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Cat. No. ARG33823

HSPB1 Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

The HSPB1 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the A-549 lung adenocarcinoma line, targeting HSPB1 (HSP27). HSPB1 is a stress-induced chaperone that regulates actin dynamics and apoptosis by interacting with p38 MAPK, MAPKAPK2, caspase-3, and cytochrome c. In A-549 cells, HSPB1 mediates stress resistance, apoptosis evasion, and migration, making this knockout ideal for lung cancer and signaling research. Key applications include western blotting, apoptosis and migration assays, phospho-HSPB1 analysis, and drug sensitivity testing for functional genomics and target validation. The polyclonal format enables robust population-level knockout studies.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    A549

    Sex of Donor

    Male

    Age

    58 years

    Derived From Site

    Lung

    Gene Name

    HSPB1

    Gene Identifier

    NCBI Gene ID 3315

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% COâ‚‚

  • 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. It 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 HSPB1 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma cell line. This polyclonal pool provides a heterogeneous gene-disrupted model suitable for loss-of-function studies of HSPB1, avoiding artifacts associated with clonal selection. It enables robust functional genomics, target validation, and pathway analysis in a lung cancer context.

The A-549 cell line, established from an alveolar basal epithelial adenocarcinoma, is a widely used model for lung adenocarcinoma and alveolar type II pneumocyte biology. Its epithelial origin and well-characterized mutational profile make it ideal for investigating oncogenic signaling, stress responses, and therapeutic resistance mechanisms.

HSPB1 encodes the small heat shock protein HSP27, which functions as an ATP-independent molecular chaperone preventing protein aggregation and regulating actin cytoskeleton dynamics. Under stress conditions, p38 MAPK activates MAPKAPK2, leading to phosphorylation of HSPB1 and a shift from large oligomers to dimers. Phosphorylated HSPB1 stabilizes actin filaments and sequesters pro-apoptotic factors including cytochrome c and caspase-3, thereby blocking apoptosis. HSPB1 interacts with CRYAB, HSPB6, HSP70, and Daxx, and modulates NF-??B and Akt signaling. Upstream regulators include heat shock, oxidative stress, TNF-??, IL-1, and HSF1, integrating diverse stress inputs to control cell survival and migration.

In the A-549 lung adenocarcinoma background, HSPB1 contributes to stress adaptation, apoptosis evasion, and cell motility, processes critical for tumor progression and drug resistance. Disruption of HSPB1 in this model allows dissection of its protective roles in MAPK pathway signaling and actin reorganization. The polyclonal knockout format captures heterogeneous responses, making it valuable for studying compensatory mechanisms and population-level effects upon HSPB1 loss.

This knockout cell population supports a range of assays including western blotting for total and phospho-HSPB1, RT-qPCR, immunofluorescence, Annexin V/PI apoptosis assays, scratch wound migration assays, and MTT drug sensitivity testing. Applications encompass investigation of lung cancer stress biology, anti-apoptotic mechanisms, cell migration, and chemoresistance. It is suitable for functional genomics and target validation campaigns. For further information, please contact Ascent Research.

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