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Cat. No. ARG39206

DNAJC13 Knockout huh-7 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Liver

  • Disease:

    Hepatocellular carcinoma

The DNAJC13 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of human hepatocellular carcinoma Huh-7 cells, disrupted for the DNAJC13 gene. DNAJC13 encodes a co-chaperone that recruits Hsc70 to endosomal clathrin coats, promoting retromer-mediated recycling of receptors such as Sortilin and CI-MPR. Loss of function disrupts endolysosomal trafficking, autophagy, and Wnt signaling, and is associated with Parkinson disease 21. The Huh-7 host line, permissive to HCV and well-suited for hepatic metabolism studies, provides a relevant model to examine DNAJC13-dependent sorting in liver cancer biology. Applications include endosomal trafficking assays, transferrin and EGFR recycling studies, immunofluorescence, autophagy flux analysis, and drug screening for trafficking modulators.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Huh-7

    Sex of Donor

    Male

    Age

    57 years

    Gene Name

    DNAJC13

    Gene Identifier

    NCBI Gene ID 23317

    Morphology

    Epithelial-like

    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 DNAJC13 Knockout Huh-7 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population derived from Huh-7 hepatocellular carcinoma cells, with targeted disruption of the DNAJC13 gene. This polyclonal format provides a heterogeneous loss-of-function model for investigating DNAJC13??s role in endosomal trafficking, avoiding the selection bias of single-cell clones. These cells are designed for advanced biomedical research into trafficking-related pathologies.

Huh-7 is a well-differentiated hepatocarcinoma line from a Japanese male, permissive to hepatitis C virus (HCV) and extensively used as a hepatic metabolism and liver cancer model. Its high endocytic activity and HCV susceptibility make it an ideal system to study how DNAJC13-dependent sorting influences hepatocyte functions, receptor recycling, and lysosomal homeostasis in a disease-relevant context.

DNAJC13 (RME-8) recruits Hsc70 to endosomal clathrin coats, driving clathrin uncoating and enabling retromer (VPS35/VPS26/VPS29)-mediated sorting of cargo receptors such as Sortilin, CI-MPR, and Wntless back to the TGN or plasma membrane. It interacts directly with clathrin, sorting nexins (SNX1/SNX2), and the WASH complex, and is regulated by Rab5, Rab7, LRRK2, and EGFR signaling. DNAJC13 loss disrupts retromer function, leading to receptor mis-sorting, lysosomal degradation defects, and aberrant Wnt pathway activation??pathways central to neurodegenerative diseases like Parkinson??s disease 21 and endosomal trafficking disorders.

In Huh-7 cells, DNAJC13 knockout models impaired endosomal-lysosomal trafficking that is critical for liver cancer cell survival, autophagy regulation, and HCV lifecycle. The polyclonal nature enables studies under heterogeneous editing backgrounds, better mimicking in vivo tissue complexity. This system facilitates dissection of how trafficking perturbations contribute to both hepatocarcinogenesis and neurodegeneration, bridging liver biology and neuropathology.

Researchers can employ these cells for endosomal sorting assays (transferrin uptake, EGFR recycling), confocal imaging of clathrin dynamics, immunofluorescence detection of endolysosomal markers (EEA1, Rab5, LAMP1), and autophagy flux analysis (LC3 turnover). Additional applications include lysosomal enzyme activity measurements, co-chaperone function assays, and drug screening for trafficking modulators. Wound healing assays further enable evaluation of DNAJC13??s impact on hepatocellular carcinoma cell migration. For detailed product specifications, please contact Ascent Research.

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