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<t>AML</t> <t>cell</t> sensitivity to CDK8/19i correlates with their metabolic properties. A. AML cell lines and their sensitivity to CCNC KO (CRISPR_CCNC (DepMap Public 25Q3+Score, Chronos)) and siRNA CCNC (siRNA_CCNC, (Achilles+DRIVE+Marcotte, DEMETER2)) as determined by DepMap or CDK8/19i as determined by minIC50 from published data. B . Distribution ridgeplots of CDK8/19i sensitive and resistant AML cells based on their average sensitivity to gene KO (DepMap, Chronos) in the groups determined using the Hallmark database. Data transformed using z-scaling. Groups of KO in which the greatest differences between groups of cells are expected are marked in green. C . Heatmap of genes whose KO directly correlates with AML sensitivity to CDK8/19i. Data was obtained from the DepMap (Public 25Q3+Score, Chronos) using Spearman correlation. Data were transformed using z-scaling. E . Distribution ridgeplots of CDK8/19i sensitive and resistant AML cells based on their metabolic indices (genes obtained from DepMap Expression Public 25Q3 database). The indices with the greatest differences between CDK8/19i sensitive and resistant AML cells are presented. G . A schematic diagram summarizing the major cellular processes that may be involved in the sensitivity of AML cells to CDK8/19i.
Human Aml Cell Lines Mv4, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human aml cell lines mv4 - by Bioz Stars, 2026-06
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ATCC human mv4
<t>AML</t> <t>cell</t> sensitivity to CDK8/19i correlates with their metabolic properties. A. AML cell lines and their sensitivity to CCNC KO (CRISPR_CCNC (DepMap Public 25Q3+Score, Chronos)) and siRNA CCNC (siRNA_CCNC, (Achilles+DRIVE+Marcotte, DEMETER2)) as determined by DepMap or CDK8/19i as determined by minIC50 from published data. B . Distribution ridgeplots of CDK8/19i sensitive and resistant AML cells based on their average sensitivity to gene KO (DepMap, Chronos) in the groups determined using the Hallmark database. Data transformed using z-scaling. Groups of KO in which the greatest differences between groups of cells are expected are marked in green. C . Heatmap of genes whose KO directly correlates with AML sensitivity to CDK8/19i. Data was obtained from the DepMap (Public 25Q3+Score, Chronos) using Spearman correlation. Data were transformed using z-scaling. E . Distribution ridgeplots of CDK8/19i sensitive and resistant AML cells based on their metabolic indices (genes obtained from DepMap Expression Public 25Q3 database). The indices with the greatest differences between CDK8/19i sensitive and resistant AML cells are presented. G . A schematic diagram summarizing the major cellular processes that may be involved in the sensitivity of AML cells to CDK8/19i.
Human Mv4, 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/human mv4/product/ATCC
Average 99 stars, based on 1 article reviews
human mv4 - by Bioz Stars, 2026-06
99/100 stars
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AML cell sensitivity to CDK8/19i correlates with their metabolic properties. A. AML cell lines and their sensitivity to CCNC KO (CRISPR_CCNC (DepMap Public 25Q3+Score, Chronos)) and siRNA CCNC (siRNA_CCNC, (Achilles+DRIVE+Marcotte, DEMETER2)) as determined by DepMap or CDK8/19i as determined by minIC50 from published data. B . Distribution ridgeplots of CDK8/19i sensitive and resistant AML cells based on their average sensitivity to gene KO (DepMap, Chronos) in the groups determined using the Hallmark database. Data transformed using z-scaling. Groups of KO in which the greatest differences between groups of cells are expected are marked in green. C . Heatmap of genes whose KO directly correlates with AML sensitivity to CDK8/19i. Data was obtained from the DepMap (Public 25Q3+Score, Chronos) using Spearman correlation. Data were transformed using z-scaling. E . Distribution ridgeplots of CDK8/19i sensitive and resistant AML cells based on their metabolic indices (genes obtained from DepMap Expression Public 25Q3 database). The indices with the greatest differences between CDK8/19i sensitive and resistant AML cells are presented. G . A schematic diagram summarizing the major cellular processes that may be involved in the sensitivity of AML cells to CDK8/19i.

Journal: bioRxiv

Article Title: The sensitivity of acute myeloid leukemia to CDK8/19 inhibitors is determined by their metabolic profile

doi: 10.64898/2025.12.14.694205

Figure Lengend Snippet: AML cell sensitivity to CDK8/19i correlates with their metabolic properties. A. AML cell lines and their sensitivity to CCNC KO (CRISPR_CCNC (DepMap Public 25Q3+Score, Chronos)) and siRNA CCNC (siRNA_CCNC, (Achilles+DRIVE+Marcotte, DEMETER2)) as determined by DepMap or CDK8/19i as determined by minIC50 from published data. B . Distribution ridgeplots of CDK8/19i sensitive and resistant AML cells based on their average sensitivity to gene KO (DepMap, Chronos) in the groups determined using the Hallmark database. Data transformed using z-scaling. Groups of KO in which the greatest differences between groups of cells are expected are marked in green. C . Heatmap of genes whose KO directly correlates with AML sensitivity to CDK8/19i. Data was obtained from the DepMap (Public 25Q3+Score, Chronos) using Spearman correlation. Data were transformed using z-scaling. E . Distribution ridgeplots of CDK8/19i sensitive and resistant AML cells based on their metabolic indices (genes obtained from DepMap Expression Public 25Q3 database). The indices with the greatest differences between CDK8/19i sensitive and resistant AML cells are presented. G . A schematic diagram summarizing the major cellular processes that may be involved in the sensitivity of AML cells to CDK8/19i.

Article Snippet: Human AML cell lines MV4;11, KG-1 (Russian Collection of Cell Cultures, Saint-Petersburg, Russia), THP-1 (TIB-202 TM, ATCC), Kasumi-1 (the cells were provided by the Department of Genetics, Faculty of Biology, Belarusian State University) were propagated in RPMI-1640 (PanEco, Moscow, Russia) with 10% fetal bovine serum (Biosera, Cholet, France), 2 mM L-glutamine, 100 U/mL penicillin and 100 μg/mL streptomycin (PanEco) at 37°C and 5% CO2 in humidified atmosphere.

Techniques: CRISPR, Transformation Assay, Expressing