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Cat. No. ARG36288

BAG5 Knockout KYSE30 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Esophagus

  • Disease:

    Squamous cell carcinoma

The BAG5 Knockout KYSE-30 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal population in which BAG5 is disrupted in the human esophageal squamous cell carcinoma line KYSE-30. BAG5 acts as a co-chaperone and nucleotide exchange factor for Hsp70, regulating protein folding, autophagy, and apoptosis through interactions with Hsp70, Parkin, and BCL-2. Loss of BAG5 compromises proteostasis and enhances susceptibility to proteotoxic stress, making this model valuable for studying chaperone-mediated autophagy, drug resistance, and apoptotic signaling in esophageal cancer. Typical assays include western blotting, flow cytometric apoptosis analysis, co-immunoprecipitation, migration/invasion assays, and drug sensitivity testing.

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Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    KYSE-30

    Sex of Donor

    Female

    Age

    64 years

    Gene Name

    BAG5

    Gene Identifier

    NCBI Gene ID 9529

    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 BAG5 Knockout KYSE-30 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which BAG5 gene disruption has been introduced into the KYSE-30 human esophageal squamous cell carcinoma line. This heterogeneous pool models BAG5 loss-of-function without clonal selection, making it suitable for population-level phenotypic analyses, drug-response profiling, and omics studies.

KYSE-30 is a well-characterized cell line derived from a human esophageal squamous cell carcinoma, displaying epithelial morphology and robust tumorigenic capacity. It serves as a faithful model for studying esophageal carcinogenesis, metastasis, and therapeutic resistance, and is widely used to explore the molecular underpinnings of ESCC progression and therapy response.

BAG5 encodes a nucleotide exchange factor for Hsp70, facilitating substrate release and thereby regulating protein quality control. It directly interacts with Hsp70, Hsc70, Parkin, PINK1, and BCL-2, and functions at the intersection of chaperone-mediated protein folding, autophagy, and apoptosis. BAG5 expression is induced by heat shock and proteotoxic stress, and its activity modulates downstream LC3 lipidation, caspase activation, and Parkin translocation to mitochondria, processes critical for cellular stress adaptation.

In KYSE-30 cells, BAG5 knockout compromises Hsp70 chaperone cycle function, impairing autophagic clearance of protein aggregates and sensitizing cells to proteotoxic stress and apoptosis. This disruption is particularly relevant to esophageal cancer biology, where protein homeostasis pathways are frequently dysregulated to support malignant growth and drug resistance. The model thus enables dissection of BAG5-dependent quality control mechanisms in ESCC survival and therapy adaptation.

Applications include investigating protein homeostasis through western blotting and co-immunoprecipitation of BAG5 partners such as Hsp70 and Parkin, assessing autophagy flux via LC3 lipidation, and measuring apoptosis using flow cytometry. Migration, invasion, and drug sensitivity assays can evaluate the impact of BAG5 loss on metastatic potential and chemoresistance. These polyclonal cells are also suited for transcriptomic and proteomic analyses to map stress response networks. For additional information or to request custom models, contact Ascent Research.

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