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Cat. No. ARG27563

HMGXB4 Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

The HMGXB4 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the near-haploid HAP1 cell line, targeting the HMGXB4 gene. HMGXB4 encodes an HMG-box transcription factor that modulates Wnt/??-catenin signaling through interactions with CTNNB1 and TCF7L2, regulating genes such as AXIN2 and CCND1. This model facilitates functional genomics, Wnt pathway analysis, and cancer cell biology research. The haploid HAP1 background ensures clear genotype-phenotype relationships, making it ideal for high-throughput assays and drug target validation in oncogenic and developmental contexts.

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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

    HMGXB4

    Gene Identifier

    NCBI Gene ID 10042

    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 HMGXB4 Knockout HAP1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of HMGXB4. HMGXB4 encodes an HMG-box transcription factor that modulates gene expression through DNA binding and chromatin interactions, with roles in Wnt/??-catenin signaling. This polyclonal knockout pool, derived from the HAP1 near-haploid cell line, offers a robust loss-of-function model for functional studies, free from clonal bias.

HAP1 cells, originating from the KBM-7 chronic myeloid leukemia line, feature a near-haploid karyotype that simplifies genetic analyses. Their stable, fibroblast-like morphology and rapid growth support high-throughput assays and knockout screens. Haploidy ensures that single-gene disruptions produce clear phenotypes, enabling direct genotype-phenotype correlations. This background minimizes functional redundancy, making HAP1 a gold standard for gene function studies, particularly in cancer biology and signal transduction.

HMGXB4 participates in chromatin organization and transcriptional regulation, acting as a cofactor in Wnt signaling. It interacts with ??-catenin (CTNNB1), TCF7L2, and LEF1 on target gene promoters. Activated by WNT3A through FZD/LRP5/6, the pathway stabilizes CTNNB1 via DVL and GSK3B inhibition. HMGXB4 then modulates expression of AXIN2, CCND1, and MYC. Its interactions with chromatin remodeling complexes confer context-dependent control over proliferation and differentiation.

Combining HMGXB4 knockout with the HAP1 haploid background creates a powerful system for investigating transcriptional control mechanisms. The absence of a second allele eliminates confounding wild-type expression, enhancing signal-to-noise in phenotypic assays. This model is particularly suited for dissecting Wnt pathway dynamics, as HAP1 cells retain a functional Wnt signaling cascade. Researchers can explore how HMGXB4 loss affects chromatin landscape and target gene transcription without interference from redundant HMG-box factors.

Research applications encompass functional genomics (RNA-seq, ChIP-qPCR), Wnt pathway interrogation using luciferase reporters and co-immunoprecipitation of CTNNB1/LEF1 complexes, and cancer cell biology (proliferation, migration/invasion assays). The polyclonal format supports bulk population studies and drug target validation via high-content screening for HMGXB4-related pathways. These cells advance research into transcriptional dysregulation in developmental disorders and leukemogenesis. For further inquiries, contact Ascent Research.

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