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Cat. No. ARG36189

KAT7 Knockout HT29 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

The KAT7 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from HT29 colorectal adenocarcinoma cells. This model disrupts the histone acetyltransferase KAT7, which acetylates histones H3/H4 to regulate DNA replication licensing and cell cycle progression via interactions with MCM2-7, CDT1, and TP53. Ideal for studying epigenetic control of colorectal cancer, applications include ChIP-qPCR, cell cycle analysis, proliferation assays, and RNA-seq. The polyclonal nature captures heterogeneous responses, supporting inhibitor screening and functional genomics research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HT29

    Gene Name

    Kat7

    Gene Identifier

    NCBI Gene ID 11143

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    McCoy's 5A

    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 HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HT29 colorectal adenocarcinoma cell line, engineered to disrupt the KAT7 gene. This genetically diverse pool of edited cells provides a robust loss-of-function model for investigating the functional consequences of KAT7 ablation in colorectal cancer contexts, circumventing the clonal selection bias inherent in monoclonal cell lines.

HT29 is a well-characterized human colorectal adenocarcinoma cell line with epithelial morphology, widely employed as a model system for intestinal epithelial biology, drug transport studies, and colorectal cancer research. Its predictable growth kinetics and responsiveness to differentiation agents make it an ideal host for gene knockout studies.

KAT7 (MYST2/HBO1) encodes a histone acetyltransferase that preferentially acetylates histones H3 and H4 at replication origins, thereby licensing DNA replication and regulating chromatin remodeling. KAT7 operates within multiprotein complexes containing JADE1, ING4, EAF6, and BRPF2, and its enzymatic activity is governed by upstream regulators including E2F1, CDK2, and ING5. Downstream, KAT7-mediated acetylation promotes MCM2-7 helicase loading via interactions with ORC1 and CDT1, and directly acetylates TP53 at key residues, modulating p53 transcriptional activity. Additionally, KAT7 influences expression of cell cycle regulators such as CCND1, linking epigenetic modification to cell proliferation control.

In colorectal adenocarcinoma, disruption of KAT7 impairs histone acetylation dynamics, leading to defective DNA replication licensing and perturbed cell cycle gene expression, which can attenuate the proliferative capacity of HT29 cells. The concurrent alteration of p53 acetylation status may further modulate apoptosis or cell cycle arrest, highlighting the model??s utility for dissecting epigenetic contributions to tumorigenesis and exploring therapeutic vulnerabilities in colorectal cancer.

This polyclonal knockout cell product is suitable for a broad range of assays, including Western blotting and ChIP-qPCR to assess histone acetylation changes, RT-qPCR for cell cycle gene profiling, flow cytometry-based cell cycle and apoptosis analyses, and MTT or colony formation assays to measure proliferation. The heterogeneous population enables transcriptome-wide RNA-seq studies and high-throughput screening of epigenetic inhibitors, providing a versatile tool for functional validation of KAT7 in colon adenocarcinoma. For further technical assistance or to discuss custom applications, please contact Ascent Research.

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