Quick Order Cart

Cat. No. ARG40124

DYDC1 Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

This product provides a CRISPR/Cas9-edited polyclonal knockout population of DYDC1 in the human near-haploid HAP1 cell line. DYDC1 is a putative scaffolding component of histone H3K4 methyltransferase complexes, interacting with ASH2L, RBBP5, WDR5, and MLL family proteins to regulate chromatin modification and transcriptional activation. The polyclonal format offers a robust loss-of-function model for studying epigenetic mechanisms in a cancer-derived background. The engineered cells enable investigation of DYDC1??s role in H3K4 methylation dynamics and downstream gene expression programs, with applications in chromatin biology, cancer epigenetics, synthetic lethality screening, and drug target validation using techniques such as ChIP-seq, western blotting, and cell proliferation assays.

Inquire Now

In stock

Ships next business day


Ask a Question

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

    DYDC1

    Gene Identifier

    NCBI Gene ID 143241

    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 DYDC1 Knockout HAP1 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population for targeted DYDC1 gene disruption in a human near-haploid background. This loss-of-function model permits investigation of DYDC1 biology without confounding allele complementation typical of diploid lines. The polyclonal format harbors a heterogeneous knockout genotype pool, making it suitable for pooled genetic screens and gene essentiality analyses.

HAP1 cells are a human near-haploid fibroblastoid line derived from KBM-7 chronic myeloid leukemia cells. Their haploid karyotype simplifies knockout phenotype analysis because a single gene disruption can yield complete inactivation. These adherent, immortalized cells maintain relevant signaling and epigenetic machinery, offering a robust system for chromatin and transcription studies.

DYDC1 is a putative scaffold or regulatory component of COMPASS/Set1-like histone H3K4 methyltransferase complexes. It is predicted to interact with core factors ASH2L, RBBP5, WDR5, DPY30, and MLL family methyltransferases to promote H3K4 methylation at promoters of active genes, including HOX clusters and cell cycle regulators. DYDC1 may function downstream of oncogenic signals such as MYC and developmental pathways, integrating extracellular cues to epigenetic and transcriptional outputs. Disruption of DYDC1 is expected to reduce H3K4 methylation and alter gene expression profiles impacting proliferation and differentiation.

HAP1 cells, originating from a leukemic line, provide a relevant background for studying DYDC1’s role in cancer-related H3K4 methylation dynamics. The haploid state eliminates allele heterogeneity, enabling clear interpretation of knockout phenotypes. This model can assess DYDC1’s contribution to leukemic cell maintenance and epigenetic drug sensitivity. Moreover, the polyclonal population supports synthetic lethality screens to identify genetic dependencies that arise upon DYDC1 loss.

Researchers can utilize this product for western blotting of H3K4me1/2/3, ChIP-seq to map DYDC1-dependent genomic loci, and RNA-seq for transcriptome profiling. Targeted gene validation via RT-qPCR and proliferation or drug sensitivity assays with histone methyltransferase inhibitors are direct applications. The DYDC1 Knockout HAP1 Polyclonal Cells serve as a versatile tool for chromatin biology, cancer epigenetics, synthetic lethality screening, and drug target discovery. For additional information, please contact Ascent Research.

Reset Password

    Reach Us Questions? Click Me Here!

    Fill out the form below and a member of our team will contact you shortly!

    *Required field



      Reach Us

      Fill out the form below and a member of our team will contact you shortly!

      *Required field

      Product Inquiry (Optional)