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Cat. No. ARG39175

DNAJC1 Knockout SK-HEP-1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Adenocarcinoma

The DNAJC1 Knockout SK-HEP-1 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout population in the SK-HEP-1 hepatic adenocarcinoma line. Disruption of DNAJC1, an ER-resident J-domain co-chaperone, inactivates its stimulation of HSPA5 (BiP) ATPase activity, leading to ER proteostasis failure and UPR activation through ATF6 and XBP1-regulated pathways. This knockout pool is suited for hepatocellular carcinoma research, particularly for examining ER stress responses, drug sensitivity, and protein secretion. Common experimental approaches include Western blot detection of UPR markers, RT-qPCR analysis of XBP1 splicing, and apoptosis assays upon treatment with thapsigargin or tunicamycin.

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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

    DNAJC1

    Gene Identifier

    NCBI Gene ID 64215

    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 DNAJC1 Knockout SK-HEP-1 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout population derived from the SK-HEP-1 hepatic adenocarcinoma cell line. This product provides a pool of cells carrying targeted disruptions in the DNAJC1 gene, enabling loss-of-function analyses without clonal isolation. The heterogeneous knockout model is suitable for studying gene function in hepatocellular carcinoma research.

SK-HEP-1 is an ascites-derived human hepatic adenocarcinoma cell line serving as a well-characterized hepatocellular carcinoma model. It retains malignant properties and is widely used for investigating ER stress, drug response, oncogenic signaling, and metabolic reprogramming in liver cancer. The DNAJC1 knockout in this background permits exploration of co-chaperone biology in a pathophysiologically relevant context.

DNAJC1 encodes an ER-resident J-domain co-chaperone that activates HSP70 ATPase activity, primarily interacting with HSPA5 (BiP) to facilitate protein folding and quality control in the ER. It functions downstream of UPR transcription factors ATF6 and XBP1, and its disruption impairs ER proteostasis, triggering UPR sensors PERK and IRE1 and modulating downstream effectors including ATF4 and CHOP. DNAJC1 deficiency compromises the ER-associated degradation machinery and sensitizes cells to ER stress-induced apoptosis. Thus, DNAJC1 integrates stress signaling with chaperone networks to maintain ER homeostasis.

In SK-HEP-1 cells, DNAJC1 knockout disrupts ER protein folding capacity, exacerbating the vulnerability of hepatocellular carcinoma cells to proteotoxic stress. This model enables dissection of how ER co-chaperone loss influences tumor cell survival, secretory function, and drug sensitivity. The polyclonal nature mirrors the genetic variability that could arise upon therapeutic targeting.

Researchers can employ this knockout pool for Western blotting of UPR markers (BiP, CHOP), RT-qPCR analysis of XBP1 splicing, cell viability and apoptosis assays under ER stress induction (e.g., thapsigargin), and immunofluorescence localization of ER chaperones. Additional applications include drug sensitivity screens, protein secretion analyses, and flow cytometric quantification of apoptotic markers. For further technical information, contact Ascent Research.

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