Security Notice: Please be aware of impersonation attempts using our company name
Legitimate communications from Ascent Research will only come from official @ascentresearch.com email addresses.
Quick Order Cart

Cat. No. ARG42808

CBX8 Knockout K562 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Pleural effusion

  • Disease:

    Chronic myeloid leukemia

The CBX8 Knockout K-562 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population disrupting the CBX8 gene in K-562 cells, a human BCR-ABL-positive chronic myelogenous leukemia line. CBX8 encodes a PRC1 component that recognizes H3K27me3 and represses targets including CDKN2A and CDKN1A. Loss of CBX8 provides a tool to dissect Polycomb silencing in leukemia, enabling analysis of epigenetic regulation, cell cycle control, and hematopoietic differentiation. Applications include transcriptomic profiling, chromatin immunoprecipitation, and drug sensitivity assays. For more information, contact Ascent Research.

Inquire Now

In stock

Ships next business day


Ask a Question

Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    K562

    Sex of Donor

    Female

    Derived From Site

    In situ; Pleural effusion

    Gene Name

    CBX8

    Gene Identifier

    NCBI Gene ID 57332

    Growth Mode

    Suspension

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

The CBX8 Knockout K-562 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the human CBX8 gene. CBX8 encodes a chromobox protein that functions as a core component of Polycomb repressive complex 1 (PRC1). This product comprises a heterogeneous pool of edited cells, avoiding clone-specific artifacts and capturing a range of editing outcomes. The polyclonal format enables analysis of gene function within a population context.

The host K-562 cell line is derived from a female patient with chronic myelogenous leukemia in blast crisis and harbors the BCR-ABL fusion oncogene. K-562 cells serve as a model of multipotent hematopoietic progenitors, capable of lineage-appropriate differentiation. The BCR-ABL-positive background makes these cells particularly relevant for studying the interplay between oncogenic signaling and epigenetic regulation in leukemia.

CBX8 is a reader of H3K27me3, a histone modification deposited by PRC2. Through its chromodomain, CBX8 recruits PRC1 to chromatin, where it associates with RING1B and BMI1 to catalyze H2AK119ub, promoting chromatin compaction and transcriptional silencing. CBX8 activity is modulated by upstream regulators E2F1, MYC, and BCR-ABL signaling. Key downstream targets include the tumor suppressors CDKN2A and CDKN1A, as well as HOX genes and pro-apoptotic factors, linking CBX8 to cell cycle control and apoptosis.

In K-562 cells, BCR-ABL-driven proliferation may be sustained in part through CBX8-mediated repression of growth-restrictive genes. Knockout of CBX8 can disrupt this silencing, potentially derepressing CDKN2A and CDKN1A and impairing leukemic growth. This model thus enables dissection of how oncogenic signaling exploits Polycomb silencing to maintain an undifferentiated state, and provides a tool to study CBX8-dependent regulation of hematopoietic progenitor cell fate.

This knockout model supports a wide range of applications, from transcriptome-wide RNA-seq and targeted RT-qPCR to chromatin immunoprecipitation for H3K27me3 and H2AK119ub. Protein-level validation by Western blotting and functional assays such as flow cytometry for cell cycle and differentiation markers, colony formation, and drug sensitivity testing are readily performed. These cells facilitate research into Polycomb biology, cancer epigenetics, and leukemia therapeutic strategies. For detailed information, please contact Ascent Research.

Reset Password

    Reach Us Questions? Click Me Here!

    Fill out the form below and a member of our team will contact you shortly!

    *Required field



      Reach Us

      Fill out the form below and a member of our team will contact you shortly!

      *Required field

      Product Inquiry (Optional)