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Cat. No. ARG38148

H4C1 Knockout HEK293T Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Kidney

CRISPR/Cas9-edited polyclonal knockout HEK293T cells with disrupted H4C1 gene, encoding replication-dependent histone H4. H4C1 is regulated by NPAT and CDK2?CCyclin E, and its loss impairs nucleosome assembly and chromatin structure. This loss-of-function model supports epigenetics, cancer biology, and cell cycle research, enabling assays such as Western blot, ChIP-qPCR, and RNA-seq in a widely used host cell line.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HEK293T

    Sex of Donor

    Female

    Age

    Fetus

    Derived From Site

    Fetal kidney

    Gene Name

    H4C1

    Gene Identifier

    NCBI Gene ID 8359

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    DMEM

    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 H4C1 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the H4C1 gene in human HEK293T cells, providing a powerful loss-of-function model for investigating histone H4 biology. This product consists of a heterogeneous pool of knockout cells generated by CRISPR/Cas9-mediated gene disruption, avoiding clonal selection to preserve population-level genetic diversity while eliminating functional H4C1 expression. The polyclonal format enables robust functional studies without the artifacts that may arise from single-cell cloning, making it ideal for experiments requiring near-physiological knockout representation.

HEK293T cells are an adherent human embryonic kidney epithelial cell line immortalized with the SV40 large T antigen, widely recognized as a model system for protein expression, viral production, and cell signaling studies. Their robust growth characteristics and high transfection efficiency facilitate a broad range of assays, from transient overexpression to stable genetic manipulation. The combination of HEK293T??s experimental versatility with targeted H4C1 knockout provides a clinically and scientifically relevant platform for chromatin research.

H4C1 encodes a replication-dependent histone H4 protein, a core component of the nucleosome that packages DNA into chromatin. Histone H4 expression is tightly coupled to the cell cycle through transcriptional activation by NPAT and HINFP, which are downstream effectors of CDK2?CCyclin E and pRB?CE2F signaling. H4C1 protein interacts with histone chaperones ASF1A and the CAF-1 complex, as well as with histones H2A, H2B, and H3, to mediate replication-coupled nucleosome assembly. Additionally, histone H4 participates in higher-order chromatin organization through interactions with SWI/SNF chromatin remodeling complexes. Knockout of H4C1 disrupts these interactions, impairing proper nucleosome formation and chromatin condensation, which can lead to genome instability and dysregulated global gene expression.

In the HEK293T host cell context, H4C1 knockout allows direct examination of how histone H4 loss impacts chromatin dynamics, DNA repair, and replication-dependent nucleosome assembly. Because HEK293T cells proliferate rapidly and rely on coordinated histone production during S phase, H4C1 disruption provides a tractable system to study cell cycle-specific chromatin defects. The model is particularly valuable for dissecting the contributions of H4C1 to epigenetic regulation and for screening small molecules that may modulate chromatin structure in cancer or developmental disorders.

This polyclonal knockout cell product is suitable for a diverse array of research applications, including epigenetics, cancer biology, and cell cycle studies. Representative assays include Western blotting and RT-qPCR to confirm H4C1 loss and downstream gene expression changes, ChIP-qPCR to assess histone modifications and chromatin occupancy, flow cytometry and immunofluorescence for cell cycle and chromatin organization analysis, and RNA-seq for transcriptome-wide profiling. Proliferation assays can further reveal growth-related consequences of H4C1 knockout. For detailed technical specifications and ordering information, please contact Ascent Research.

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