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Cat. No. ARG39785

DRGX Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

The DRGX Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of near-haploid HAP1 cells carrying a targeted disruption of the DRGX gene. DRGX encodes a paired-like homeobox transcription factor that functions downstream of NEUROG2 to drive dorsal root ganglion sensory neuron differentiation and regulates key nociceptive ion channels and receptors such as SCN10A (NaV1.8) and TRPV1. This knockout pool provides a reliable loss-of-function model for studying DRGX-dependent transcriptional programs, protein interactions, and signaling pathways. It is well suited for applications in pain research, target validation, high-throughput screening, and isogenic control generation.

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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

    DRGX

    Gene Identifier

    NCBI Gene ID 644168

    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 DRGX Knockout HAP1 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the DRGX gene. This heterogeneous pool of HAP1 cells provides a loss-of-function model to study DRGX-dependent processes without single-cell cloning, allowing assessment of gene function in a population context.

HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) line from a male patient. Its near-haploid karyotype simplifies genetic manipulation and minimizes heterozygous confounding effects, making it a robust system for knockout studies. Although of leukemic origin, HAP1 cells maintain functional transcriptional and signaling pathways, and are widely used for functional genomics and drug discovery.

DRGX is a paired-like homeobox transcription factor that acts downstream of proneural factors NEUROG2 and NEUROG1 to direct dorsal root ganglion (DRG) sensory neuron differentiation. It transcriptionally regulates ion channels and receptors critical for nociception, including SCN10A (NaV1.8), TRPV1, NTRK1, and RET, as well as the transcription factor POU4F1 (BRN3A). DRGX interacts with cofactors PBX1, MEIS1, and SOX10, and is modulated by retinoic acid, BMP4, and Wnt signaling. Loss of DRGX function impairs sensory neuron specification and is linked to congenital insensitivity to pain.

In the HAP1 context, DRGX knockout provides an isogenic background for dissecting its molecular functions. While HAP1 cells are non-neuronal, they express core transcriptional machinery enabling study of transcription factor activity and interactions. The polyclonal knockout population is ideal for analyzing DRGX-dependent transcriptional changes, protein?Cprotein interactions, and pathway modulation, with the near-haploid genome ensuring unambiguous genotype?Cphenotype correlations.

Applications include western blotting for DRGX protein validation, RT-qPCR and RNA-seq for expression profiling, co-immunoprecipitation for interaction studies, reporter assays for transcriptional activity, and immunofluorescence for localization. The model supports high-throughput screens for modulators of DRGX pathways and generation of isogenic controls. For more information, contact Ascent Research.

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