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Cat. No. ARG38946

DLX1 Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

The DLX1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the near-haploid HAP1 chronic myeloid leukemia cell line, offering a genetically tractable system for targeted disruption of the DLX1 homeobox transcription factor. DLX1, activated by SHH signaling and acting in concert with DLX2, regulates GABAergic interneuron differentiation through downstream targets such as GAD1 and GAD2. This model is ideal for studying DLX1-dependent proliferation, apoptosis, and gene expression changes in a cancer background, supporting assays like western blotting, RT-qPCR, and functional proliferation (MTT, BrdU) and apoptosis (Annexin V) readouts.

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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

    DLX1

    Gene Identifier

    NCBI Gene ID 1745

    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 DLX1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 cell line, designed to disrupt the expression of the DLX1 gene. This product provides a heterogeneous pool of edited cells, facilitating robust loss-of-function studies without the clonal selection step. The knockout model enables investigation of DLX1-dependent cellular phenotypes and transcriptional networks in a defined genetic background.

HAP1 cells are a near-haploid human cell line originally derived from the KBM-7 chronic myeloid leukemia (CML) line, which was isolated from a patient in blast crisis. These cells are BCR-ABL1 positive and have been adapted to adherent growth, offering a genetically simplified platform for functional genomics. Their haploid nature reduces gene redundancy, making them particularly suitable for CRISPR-based knockout experiments and phenotypic screens.

DLX1 encodes a homeobox transcription factor that plays a critical role in embryonic development, neurogenesis, and craniofacial patterning. It functions downstream of the Sonic Hedgehog (SHH) signaling pathway, where SHH binding to PTCH1 relieves SMO inhibition, leading to GLI transcription factor activation and subsequent DLX1 expression. DLX1, often in concert with its paralog DLX2 and interacting cofactors such as MSX1, MSX2, and p300/CBP, directly regulates genes essential for GABAergic interneuron differentiation, including GAD1, GAD2, LHX6, and ARX. Additional upstream regulators like FGF8, BMP4, and FOXG1 further modulate DLX1 activity, integrating signals from multiple morphogen pathways.

In the HAP1 CML background, DLX1 knockout uncouples its neurodevelopmental functions from the neuronal context, allowing researchers to examine its role in proliferation, apoptosis, and transcriptional regulation within a cancer cell model. The BCR-ABL1 oncogenic driver may interact with DLX1-mediated transcriptional networks, offering a unique system to explore potential crosstalk between developmental transcription factors and leukemogenic signaling. This polyclonal population is well-suited for high-throughput screening and validation experiments, leveraging HAP1??s genetic tractability.

Typical applications include western blotting and RT-qPCR to confirm DLX1 ablation, Sanger sequencing to verify CRISPR-induced mutations, immunofluorescence to assess protein localization, RNA-seq for transcriptome-wide impact, and functional assays such as MTT and BrdU incorporation for proliferation, or Annexin V staining for apoptosis. This product supports investigations into neurodevelopmental gene function in a non-neuronal environment, as well as basic studies on SHH signaling and GABAergic gene regulation. For further technical details or custom requests, please contact Ascent Research.

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