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Cat. No. ARG35996

KAT7 Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

KAT7 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population, targeting the histone acetyltransferase KAT7 in the near-haploid HAP1 cell line. KAT7, catalytic subunit of the HBO1 complex, acetylates histone H4 at K5, K8, and K12 to regulate DNA replication licensing and gene transcription, operating downstream of CDK1/Cyclin B1 and interacting with CTNNB1 and p53. This model enables precise dissection of chromatin dynamics, DNA replication, and cell cycle control, with applications in cancer biology, epigenetic studies, and drug target identification using assays such as ChIP-qPCR, DNA fiber assays, and flow cytometry.

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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

    Kat7

    Gene Identifier

    NCBI Gene ID 11143

    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 KAT7 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population derived from the near-haploid HAP1 cell line, designed to disrupt the KAT7 gene. This pooled loss-of-function model enables robust study of KAT7-dependent processes in a genetically simplified background, making it suitable for functional genomics, epigenetics, and drug target validation.

HAP1 is a male, near-haploid, fibroblast-like cell line derived from the KBM-7 chronic myeloid leukemia line. Its haploid karyotype (except for disomic chromosome 8) allows complete gene inactivation with a single targeting event, rendering it a powerful system for knockout screens and mechanistic studies of gene function. The cells proliferate rapidly and are amenable to standard genetic manipulation and assay protocols.

KAT7 encodes a histone acetyltransferase that serves as the catalytic subunit of the HBO1 complex, which also contains BRPF1/2/3, JADE1/2/3, ING4/5, and MEAF6. This complex acetylates histone H4 at lysines 5, 8, and 12, promoting chromatin decompaction and the loading of replication licensing factors ORC1, Cdt1, and the MCM2-7 helicase. KAT7 activity is regulated by CDK1/Cyclin B1, Cdt1, the APC/C ubiquitin ligase, ATM/ATR kinases, and E2F transcription factors, and it converges with Wnt/??-catenin signaling through interaction with CTNNB1 and TCF7L2. KAT7 also acetylates p53 at K120 and K382, modulating its transcriptional function.

In the near-haploid HAP1 background, KAT7 disruption produces a clear loss-of-function model for investigating how histone H4 acetylation controls DNA replication licensing, cell cycle progression, and chromatin dynamics. This model is particularly relevant for cancers where KAT7 is implicated??such as acute myeloid leukemia, breast cancer, and hepatocellular carcinoma??and enables the study of oncogenic transcriptional dependencies and synthetic lethal interactions within the HBO1 network.

Key applications include ChIP-qPCR for assessing H4 acetylation at origins, DNA fiber assays for replication fork analysis, EdU incorporation with flow cytometry for cell cycle analysis, and co-immunoprecipitation to probe HBO1 complex composition. Proliferation and viability can be measured via colony formation and MTT assays. These cells also facilitate genome-wide CRISPR screens and drug sensitivity profiling. For further support, please contact Ascent Research.

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