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Cat. No. ARG36027

BAG5 Knockout HCT116 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Large intestine (colon)

  • Disease:

    Carcinoma

The BAG5 polyclonal knockout HCT 116 cells are a CRISPR/Cas9-edited cell population with targeted disruption of the BAG5 co-chaperone gene in human colorectal carcinoma cells. BAG5 negatively regulates Hsp70 chaperone activity and Parkin-dependent mitophagy, and promotes ??-synuclein aggregation. In the HCT 116 background (KRAS G13D, MSI, p53 WT), loss of BAG5 enhances proteostasis and sensitizes cells to apoptosis. This model supports research in colorectal cancer, autophagy, mitophagy, and drug screening for BAG5 interactors, compatible with western blotting, apoptosis assays, and co-immunoprecipitation.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HCT 116

    Sex of Donor

    Male

    Age

    Adult

    Derived From Site

    In situ; Colon

    Gene Name

    BAG5

    Gene Identifier

    NCBI Gene ID 9529

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    McCoy's 5A

    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

This product offers a CRISPR/Cas9-edited polyclonal knockout cell population of BAG5 in the human colorectal carcinoma HCT 116 cell line. The polyclonal format comprises a heterogeneous mixture of cells with targeted disruption of BAG5, delivering a robust loss-of-function model without requiring single-cell cloning. It is designed for reliable interrogation of BAG5-dependent pathways in a cancer-relevant background.

HCT 116 is an extensively characterized colorectal epithelial cell line harboring a KRAS G13D mutation, microsatellite instability, and wild-type p53. This genetic makeup renders it a valuable platform for studying oncogenic signaling, stress responses, and protein homeostasis. The BAG5 knockout counterpart builds on this well-defined background, enabling precise dissection of co-chaperone functions in tumor cell biology.

BAG5 encodes a co-chaperone that inhibits Hsp70 ATPase activity and negatively regulates Parkin-mediated mitophagy by impairing Parkin ubiquitination. It also promotes ??-synuclein aggregation, linking it to neurodegenerative pathology. BAG5 is activated by cellular stress and proteasome inhibition, and it suppresses Hsp70 chaperone function, Parkin-dependent mitochondrial clearance, and apoptosis signaling. Molecular partners include Hsp70/Hsc70, ??-synuclein, Parkin, and CHIP, placing BAG5 at the crossroads of proteasomal and autophagic degradation pathways.

In HCT 116 cells, BAG5 knockout removes the inhibitory constraint on Hsp70 and Parkin, thereby enhancing protein quality control and mitophagy, and sensitizing cells to apoptosis. This shift provides insight into how colorectal cancer cells adapt to proteotoxic stress and offers a model to study the role of chaperone networks in tumor cell survival and therapy resistance.

Applications for these polyclonal knockout cells span colorectal cancer research, proteostasis and autophagy studies, and Parkinson??s disease modeling. They support western blotting, RT-qPCR, apoptosis and mitophagy assays, co-immunoprecipitation, and Hsp70 ATPase activity measurement. High-throughput screening for BAG5?CHsp70?CParkin pathway modulators is also feasible. For more information, please contact Ascent Research.

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