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Cat. No. ARG27661

KATNBL1 Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

KATNBL1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited knockout population targeting the p80 regulatory subunit of katanin in a near-haploid human cell line. This model enables loss-of-function studies of microtubule severing, essential for mitotic spindle assembly, chromosome segregation, and cytoskeletal organization. KATNBL1 functions downstream of Aurora A kinase and PLK1, and interacts with KATNA1 to modulate microtubule dynamics. Ideal for investigating cell division mechanisms and microtubule-related pathologies, the knockout cells support applications such as immunofluorescence imaging, live-cell microscopy, flow cytometry, and drug screening. The HAP1 background simplifies genetic analysis, making this product a valuable tool for functional genomics, cancer biology, and neurobiology research.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    HAP1

    Sex of Donor

    Male

    Age

    40 years

    Derived From Site

    Bone marrow

    Gene Name

    KATNBL1

    Gene Identifier

    NCBI Gene ID 79768

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    IMDM

    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 KATNBL1 Knockout HAP1 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population engineered for targeted disruption of the KATNBL1 gene. This loss-of-function model is generated in HAP1 cells, providing a powerful tool to investigate the role of the p80 regulatory subunit of the katanin microtubule-severing complex. The polyclonal nature of the population ensures a broad representation of knockout alleles while maintaining a near-complete loss of KATNBL1 function across the cell pool, making it ideally suited for high-throughput functional genomics, phenotypic screening, and detailed cell biology analyses.

The HAP1 host cells are a near-haploid human fibroblast-like cell line derived from the KBM-7 chronic myeloid leukemia line. These cells stably maintain a haploid karyotype for most chromosomes, enabling unambiguous gene knockout by disruption of a single allele. HAP1 cells exhibit adherent, fibroblastoid morphology and retain expression of key signaling and adhesion proteins, facilitating studies of mitosis, cytoskeletal dynamics, and genetic interaction networks without the complexity of diploid compensation.

KATNBL1 encodes the non-catalytic p80 subunit of katanin, which directs the p60 catalytic subunit (KATNA1) to microtubules and stimulates ATP-dependent severing. Functioning downstream of mitotic kinases Aurora A and PLK1, KATNBL1 is phosphorylated to activate severing activity during spindle assembly, thereby regulating spindle length and chromosome segregation. Beyond mitosis, katanin influences interphase microtubule dynamics and participates in cellular processes such as cytokinesis and neurite outgrowth. KATNBL1 forms complexes with KATNA1 and interacts with microtubule-severing proteins spastin and fidgetin, integrating signals from multiple pathways to govern cytoskeletal remodeling.

Combining KATNBL1 knockout with the HAP1 haploid background creates a genetically simplified platform to dissect katanin-dependent mechanisms in cell division and microtubule organization. The absence of a second allele eliminates masking effects, enabling clear-cut phenotypic assessment. This model is particularly valuable for genome-wide screens seeking to uncover modulators of spindle assembly checkpoints, chromosomal stability, and cell cycle progression, areas directly relevant to aneuploidy in cancer and neurodevelopmental disorders.

Typical research applications employing these cells include immunofluorescence microscopy to examine mitotic spindle morphology, live-cell imaging to monitor microtubule dynamics in real time, and flow cytometry for cell cycle profiling. The knockout cells are also used for Western blotting validation of katanin subunits and for phenotypic rescue assays to confirm gene-specific effects. In neurobiology, they serve as a model for studying neurite outgrowth regulation. Moreover, the polyclonal population supports small-molecule screening campaigns aimed at identifying compounds that compensate for defective microtubule severing. For further information, please contact Ascent Research.

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