

    SMIM3 knockdown reduced the proliferation of AML cells in nude mice by inhibiting PI3K-AKT signaling pathway. A – D , F – I SMIM3 -KD inhibits tumor growth in Kasumi-1 and THP-1 cells. E , J The expression of PI3K-AKT signaling pathway proteins in tumor tissues by Western blot. CTRL, control; KD, knockdown; ***P < 0.001 compared with CTRL cells

    Journal: Journal of Translational Medicine

    Article Title: Downregulation of SMIM3 inhibits growth of leukemia via PI3K-AKT signaling pathway and correlates with prognosis of adult acute myeloid leukemia with normal karyotype

    doi: 10.1186/s12967-022-03831-8

    Figure Lengend Snippet: SMIM3 knockdown reduced the proliferation of AML cells in nude mice by inhibiting PI3K-AKT signaling pathway. A – D , F – I SMIM3 -KD inhibits tumor growth in Kasumi-1 and THP-1 cells. E , J The expression of PI3K-AKT signaling pathway proteins in tumor tissues by Western blot. CTRL, control; KD, knockdown; ***P < 0.001 compared with CTRL cells

    Article Snippet: The human AML cell line Kasumi-1 was purchased from American Type Culture Collection (Manassas, VA, USA).

    Techniques: Expressing, Western Blot