experimental models thp 1 cells Search Results


hl-60 shsdha #1 cells  (Shanghai Model Organisms Center)
90
Shanghai Model Organisms Center hl-60 shsdha #1 cells
a Correlation analysis between SDHA mRNA levels and succinate levels in primary AML samples ( n = 25). b The succinate levels of cells and plasma in the bone marrow of primary AML sample and non-AML samples. c The succinate levels of bone marrow cells and peripheral plasma in AML <t>orthotopic</t> <t>xenograft</t> mice and normal mice. d Correlation analysis between IC 50 of different chemotherapy drugs on primary AML samples and the succinate levels of these samples. a , d Pearson correlation coefficient r was calculated by GraphPad Prism. Data are presented as mean ± 95% confidence bands. The significance analysis was conducted by simple linear regression. e SDHA was knocked down in HL-60 cells using lentiviral infection, followed by two rounds of puromycin selection to establish stable SDHA knockdown cell lines. Then the succinate levels of HL-60 <t>shCtrl</t> cells and HL-60 shSDHA cells, and the effects of SDHA knock down were detected. The HL-60 shCtrl and HL-60 shSDHA cells used in the following are the same as the cells used here. ( f ) The clone formation rates of shCtrl cells and shSDHA HL-60 cells. g The clone formation rates of HL-60 cells after treated with different concentrations of succinate for 10 ~ 14 days. Suc: succinate. h The effect of SDHA knocked down in the tumors of AML xenograft models. i Tumor growth of the shCtrl and shSDHA HL-60 cells derived xenografts in NSG mice. Tumor volume growth curves are based as mean ± SE ( n = 5). j , k shCtrl and shSDHA HL-60 cells were treated with three gradient concentrations of chemotherapy drugs ( j ) or 50 % peak plasma concentration (PPC) of targeted drugs for three days ( k ). The resistance index is calculated using the area under the curve (AUC) of cell viability at three chemotherapy drug concentrations. A larger resistance index indicates greater drug resistance. b – c , e – g , Data are presented as mean ± SD; ( b – c , e – g , i – k ) The significance analysis was conducted by two-tailed unpaired Student’s t -test. e – g Three independent experiments were performed. Source data are provided as a Source Data file.
Hl 60 Shsdha #1 Cells, supplied by Shanghai Model Organisms Center, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/hl-60 shsdha #1 cells/product/Shanghai Model Organisms Center
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hl-60 shsdha #1 cells - by Bioz Stars, 2026-03
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monocytic hiv-1 latent model cell lines thp-1 nluc #225  (Nacalai)
90
Nacalai monocytic hiv-1 latent model cell lines thp-1 nluc #225
a Correlation analysis between SDHA mRNA levels and succinate levels in primary AML samples ( n = 25). b The succinate levels of cells and plasma in the bone marrow of primary AML sample and non-AML samples. c The succinate levels of bone marrow cells and peripheral plasma in AML <t>orthotopic</t> <t>xenograft</t> mice and normal mice. d Correlation analysis between IC 50 of different chemotherapy drugs on primary AML samples and the succinate levels of these samples. a , d Pearson correlation coefficient r was calculated by GraphPad Prism. Data are presented as mean ± 95% confidence bands. The significance analysis was conducted by simple linear regression. e SDHA was knocked down in HL-60 cells using lentiviral infection, followed by two rounds of puromycin selection to establish stable SDHA knockdown cell lines. Then the succinate levels of HL-60 <t>shCtrl</t> cells and HL-60 shSDHA cells, and the effects of SDHA knock down were detected. The HL-60 shCtrl and HL-60 shSDHA cells used in the following are the same as the cells used here. ( f ) The clone formation rates of shCtrl cells and shSDHA HL-60 cells. g The clone formation rates of HL-60 cells after treated with different concentrations of succinate for 10 ~ 14 days. Suc: succinate. h The effect of SDHA knocked down in the tumors of AML xenograft models. i Tumor growth of the shCtrl and shSDHA HL-60 cells derived xenografts in NSG mice. Tumor volume growth curves are based as mean ± SE ( n = 5). j , k shCtrl and shSDHA HL-60 cells were treated with three gradient concentrations of chemotherapy drugs ( j ) or 50 % peak plasma concentration (PPC) of targeted drugs for three days ( k ). The resistance index is calculated using the area under the curve (AUC) of cell viability at three chemotherapy drug concentrations. A larger resistance index indicates greater drug resistance. b – c , e – g , Data are presented as mean ± SD; ( b – c , e – g , i – k ) The significance analysis was conducted by two-tailed unpaired Student’s t -test. e – g Three independent experiments were performed. Source data are provided as a Source Data file.
Monocytic Hiv 1 Latent Model Cell Lines Thp 1 Nluc #225, supplied by Nacalai, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/monocytic hiv-1 latent model cell lines thp-1 nluc #225/product/Nacalai
Average 90 stars, based on 1 article reviews
monocytic hiv-1 latent model cell lines thp-1 nluc #225 - by Bioz Stars, 2026-03
90/100 stars
  Buy from Supplier

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a Correlation analysis between SDHA mRNA levels and succinate levels in primary AML samples ( n = 25). b The succinate levels of cells and plasma in the bone marrow of primary AML sample and non-AML samples. c The succinate levels of bone marrow cells and peripheral plasma in AML orthotopic xenograft mice and normal mice. d Correlation analysis between IC 50 of different chemotherapy drugs on primary AML samples and the succinate levels of these samples. a , d Pearson correlation coefficient r was calculated by GraphPad Prism. Data are presented as mean ± 95% confidence bands. The significance analysis was conducted by simple linear regression. e SDHA was knocked down in HL-60 cells using lentiviral infection, followed by two rounds of puromycin selection to establish stable SDHA knockdown cell lines. Then the succinate levels of HL-60 shCtrl cells and HL-60 shSDHA cells, and the effects of SDHA knock down were detected. The HL-60 shCtrl and HL-60 shSDHA cells used in the following are the same as the cells used here. ( f ) The clone formation rates of shCtrl cells and shSDHA HL-60 cells. g The clone formation rates of HL-60 cells after treated with different concentrations of succinate for 10 ~ 14 days. Suc: succinate. h The effect of SDHA knocked down in the tumors of AML xenograft models. i Tumor growth of the shCtrl and shSDHA HL-60 cells derived xenografts in NSG mice. Tumor volume growth curves are based as mean ± SE ( n = 5). j , k shCtrl and shSDHA HL-60 cells were treated with three gradient concentrations of chemotherapy drugs ( j ) or 50 % peak plasma concentration (PPC) of targeted drugs for three days ( k ). The resistance index is calculated using the area under the curve (AUC) of cell viability at three chemotherapy drug concentrations. A larger resistance index indicates greater drug resistance. b – c , e – g , Data are presented as mean ± SD; ( b – c , e – g , i – k ) The significance analysis was conducted by two-tailed unpaired Student’s t -test. e – g Three independent experiments were performed. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Succinate dehydrogenase deficiency-driven succinate accumulation induces drug resistance in acute myeloid leukemia via ubiquitin-cullin regulation

doi: 10.1038/s41467-024-53398-9

Figure Lengend Snippet: a Correlation analysis between SDHA mRNA levels and succinate levels in primary AML samples ( n = 25). b The succinate levels of cells and plasma in the bone marrow of primary AML sample and non-AML samples. c The succinate levels of bone marrow cells and peripheral plasma in AML orthotopic xenograft mice and normal mice. d Correlation analysis between IC 50 of different chemotherapy drugs on primary AML samples and the succinate levels of these samples. a , d Pearson correlation coefficient r was calculated by GraphPad Prism. Data are presented as mean ± 95% confidence bands. The significance analysis was conducted by simple linear regression. e SDHA was knocked down in HL-60 cells using lentiviral infection, followed by two rounds of puromycin selection to establish stable SDHA knockdown cell lines. Then the succinate levels of HL-60 shCtrl cells and HL-60 shSDHA cells, and the effects of SDHA knock down were detected. The HL-60 shCtrl and HL-60 shSDHA cells used in the following are the same as the cells used here. ( f ) The clone formation rates of shCtrl cells and shSDHA HL-60 cells. g The clone formation rates of HL-60 cells after treated with different concentrations of succinate for 10 ~ 14 days. Suc: succinate. h The effect of SDHA knocked down in the tumors of AML xenograft models. i Tumor growth of the shCtrl and shSDHA HL-60 cells derived xenografts in NSG mice. Tumor volume growth curves are based as mean ± SE ( n = 5). j , k shCtrl and shSDHA HL-60 cells were treated with three gradient concentrations of chemotherapy drugs ( j ) or 50 % peak plasma concentration (PPC) of targeted drugs for three days ( k ). The resistance index is calculated using the area under the curve (AUC) of cell viability at three chemotherapy drug concentrations. A larger resistance index indicates greater drug resistance. b – c , e – g , Data are presented as mean ± SD; ( b – c , e – g , i – k ) The significance analysis was conducted by two-tailed unpaired Student’s t -test. e – g Three independent experiments were performed. Source data are provided as a Source Data file.

Article Snippet: For the xenograft experiment, 1 × 10 7 HL-60 shCtrl cells or shSDHA (#1 and #2) cells were injected subcutaneously into female NOD-SCID IL-2receptor gamma null (NSG) mice (Shanghai Model Organisms).

Techniques: Clinical Proteomics, Infection, Selection, Knockdown, Derivative Assay, Concentration Assay, Two Tailed Test

a Schematic view of the proteome and transcriptome sequencing results of HL-60 cells treated by 6 mM succinate for 3 h or 24 h. b Heat map display of the upregulated proteins (cluster I + II in Fig. 3a) both in the proteome of succinate 3 h and 24 h groups, and their corresponding mRNA levels. Three replicate results were demonstrated. c NES scores of the most altered gene signatures derived from GSEA in succinate-treated proteome compared to control condition. The p -values of all results are less than 0.05. Overlaying the proteins upregulated by succinate from the four pro-cancer gene signatures (in red) with the 255 proteins in cluster (I + II), 34 proteins were identified. Subsequently, we analyzed the correlation of these 34 proteins with AML prognosis and found that high expression of WEE1 and TUBG1 was significantly associated with AML prognosis. d The relative protein levels of WEE1 and TUBG1 in succinate group compared to control group in proteome data. e Detection of WEE1 protein level (left) and mRNA level (right) in HL-60 cells after treated by 6 mM succinate. f , g WEE1 was knocked down in shSDHA and shCtrl HL-60 cells. Then cytarabine and IDA of indicated concentrations were treated on the above cells for three days, followed by the detection of cell viability. Cyta: cytarabine; IDA: idarubicin HCl. h GSEA analysis for the upregulated proteins under MLN4924, MG132 or CQ treatment in succinate v.s . control condition. The succinate group contains both succinate 3 h treatment group and 24 h treatment group. i Detection of cullin neddylation level in HL-60 and NB4 cells after treated with 6 mM succinate for indicated time. j Detection of cullin neddylation in SDHA stably-knocked down HL-60 and NB4 cells. k , l Detection of the interaction between exogenous UBC12 and endogenous UBE1C ( k ) or recombinant UBE1C ( l ) in 293 T cells after transfected with UBC12, followed by treatment with succinate. R: recombinant. a – g , i – l Three independent experiments were performed; d-f, Data are presented as mean ± SD; a – h The significance analysis was conducted by two-tailed unpaired Student’s t -test. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Succinate dehydrogenase deficiency-driven succinate accumulation induces drug resistance in acute myeloid leukemia via ubiquitin-cullin regulation

doi: 10.1038/s41467-024-53398-9

Figure Lengend Snippet: a Schematic view of the proteome and transcriptome sequencing results of HL-60 cells treated by 6 mM succinate for 3 h or 24 h. b Heat map display of the upregulated proteins (cluster I + II in Fig. 3a) both in the proteome of succinate 3 h and 24 h groups, and their corresponding mRNA levels. Three replicate results were demonstrated. c NES scores of the most altered gene signatures derived from GSEA in succinate-treated proteome compared to control condition. The p -values of all results are less than 0.05. Overlaying the proteins upregulated by succinate from the four pro-cancer gene signatures (in red) with the 255 proteins in cluster (I + II), 34 proteins were identified. Subsequently, we analyzed the correlation of these 34 proteins with AML prognosis and found that high expression of WEE1 and TUBG1 was significantly associated with AML prognosis. d The relative protein levels of WEE1 and TUBG1 in succinate group compared to control group in proteome data. e Detection of WEE1 protein level (left) and mRNA level (right) in HL-60 cells after treated by 6 mM succinate. f , g WEE1 was knocked down in shSDHA and shCtrl HL-60 cells. Then cytarabine and IDA of indicated concentrations were treated on the above cells for three days, followed by the detection of cell viability. Cyta: cytarabine; IDA: idarubicin HCl. h GSEA analysis for the upregulated proteins under MLN4924, MG132 or CQ treatment in succinate v.s . control condition. The succinate group contains both succinate 3 h treatment group and 24 h treatment group. i Detection of cullin neddylation level in HL-60 and NB4 cells after treated with 6 mM succinate for indicated time. j Detection of cullin neddylation in SDHA stably-knocked down HL-60 and NB4 cells. k , l Detection of the interaction between exogenous UBC12 and endogenous UBE1C ( k ) or recombinant UBE1C ( l ) in 293 T cells after transfected with UBC12, followed by treatment with succinate. R: recombinant. a – g , i – l Three independent experiments were performed; d-f, Data are presented as mean ± SD; a – h The significance analysis was conducted by two-tailed unpaired Student’s t -test. Source data are provided as a Source Data file.

Article Snippet: For the xenograft experiment, 1 × 10 7 HL-60 shCtrl cells or shSDHA (#1 and #2) cells were injected subcutaneously into female NOD-SCID IL-2receptor gamma null (NSG) mice (Shanghai Model Organisms).

Techniques: Sequencing, Derivative Assay, Control, Expressing, Stable Transfection, Recombinant, Transfection, Two Tailed Test

a H1299 cells were treated with 82 FDA approved anti-cancer drugs for three days (25% PPC). The final relative succinate Level= the succinate level /the survival rate. b HL-60 cells were treated with the top7 drugs (25 % PPC, three days) in Fig. 6a. Two independent experiments were performed; Data are presented as mean ( n = 2). c shCtrl and shSDHA HL-60 cells were treated with 500 nM fludarabine for three days. d Detection of UBC12 phosphorylation in HL-60 cells after treated with 500 nM fludarabine for three days, followed by treatment of 6 mM succinate for 3 h before collecting the samples. The samples derive from the same experiment but different gels for p-UBC12 and another for UBC12 were processed in parallel. e Detection of cullin neddylation in HL-60 cells after treated with 500 nM fludarabine for three days, followed by treatment of 6 mM succinate for indicated time before collecting the samples. The samples derive from the same experiment but different gels for cul1 and another for cul3 were processed in parallel. f – g shCtrl and shSDHA HL-60 cells were treated with fludarabine ( f ) and CB-839 ( g ) for three days respectively. h shCtrl and shSDHA HL-60 cells were seeded in soft agar, followed by treatment with 200 nM fludarabine. After two weeks, the clones were stained and counted. i , shCtrl and shSDHA HL-60 cells were treated with 500 nM fludarabine for three days, and the apoptosis rates were detected. j Detection of intracellular succinate levels (left) and cell viability (right) of HL-60 shSDHA cells after treated by a series of concentrations of fludarabine for three days. k – l Cytarabine, IDA or fludarabine were treated individually or in combination to indicated cells for three days. IDA: idarubicin HCl. c , f – l Three independent experiments were performed. Data are presented as mean ± SD ( n = 3); The significance analysis were conducted by two-tailed Student’s t -test or one-way ANOVA for Fig. 6c, f – l . Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Succinate dehydrogenase deficiency-driven succinate accumulation induces drug resistance in acute myeloid leukemia via ubiquitin-cullin regulation

doi: 10.1038/s41467-024-53398-9

Figure Lengend Snippet: a H1299 cells were treated with 82 FDA approved anti-cancer drugs for three days (25% PPC). The final relative succinate Level= the succinate level /the survival rate. b HL-60 cells were treated with the top7 drugs (25 % PPC, three days) in Fig. 6a. Two independent experiments were performed; Data are presented as mean ( n = 2). c shCtrl and shSDHA HL-60 cells were treated with 500 nM fludarabine for three days. d Detection of UBC12 phosphorylation in HL-60 cells after treated with 500 nM fludarabine for three days, followed by treatment of 6 mM succinate for 3 h before collecting the samples. The samples derive from the same experiment but different gels for p-UBC12 and another for UBC12 were processed in parallel. e Detection of cullin neddylation in HL-60 cells after treated with 500 nM fludarabine for three days, followed by treatment of 6 mM succinate for indicated time before collecting the samples. The samples derive from the same experiment but different gels for cul1 and another for cul3 were processed in parallel. f – g shCtrl and shSDHA HL-60 cells were treated with fludarabine ( f ) and CB-839 ( g ) for three days respectively. h shCtrl and shSDHA HL-60 cells were seeded in soft agar, followed by treatment with 200 nM fludarabine. After two weeks, the clones were stained and counted. i , shCtrl and shSDHA HL-60 cells were treated with 500 nM fludarabine for three days, and the apoptosis rates were detected. j Detection of intracellular succinate levels (left) and cell viability (right) of HL-60 shSDHA cells after treated by a series of concentrations of fludarabine for three days. k – l Cytarabine, IDA or fludarabine were treated individually or in combination to indicated cells for three days. IDA: idarubicin HCl. c , f – l Three independent experiments were performed. Data are presented as mean ± SD ( n = 3); The significance analysis were conducted by two-tailed Student’s t -test or one-way ANOVA for Fig. 6c, f – l . Source data are provided as a Source Data file.

Article Snippet: For the xenograft experiment, 1 × 10 7 HL-60 shCtrl cells or shSDHA (#1 and #2) cells were injected subcutaneously into female NOD-SCID IL-2receptor gamma null (NSG) mice (Shanghai Model Organisms).

Techniques: Phospho-proteomics, Clone Assay, Staining, Two Tailed Test

a Correlation analysis between IC 50 of fludarabine on primary AML samples and the succinate levels of these samples. Pearson correlation coefficient r was calculated by GraphPad Prism. Data are presented as mean ± 95% confidence bands. The significance analysis was conducted by simple linear regression. b – f The effect of fludarabine and cytarabine on the tumor burden of shCtrl group and shSDHA group NSG mice. ( b ) Tumor growth of the xenografts models. ( c ) Relative tumor volumes of the xenograft models. d Effects of fludarabine and cytarabine on shCtrl group and shSDHA group tumor size and tumor weight at pre-dose and post-dose. RTV, relative tumor volume; T/C (%) = RTV Treatment /RTV control × 100. Data are represented as mean ± SE ( n = 6); ( e ) Images of tumors in each treatment group. f The succinate levels in shSDHA group tumor tissues. The significance analysis was conducted by two-tailed paired Student’s t -test for ( b ) and unpaired Student’s t -test for ( c , d , f ). g The survival time of AML PDX with high succinate levels treated by fludarabine (40 mg/kg) or cytarabine (60 mg/kg) by intraperitoneal injection every other day. The significance analysis was conducted by Log-rank test. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Succinate dehydrogenase deficiency-driven succinate accumulation induces drug resistance in acute myeloid leukemia via ubiquitin-cullin regulation

doi: 10.1038/s41467-024-53398-9

Figure Lengend Snippet: a Correlation analysis between IC 50 of fludarabine on primary AML samples and the succinate levels of these samples. Pearson correlation coefficient r was calculated by GraphPad Prism. Data are presented as mean ± 95% confidence bands. The significance analysis was conducted by simple linear regression. b – f The effect of fludarabine and cytarabine on the tumor burden of shCtrl group and shSDHA group NSG mice. ( b ) Tumor growth of the xenografts models. ( c ) Relative tumor volumes of the xenograft models. d Effects of fludarabine and cytarabine on shCtrl group and shSDHA group tumor size and tumor weight at pre-dose and post-dose. RTV, relative tumor volume; T/C (%) = RTV Treatment /RTV control × 100. Data are represented as mean ± SE ( n = 6); ( e ) Images of tumors in each treatment group. f The succinate levels in shSDHA group tumor tissues. The significance analysis was conducted by two-tailed paired Student’s t -test for ( b ) and unpaired Student’s t -test for ( c , d , f ). g The survival time of AML PDX with high succinate levels treated by fludarabine (40 mg/kg) or cytarabine (60 mg/kg) by intraperitoneal injection every other day. The significance analysis was conducted by Log-rank test. Source data are provided as a Source Data file.

Article Snippet: For the xenograft experiment, 1 × 10 7 HL-60 shCtrl cells or shSDHA (#1 and #2) cells were injected subcutaneously into female NOD-SCID IL-2receptor gamma null (NSG) mice (Shanghai Model Organisms).

Techniques: Control, Two Tailed Test, Injection