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Cat. No. ARG37707

H1-0 Knockout HEK293T Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Kidney

The H1-0 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in the HEK293T human embryonic kidney epithelial line, featuring targeted disruption of the H1-0 gene encoding linker histone H1.0. Loss of H1.0, a key chromatin compaction factor that interacts with HMGB1, HP1, and NAP1L1, leads to chromatin decondensation and derepression of pluripotency genes such as POU5F1 and NANOG, as well as cell cycle regulators like CCND1. This model is ideal for studying epigenetic regulation, chromatin organization, and transcriptional control in a proliferative, transformable host. Applications include ATAC-seq, ChIP-qPCR, RNA-seq, and functional assays to explore histone function, gene silencing, and cancer-related pathways. For more information, contact Ascent Research.

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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

    H1-0

    Gene Identifier

    NCBI Gene ID 3005

    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 H1-0 Knockout HEK293T Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the human H1-0 gene has been disrupted via CRISPR/Cas9-mediated gene targeting. This product provides a heterogeneous pool of edited HEK293T cells harboring loss-of-function mutations in the H1-0 locus, enabling robust functional studies of linker histone H1.0 without clonal selection. The polyclonal format captures diverse editing events across the cell population, offering a representative model for investigating H1-0-dependent phenotypes while minimizing clonal bias.

HEK293T cells are a widely used human embryonic kidney epithelial cell line transformed with adenovirus 5 DNA and stably expressing the SV40 large T antigen. This background confers high transfectability, rapid proliferation, and the capacity for efficient viral production, making HEK293T a versatile host for gene perturbation studies. Their epithelial origin and transformed state provide a relevant context for examining chromatin dynamics in a proliferative cellular environment.

H1-0 encodes histone H1.0, a linker histone that binds nucleosomal linker DNA to promote chromatin compaction and transcriptional repression. It functions downstream of transcriptional regulators such as SP1, AP-1, and E2F1, and is regulated by the RB1 tumor suppressor and growth factor signaling. H1.0 interacts with nucleosomes, HMGB1, HP1, PARP1, NAP1L1, and CAF-1 to stabilize higher-order chromatin structure. Its loss leads to chromatin decondensation and derepression of downstream targets including pluripotency factors POU5F1, NANOG, and SOX2, as well as the cell cycle regulator CCND1, thereby altering the epigenetic landscape and gene expression programs.

In the HEK293T background, disruption of H1-0 disrupts normal chromatin organization, potentially affecting global transcription, cell cycle progression, and genome stability. Given the cell line’s transformed phenotype and high expression of viral oncoproteins, this knockout model enables dissection of how linker histone H1.0 maintains repression of developmental and proliferative genes in a context susceptible to epigenetic rewiring. It offers a powerful system to study the interplay between chromatin structure, oncogenic transformation, and gene silencing.

This polyclonal knockout cell population is suitable for a broad range of chromatin and epigenetics research applications, including ChIP-qPCR to assess histone modifications and occupancy, ATAC-seq to map chromatin accessibility, and RNA-seq for transcriptome profiling. Additional applications include western blotting and immunofluorescence for protein analysis, reporter assays for transcriptional activity, and cell proliferation or flow cytometry?Cbased assays to evaluate cell cycle effects. These cells provide a valuable tool for investigating histone function, gene regulation, and mechanisms of cancer and developmental diseases. For further details or technical support, please contact Ascent Research.

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