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Cat. No. ARG37183

HSPB8 Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

This product provides a CRISPR/Cas9-edited polyclonal knockout population of HeLa cells with targeted disruption of the HSPB8 gene. HSPB8 is a stress-induced molecular chaperone that partners with BAG3 and HSC70 to mediate chaperone-assisted selective autophagy, preventing toxic protein aggregation and promoting cell survival. Loss of HSPB8 in the widely used HeLa cervical adenocarcinoma model enables investigation of autophagy-dependent proteostasis, cancer cell stress responses, and neurodegeneration-related pathways. The knockout cells are suitable for assays including Western blotting, immunofluorescence, co-immunoprecipitation, autophagy flux analysis, and drug sensitivity screening.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HeLa

    Sex of Donor

    Female

    Age

    31 years

    Gene Name

    HSPB8

    Gene Identifier

    NCBI Gene ID 26353

    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 HSPB8 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the HeLa cell line, in which the HSPB8 gene has been disrupted to create a loss-of-function model. Supplied as a mixed population with diverse editing events, this polyclonal knockout model enables HSPB8 functional studies without clonal selection bias. CRISPR/Cas9 targeting critical exons results in ablated full-length HSPB8 protein expression.

HeLa is a human epithelioid cervical adenocarcinoma line isolated in 1951, widely used for cancer biology, signal transduction, and autophagy research due to robust growth and well-characterized signaling networks. HeLa cells endogenously express HSPB8 and associated chaperone components, offering a physiologically relevant system to study stress-induced protein quality control and cell survival.

HSPB8 is an ATP-independent chaperone upregulated by stress via HSF1 and cytokines like TNF-alpha and IL-1beta through MAPK signaling. It forms a complex with BAG3 and HSC70, recruiting autophagic receptor SQSTM1/p62 and ubiquitinated cargo. The complex links to dynein and microtubules for delivery to LC3-positive autophagosomes in the CASA pathway. HSPB8 promotes aggrephagy and proteostasis, impacting cell survival and cytoskeletal integrity, with further interactions including HSPB1 and HSPB6.

In HeLa cells, HSPB8 knockout perturbs CASA, sensitizing cells to proteotoxic stress and providing a cancer-relevant model for autophagy?Caggregation interplay. This system is valuable for studying HSPB8’s roles in oncogenic stress responses, and for modeling neurodegenerative diseases like Charcot-Marie-Tooth disease type 2L and distal hereditary motor neuropathy, where HSPB8 mutations impair autophagic clearance. The knockout also enables analysis of MAPK-mediated survival and apoptosis regulation.

Applications include Western blotting, RT-qPCR, immunofluorescence, co-immunoprecipitation, autophagy flux assays, protein aggregation analysis, cell viability, migration, and drug sensitivity screening. The polyclonal population supports pooled functional genomics and bulk biochemical studies. Typical research areas are chaperone-assisted autophagy mechanisms, protein aggregation disease modeling, cancer stress adaptation, and high-throughput screening of HSPB8?CBAG3?CHSC70 axis modulators. For further information, contact Ascent Research.

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