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Cat. No. ARG35984

HDAC8 Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

CRISPR/Cas9-edited polyclonal HDAC8 knockout HAP1 cells provide a loss-of-function model for studying histone deacetylase 8. HDAC8 deacetylates histones and SMC3, regulating chromatin structure and cohesin recycling. Disruption enables investigation of epigenetic regulation, cancer, and cohesinopathies. These near-haploid HAP1 cells simplify genetic analysis and offer reliable knockout efficiency. Applications include Western blotting for acetyl-histones, ChIP, and drug sensitivity assays, supporting drug target validation and functional genomics.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HAP1

    Sex of Donor

    Male

    Age

    40 years

    Derived From Site

    Bone marrow

    Gene Name

    HDAC8

    Gene Identifier

    NCBI Gene ID 55869

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    IMDM

    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 HDAC8 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 human cell line. This model features targeted disruption of the HDAC8 gene, which encodes histone deacetylase 8. The polyclonal format provides a heterogeneous pool of knockout cells, enabling robust loss-of-function studies while minimizing clonal selection effects.

HAP1 is a near-haploid human cell line originating from the KBM-7 chronic myeloid leukemia line. With a single set of chromosomes in most genomic regions, HAP1 cells simplify genetic analyses and enhance CRISPR editing efficiency. Their adherent growth and stable karyotype make them well-suited for functional genomics and reproducible knockout experiments in epigenetic and cancer research.

HDAC8 is a class I histone deacetylase that removes acetyl groups from histones H3 (K9, K14, K56) and H4 (K16), promoting chromatin compaction and transcriptional silencing. It also targets non-histone substrates such as SMC3, p53, and cortactin. HDAC8 is regulated by PKA phosphorylation and association with the MTA1/NuRD corepressor complex. A key function is deacetylation of SMC3 within the cohesin recycling pathway, which is essential for cohesin loading onto chromatin, affecting sister chromatid cohesion and gene regulation. HDAC8 interacts with HSP70, Hsp90, and cooperates with HDAC3 in nuclear processes.

In HAP1 cells, HDAC8 disruption offers a clear phenotypic window due to the haploid background, facilitating study of cohesin dynamics, cell cycle regulation, and apoptosis. This model is particularly relevant for Cornelia de Lange syndrome, neuroblastoma, colorectal cancer, and inflammatory diseases. The polyclonal knockout population enables unbiased assessment of HDAC8-dependent phenotypes without clonal variation, supporting both mechanistic and translational research.

Applications include functional genomics screens, drug target validation, and epigenetic mechanism studies. Assays such as Western blotting for acetyl-histones, RT-qPCR, ChIP for histone marks, immunofluorescence for cohesin localization, and flow cytometry for apoptosis/cell cycle are recommended. HDAC inhibitor sensitivity testing (e.g., Vorinostat) and migration assays further expand utility. For additional information, please contact our technical support team.

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