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Cat. No. ARG37202

KIF2A Knockout Hela Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Uterus (cervix)

  • Disease:

    Adenocarcinoma

CRISPR/Cas9-edited polyclonal knockout HeLa cell population with targeted KIF2A gene disruption. KIF2A is a kinesin-13 microtubule depolymerase that governs mitotic spindle assembly and chromosome segregation, regulated by Aurora A/B, Plk1, and CDK1/cyclin B, and interacting with MCAK and EB1. This loss-of-function model is ideal for studying microtubule dynamics, mitotic checkpoint control, and chromosomal instability in a cancer cell background. HeLa cells are HPV-18 positive, p53/Rb-inactivated, and highly aneuploid, offering a relevant system for exploring KIF2A-dependent spindle defects and cell cycle dysregulation. Suitable for Western blotting, immunofluorescence, live-cell imaging, and drug sensitivity assays in applications spanning cancer biology, neurodevelopment, and epilepsy research.

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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

    KIF2A

    Gene Identifier

    NCBI Gene ID 3796

    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 KIF2A Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for investigating KIF2A function. This product consists of a heterogeneous pool of HeLa cells harboring targeted disruptions in the KIF2A gene, providing a loss-of-function model without clonal selection. The polyclonal format preserves genetic diversity while eliminating wild-type KIF2A expression, enabling robust phenotypic analyses in mitotic and cytoskeletal research.

HeLa cells are a widely used human cervical adenocarcinoma line, originally derived from an HPV-18-positive tumor. Their immortalized nature, rapid doubling time, and characteristic aneuploid karyotype make them a cornerstone of cancer research. Inactivation of the p53 and retinoblastoma (Rb) tumor suppressors contributes to their unchecked proliferation and genomic instability, providing a relevant background for studying mitotic regulators.

KIF2A encodes a kinesin-13 family microtubule depolymerase essential for mitotic spindle assembly and chromosome segregation. The protein localizes to centrosomes and spindle microtubules, where it catalyzes ATP-dependent depolymerization to control microtubule dynamics. Its activity is regulated by Aurora A, Aurora B, Plk1, and CDK1/cyclin B kinases, and it interacts with factors such as KIF18A, MCAK/KIF2C, EB1, MAP1B, and TIP150 to modulate kinetochore?Cmicrotubule attachments and spindle length. KIF2A functions within the mitotic spindle assembly checkpoint and microtubule cytoskeleton organization pathways.

Given HeLa cells’ reliance on precise mitotic control despite their aneuploidy, disruption of KIF2A is expected to induce pronounced spindle defects, aberrant chromosome alignment, and mitotic delay or catastrophe. This sensitization underscores the dependence of chromosomally unstable cancer cells on microtubule-regulating enzymes. Coupled with the loss of G1/S checkpoint integrity via p53 and Rb inactivation, KIF2A knockout HeLa cells provide a powerful system to interrogate the interplay between spindle dynamics and cell cycle progression in a tumor-relevant context.

These polyclonal knockout cells facilitate diverse research applications including cancer biology, cell cycle checkpoint studies, microtubule dynamics research, neuronal migration, and epilepsy investigation. They are compatible with Western blotting for protein level assessment, immunofluorescence staining of ??-tubulin for spindle morphology, and live-cell imaging using SiR-tubulin to monitor real-time mitotic events. Flow cytometry with propidium iodide enables cell cycle distribution analysis, while co-immunoprecipitation identifies KIF2A interaction partners. Additional assays include qRT-PCR for KIF2A transcript levels, scratch wound healing for migration, and paclitaxel sensitivity testing to evaluate chemotherapeutic response. For further information, contact Ascent Research.

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