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Cat. No. ARG36726

HDAC1 Knockout SKOV3 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Ovary

  • Disease:

    Ovarian serous cystadenocarcinoma

The HDAC1 Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting histone deacetylase 1 in the human ovarian adenocarcinoma cell line SK-OV-3. HDAC1 deacetylates histones and non-histone proteins such as p53, functioning within corepressor complexes containing SIN3A and RBBP4/7 to repress transcription of tumor suppressors like CDKN1A and BAX. This knockout model is suited for studying epigenetic regulation, HDAC inhibitor drug development, ovarian cancer progression, and apoptosis mechanisms. Key applications include Western blotting, RT-qPCR, ChIP, immunofluorescence, and flow cytometry to assess changes in gene expression, histone acetylation, and cell cycle distribution.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    SKOV3

    Sex of Donor

    Female

    Age

    64 years

    Derived From Site

    Ascites

    Gene Name

    HDAC1

    Gene Identifier

    NCBI Gene ID 3065

    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 HDAC1 Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population that disrupts the gene encoding histone deacetylase 1 (HDAC1) in the human ovarian cancer cell line SK-OV-3. This polyclonal knockout model provides a heterogeneous loss-of-function system, enabling researchers to investigate the functional consequences of HDAC1 depletion without clonal isolation artifacts. The product is supplied as a ready-to-use polyclonal pool, supporting both short-term perturbation studies and long-term stable culture experiments.

SK-OV-3 is a well-characterized epithelial ovarian adenocarcinoma cell line derived from the ascites of a patient with advanced ovarian cancer. It carries a TP53 mutation and is extensively employed in ovarian cancer research, serving as a benchmark model for studying tumor biology, metastasis, and chemoresistance. The cell line??s aggressive phenotype and established use in drug sensitivity screens make it a relevant host for targeted gene disruption studies, particularly in the context of epigenetic dysregulation.

HDAC1 functions as a core transcriptional repressor by catalyzing the removal of acetyl groups from lysine residues on histone H3 and H4 tails, leading to chromatin compaction and gene silencing. Beyond histones, it deacetylates non-histone substrates such as p53, E2F1, and NF-??B, thereby modulating cell cycle progression, apoptosis, and DNA damage responses. HDAC1 associates with large multiprotein complexes containing SIN3A, MTA1/2, RBBP4/7, SAP18, SAP30, NCOR1, and SMRT. Its enzymatic activity is regulated by upstream kinases including CK2, PKA, and PKC, and it transcriptionally represses key tumor suppressors such as CDKN1A (p21) and BAX, while also influencing RB1 and c-MYC expression.

In ovarian cancer, HDAC1 is frequently overexpressed and contributes to oncogenesis by silencing pro-apoptotic and cell cycle regulatory genes. Disruption of HDAC1 in the SK-OV-3 background allows dissection of its role in maintaining the malignant phenotype, including its impact on transcriptional programs, apoptosis, and response to chemotherapy. The polyclonal knockout population retains the heterogeneous genetic landscape of the parental line, making it suitable for studies that require a diverse cell pool, such as drug resistance modeling or genome-wide screening, while avoiding the biases of single-cell clones.

These HDAC1 knockout polyclonal cells are ideal for a range of experimental applications, including epigenetic regulation research, HDAC inhibitor development and validation, and mechanistic studies of ovarian cancer progression. Researchers can employ representative assays such as Western blotting to confirm HDAC1 ablation and assess histone H3/H4 acetylation, RT-qPCR to monitor CDKN1A and BAX transcript levels, ChIP-qPCR to evaluate histone acetylation at target gene promoters, immunofluorescence for global acetyl-lysine detection, and flow cytometry to examine cell cycle arrest and apoptosis. Additional functional assays, including migration, invasion, and HDAC activity measurements, can further elucidate the phenotypic consequences of HDAC1 loss. For technical inquiries or to order this product, please contact Ascent Research.

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