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Cat. No. ARG33393

HSPB1 Knockout HT29 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

The HSPB1 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-mediated loss-of-function model in human colorectal adenocarcinoma HT29 cells. HSPB1 (Hsp27) is a molecular chaperone that suppresses apoptosis by binding cytochrome c and procaspase-3, and promotes survival via p38 MAPK/AKT/NF-??B signaling and actin stabilization. This polyclonal knockout population is ideal for studying HSPB1 in colorectal cancer proliferation, chemoresistance, and metastasis. Suitable applications include western blotting, apoptosis assays, migration studies, and cytoskeletal analysis, supporting drug screening and stress response research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HT29

    Gene Name

    HSPB1

    Gene Identifier

    NCBI Gene ID 3315

    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

The HSPB1 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of HT29 human colorectal adenocarcinoma cells with disrupted HSPB1 expression. This loss-of-function model enables investigation of heat shock protein beta-1 (HSPB1) in a colorectal cancer context. The polyclonal format preserves genetic heterogeneity, reflecting tumor diversity in experimental designs. It is suited for researchers requiring robust perturbation of HSPB1 in a well-established colon cancer cell line.

The HT29 cell line, derived from colorectal adenocarcinoma of a 44-year-old Caucasian female, displays epithelial morphology and intestinal marker expression, serving as a standard model for colorectal cancer and intestinal biology. Its tumorigenic capacity and defined signaling landscape make it ideal for dissecting oncogenic pathways and therapeutic responses in colon cancer research.

HSPB1 (Hsp27) is a stress-induced molecular chaperone activated by p38 MAPK, MAPKAPK2, AKT, ERK, and JNK downstream of stimuli like heat shock, oxidative stress, and cytokines (TNF-??, IL-1??). It inhibits apoptosis by sequestering cytochrome c and procaspase-3, blocking caspase activation. Additionally, HSPB1 stabilizes actin filaments and promotes survival via IKK-mediated NF-??B activation. It interacts with CRYAB, HSPB8, and modulates translation through eIF4E. Thus, HSPB1 integrates p38 MAPK stress signaling, AKT survival cascades, and cytoskeletal regulation.

In HT29 cells, HSPB1 contributes to proliferation, chemoresistance (e.g., cisplatin), and metastatic potential. The polyclonal HSPB1 knockout population permits rigorous examination of its roles in apoptosis, drug sensitivity, and invasion. This model is particularly relevant for colorectal cancer research, where HSPB1 overexpression often correlates with poor prognosis and resistance. The heterogeneous knockout pool supports population-based assays, such as drug screening and signaling analyses, bridging in vitro findings with tumor heterogeneity.

Applications include western blotting, RT-qPCR, MTT and Annexin V assays, Transwell migration, wound healing, cisplatin sensitivity testing, phalloidin staining, co-immunoprecipitation, and phospho-p38 ELISA. These tools facilitate studies on stress response, cytoskeletal dynamics, targeted therapy screening, and metastasis mechanisms. The HSPB1 Knockout HT29 Polyclonal Cells are a versatile resource for colorectal cancer and stress biology research. For technical inquiries, contact Ascent Research.

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