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Cat. No. ARG32543

HDAC1 Knockout SK-HEP-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

The HDAC1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human hepatic adenocarcinoma SK-HEP-1 cell line. This product provides a loss-of-function model for histone deacetylase 1 (HDAC1), enabling studies of transcriptional repression, chromatin dynamics, and signaling networks involving TP53, MYC, and the CoREST complex. These knockout cells are ideal for liver cancer research applications, including HDAC inhibitor drug screening, gene expression profiling by RNA-seq or RT-qPCR, and functional assays such as apoptosis detection and migration analysis. For further details, please 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

    SK-HEP-1

    Sex of Donor

    Male

    Age

    52 years

    Gene Name

    HDAC1

    Gene Identifier

    NCBI Gene ID 3065

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM (with NEAA)

    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-HEP-1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population for investigating histone deacetylase 1 (HDAC1) function. Derived from the human hepatic adenocarcinoma cell line SK-HEP-1, this product offers a loss-of-function model through pooled gene disruption, enabling unbiased functional studies without clonal selection artifacts.

The SK-HEP-1 cell line, originally isolated from the ascites of a liver adenocarcinoma patient, is a widely used model for hepatic sinusoidal endothelium. It retains key characteristics of hepatocellular carcinoma, including aberrant signaling pathways, and is frequently employed in cancer biology, metastasis research, and drug screening.

HDAC1 encodes a class I histone deacetylase that catalyzes deacetylation of histone H3 and H4 tails, leading to chromatin compaction and transcriptional repression. It functions within large corepressor complexes, such as those formed with SIN3A, CoREST, and the NuRD components MTA2, RBBP4, RBBP7, and CHD4. Upstream regulation by CK2 and transcription factors TP53 and MYC modulates HDAC1 activity, which in turn directly affects the acetylation status of downstream targets including TP53, E2F1, and STAT3. Through these interactions, HDAC1 interfaces with the Wnt/??-catenin (CTNNB1), Notch (NOTCH1), TGF-?? (SMAD2), and p53 (TP53/CDKN1A) pathways, governing cell cycle progression, apoptosis, and differentiation.

In the SK-HEP-1 background, HDAC1 deletion is expected to relieve repression of tumor suppressive genes and may impair proliferation, survival, and epithelial-mesenchymal transition. This knockout population thus offers a powerful tool to dissect HDAC1??s specific contributions to liver adenocarcinoma biology, including its roles in chromatin remodeling and gene regulation that drive hepatocellular carcinoma phenotypes within a sinusoidal endothelial setting.

Researchers can employ this product for chromatin immunoprecipitation?CqPCR (ChIP-qPCR) to map histone acetylation landscapes, RNA-seq or RT-qPCR to profile transcriptomic changes, and functional assays such as apoptosis and migration tests. The polyclonal knockout cells also provide an isogenic platform for HDAC inhibitor screening, enabling assessment of compound efficacy and identification of synthetic lethal interactions. For more details, please contact Ascent Research.

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