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Cat. No. ARG39308

DNAJC5 Knockout HGC-27 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Stomach

  • Disease:

    Carcinoma

DNAJC5 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the DNAJC5 gene in the human gastric carcinoma cell line HGC-27. DNAJC5 encodes cysteine string protein alpha (CSP??), a co-chaperone for Hsc70 (HSPA8) that is essential for SNARE complex assembly, synaptic vesicle exocytosis, and lysosomal function. CSP?? interacts with SNAP-25, syntaxin-1, and VAMP2, and its loss disrupts these molecular interactions. This knockout model supports investigations into non-neuronal vesicle trafficking, lysosomal storage disorders, and secretory pathway alterations in gastric cancer. Researchers can also apply it to drug discovery for neurodegeneration, including neuronal ceroid lipofuscinosis and Parkinson??s disease, leveraging assays such as Western blotting, immunoprecipitation, and lysosomal function analyses.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HGC-27

    Sex of Donor

    Unknown

    Age

    Unknown

    Derived From Site

    Metastatic; Lymph node

    Gene Name

    DNAJC5

    Gene Identifier

    NCBI Gene ID 80331

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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 DNAJC5 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the DNAJC5 gene has been disrupted in the human gastric carcinoma line HGC-27. This mixed population provides a loss-of-function model to study cysteine string protein alpha (CSP??), avoiding clonal biases while enabling robust target gene disruption. The product is suited for target validation, pathway dissection, and drug screening applications.

HGC-27 cells were isolated from a metastatic lymph node of a human gastric adenocarcinoma (undifferentiated type) and are extensively used as a model for gastric cancer progression, drug resistance, and metastasis. The cell background endogenously expresses the exocytic and vesicle trafficking machinery, making it permissive for functional characterization of CSP?? in a carcinoma context.

DNAJC5 encodes CSP??, a co-chaperone that cooperates with Hsc70 (HSPA8) to facilitate SNARE complex assembly. CSP?? directly interacts with SNARE proteins STX1A (syntaxin-1), SNAP25, and VAMP2, and functionally couples to voltage-gated Ca2+ channels and clathrin. Upstream regulators include Hsc70, synaptic activity, and cellular stress signals; downstream, CSP?? promotes SNARE-mediated vesicle exocytosis and lysosomal secretion. Disruption of DNAJC5 eliminates CSP?? co-chaperone activity, impairing SNARE complex formation and synaptic-like vesicle exocytosis, thereby perturbing lysosomal function and cellular homeostasis.

In the HGC-27 gastric cancer system, CSP?? loss may specifically alter secretory and lysosomal pathways dependent on SNARE-mediated fusion. Given the role of exocytosis in cancer cell invasion and therapy resistance, this knockout model offers a tool to dissect CSP????s contribution to gastric cancer pathogenesis. Moreover, DNAJC5 mutations are linked to neuronal ceroid lipofuscinosis (Kufs disease) and Parkinson??s disease, so these cells provide a non-neuronal platform to examine conserved neuroprotective and lysosomal dysregulation mechanisms.

Typical assays for characterizing this product include Western blotting for CSP??, RT-qPCR for DNAJC5 expression, immunofluorescence for synaptic vesicle markers, and co-immunoprecipitation for Hsc70 interaction. Functional studies may involve SNARE complex assembly assays, lysosomal function tests, cell viability, and migration/invasion analyses. The knockout model supports investigations into synaptic-like vesicle trafficking in non-neuronal cells, lysosomal storage disorders, secretory pathway alterations in gastric cancer, and drug discovery for neurodegeneration. For further information, please contact Ascent Research.

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