Genome-edited Cells
Pleural effusion
The MYC Knockout K562 Cell Line is a CRISPR/Cas9-edited knockout cell line in the K562 erythroleukemia background, providing a loss-of-function model for the MYC transcription factor. MYC heterodimerizes with MAX to regulate proliferation (via CCND1, CCNE1) and apoptosis (via BCL2 and BIM), and its expression is controlled by MAPK/ERK and PI3K/AKT pathways. This model is particularly relevant for studying BCR-ABL-driven leukemogenesis. Key applications include cancer biology, cell cycle analysis, apoptosis assays, and drug resistance profiling. Researchers can employ Western blotting, flow cytometry, and proliferation assays to characterize MYC-dependent phenotypes, making this knockout line a versatile tool for functional genomics and therapeutic target validation.
BID Knockout MES-OV Polyclonal Cells
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IFT140 Knockout HGC-27 Polyclonal Cells
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JAG1 Knockout 143B Polyclonal Cells
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IGF2 Knockout PATU8988T Polyclonal Cells
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LMNB1 Knockout AGS Polyclonal Cells
Cat. No. ARG2895
CHN1 Knockout AGS Polyclonal Cells
Cat. No. ARG2756
The MYC Knockout K562 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the K562 human erythroleukemia cell line, engineered to abolish MYC protein expression through targeted gene disruption. This stable knockout model eliminates functional MYC without reliance on transient RNA interference, offering a reliable system for investigating MYC-dependent transcriptional programs and phenotypic outcomes in both acute and long-term studies of leukemic and erythroid biology.
The parental K562 cell line originated from a pleural effusion of a 53-year-old female with chronic myelogenous leukemia in blast crisis. These BCR-ABL-positive cells exhibit erythroid progenitor characteristics and serve as a key hematopoietic malignancy model for studying erythroid differentiation, oncogenic signaling, and leukemogenesis.
MYC encodes a basic helix-loop-helix leucine zipper transcription factor that heterodimerizes with MAX to bind E-box sequences (CACGTG) and regulate target gene transcription. MYC-driven transcriptional programs control cell cycle entry via cyclins D1 and E (CCND1, CCNE1) and CDK4, promote proliferation through E2F1, and suppress apoptosis by upregulating BCL2 while repressing pro-apoptotic BIM (BCL2L11). MYC also boosts metabolism (LDHA, ODC1) and ribosome biogenesis. Upstream signals from MAPK/ERK, PI3K/AKT, Wnt/??-catenin, and JAK/STAT converge on MYC, and its activity is modulated by interactions with MAX, MIZ-1, TRRAP, and EP300. Knockout of MYC in K562 disrupts these transcriptional networks, leading to impaired G1/S transition, reduced metabolic output, and sensitization to apoptosis.
Within the K562 BCR-ABL-driven leukemic environment, MYC integrates proliferative and anti-apoptotic signals. Disrupting MYC allows researchers to dissect its specific contributions to cell cycle progression, survival, and differentiation independently of upstream kinase activity. This model is especially useful for exploring MYC-dependent vulnerabilities, testing synergistic effects with BCR-ABL inhibitors, and studying alterations in erythroid maturation.
Widely applicable to cancer biology, cell cycle research, and apoptosis studies, this knockout cell line supports assays such as Western blotting for MYC and downstream targets, RT-qPCR for transcriptional changes, flow cytometry for cell cycle and Annexin V apoptosis, and proliferation assays (MTT, BrdU). Advanced applications include RNA-seq, ChIP-qPCR for MYC binding, and co-immunoprecipitation for protein complex analysis, enabling functional genomics and drug sensitivity profiling. For technical inquiries or to order, please contact Ascent Research.
