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Cat. No. ARG42786

CBX5 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

CBX5 Knockout Jurkat Polyclonal Cells offer a CRISPR/Cas9-edited heterogeneous knockout population for loss-of-function analysis of HP1?? in human T-cell leukemia. CBX5 binds H3K9me2/3 marks deposited by SUV39H1/2, mediating heterochromatin formation and transcriptional silencing, with roles in genome stability and senescence. Suitable for heterochromatin biology, leukemia pathogenesis, DNA damage, and HIV latency studies, this model supports ChIP-qPCR, RNA-seq, and apoptosis assays. Contact Ascent Research for additional information.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Jurkat

    Cell Type

    T cell line

    Sex of Donor

    Male

    Age

    14 years

    Derived From Site

    In situ; Peripheral blood

    Gene Name

    CBX5

    Gene Identifier

    NCBI Gene ID 23468

    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 CBX5 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat T lymphoblast cell line, providing a loss-of-function model for the heterochromatin protein HP1??. This heterogeneous pool results from CRISPR/Cas9-mediated disruption of the CBX5 gene, enabling population-level studies of chromatin regulation in a T-cell leukemia background without clonal selection.

Jurkat cells are a widely used model of acute T-cell leukemia, originating from a patient with acute lymphoblastic leukemia. These immortalized T lymphoblasts maintain key T-cell receptor signaling and apoptotic pathways, making them ideal for dissecting oncogenic mechanisms and epigenetic control in hematologic malignancies, with high transfection efficiency supporting reproducible gene editing.

CBX5 (HP1??) recognizes H3K9me2/3 marks deposited by SUV39H1 and SUV39H2 methyltransferases, recruiting partners such as CAF-1 (CHAF1A), TIF1?? (TRIM28), and Lamin B receptor to promote chromatin compaction and transcriptional silencing. Upstream kinases Aurora B and PIM1 phosphorylate CBX5 to modulate chromatin affinity, while E2F transcription factors drive its expression. CBX5 represses E2F target genes, the IL-2 promoter, and telomeric repeats, contributing to genome stability and cell cycle arrest. It also interacts with HIV-1 integrase, implicating it in viral latency.

In the Jurkat context, CBX5 knockout facilitates investigation of heterochromatin-mediated gene silencing in T-cell leukemogenesis, DNA damage responses, and senescence. This model is particularly valuable for exploring interactions with E2F and PIM1 pathways that control proliferation and survival in acute lymphoblastic leukemia, and for studying how chromatin architecture influences TCR-driven apoptosis and epigenetic plasticity.

Applications include ChIP-qPCR for H3K9me3 mapping, immunofluorescence for heterochromatin foci, RNA-seq for transcriptional profiling, and co-immunoprecipitation for CBX5-associated complexes. Functional assays such as apoptosis detection, senescence-associated ??-galactosidase staining, and IL-2 reporter assays, as well as HIV latency experiments, can be performed. For technical inquiries, please contact Ascent Research.

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