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Cat. No. ARG27606

IKBIP Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

IKBIP Knockout HAP1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population in the near-haploid HAP1 cell line, with targeted disruption of the IKBIP gene. The IKBIP protein directly interacts with IKBKB (IKK-??) to negatively regulate NF-??B signaling and functions as a pro-apoptotic factor in p53-dependent DNA damage responses, promoting caspase-mediated cell death. This knockout model is ideal for investigating NF-??B pathway dynamics and apoptotic signaling using luciferase reporter assays, Western blotting, co-immunoprecipitation, and flow cytometry-based apoptosis detection. It serves cancer biology research and drug sensitivity studies with IKK inhibitors, enabling validation of therapeutic targets in the NF-??B axis.

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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

    IKBIP

    Gene Identifier

    NCBI Gene ID 121457

    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

IKBIP Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population with targeted disruption of the IKBIP gene. This loss-of-function model preserves the polyclonal nature of the edited pool, avoiding clonal selection artifacts. The use of CRISPR/Cas9 introduces genetic perturbations at the IKBIP locus, generating a heterogeneous knockout population suitable for functional screening and pathway analysis.

The host cell line HAP1 is a near-haploid human fibroblast-like cell line derived from KBM-7 chronic myeloid leukemia cells. Adapted for stable haploidy and adherent growth, HAP1 cells are widely employed in genetic screens due to their haploid genome, which simplifies gene disruption and enables clear phenotypic analyses. Their adherent morphology and rapid proliferation make them compatible with various cell-based assays.

IKBIP encodes a protein that directly interacts with IKBKB (IKK-??), a central kinase in the NF-??B signaling cascade. By inhibiting IKK-?? activity, IKBIP reduces the phosphorylation and degradation of NFKBIA (I??B??), thereby attenuating NF-??B transcriptional activation mediated by RELA. IKBIP is transcriptionally regulated by TP53 in response to DNA damage and promotes apoptosis through activation of caspases such as CASP3 and CASP9. Thus, IKBIP acts as a pro-apoptotic factor linking p53-mediated stress signaling to the cell death machinery.

In the HAP1 near-haploid background, disruption of IKBIP leads to loss of protein function, enabling clear phenotypic readouts for dissecting its role in NF-??B regulation and p53-dependent apoptosis. The haploid genome ensures that gene disruption results in functional consequences without allelic redundancy. This model allows robust interrogation of IKBIP??s impact on signaling crosstalk and apoptotic responses, with the fibroblast-like character supporting high-throughput imaging and flow cytometry.

This IKBIP knockout product supports diverse applications including NF-??B luciferase reporter assays, Western blotting for IKK-??, phospho-RELA, and IKBIP, and co-immunoprecipitation to probe protein interactions. Apoptosis can be quantified using Annexin V/PI staining, caspase activity measurements, and flow cytometry. The model is valuable for cancer biology studies and drug sensitivity testing with IKK inhibitors. For additional technical information or to discuss customized solutions, please contact Ascent Research.

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