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Cat. No. ARG27602

IFT80 Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

IFT80 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting IFT80, encoding a core component of intraflagellar transport complex B, essential for ciliogenesis. Disruption of IFT80 impairs Hedgehog signaling via factors such as GLI2 and SUFU, and modulates Wnt pathway activity, linking to skeletal ciliopathies. Derived from the near-haploid HAP1 cell line, this model provides a simplified genetic background for studying ciliary protein trafficking and signaling mechanisms. Ideal for disease modeling, drug screening, and functional genomics, using assays like ciliary marker immunofluorescence and Hedgehog target gene expression analysis.

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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

    IFT80

    Gene Identifier

    NCBI Gene ID 57560

    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

IFT80 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated to disrupt the IFT80 gene in HAP1 cells. This product offers a mixed pool of gene-edited cells for loss-of-function analysis of IFT80, a core component of intraflagellar transport complex B. The knockout model is suitable for investigating ciliogenesis, cargo trafficking, and associated signaling pathways in a simplified genetic background.

HAP1 is a near-haploid, adherent human cell line derived from the chronic myeloid leukemia line KBM-7. Its haploid karyotype facilitates unambiguous gene disruption studies, as most loci are present in a single copy, eliminating heterozygosity confounds. HAP1 cells are widely adopted for CRISPR-based functional genomics due to their robust growth and compatibility with standard molecular and cellular assays.

IFT80 encodes a subunit of IFT complex B, essential for anterograde transport along ciliary microtubules and required for ciliogenesis. It interacts with IFT20, IFT27, IFT57, IFT74, IFT81, and IFT88 within the complex. The IFT80 gene is regulated by RFX transcription factors and FOXJ1. Disruption of IFT80 compromises ciliary assembly, leading to impaired Hedgehog signaling, where SMO activation and GLI2/SUFU-dependent transcription are particularly affected. IFT80 loss also disturbs Wnt pathway modulation, linking ciliary defects to developmental signaling abnormalities.

In the HAP1 near-haploid context, IFT80 disruption yields a clean loss-of-function system for dissecting ciliary biology. The single-copy nature of IFT80 simplifies genotype-phenotype correlations, making this model ideal for studying skeletal ciliopathies such as Jeune asphyxiating thoracic dystrophy and short-rib polydactyly syndrome. Researchers can directly connect IFT80 deficiency to ciliary ultrastructure defects and aberrant Hedgehog/Wnt signaling outputs.

Applications include ciliopathy disease modeling, IFT mechanistic studies, and drug screening for ciliary function modulators. Compatible assays comprise immunofluorescence for ciliary markers (acetylated tubulin, ARL13B), Western blotting for IFT complex proteins, and RT-qPCR for Hedgehog targets (GLI1, PTCH1). Cell-based functional assays further enable investigation of Wnt-related processes. This product serves as a valuable resource for ciliary signaling and rare disease research. For more information, contact Ascent Research.

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