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Cat. No. ARG27431

C17orf75 Knockout HAP1 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Bone Marrow

  • Disease:

    Chronic myeloid leukemia

The C17orf75 Knockout HAP1 Polyclonal Cells product provides a polyclonal population of the near-haploid human HAP1 cell line with CRISPR/Cas9-mediated disruption of the C17orf75 gene. This uncharacterized gene's knockout enables functional studies to elucidate its biological role. The haploid background simplifies loss-of-function analysis, and the polyclonal format reduces clonal artifacts. Applications include functional genomics, knockout screening, and downstream assays such as RT-qPCR, western blotting, and DNA sequencing. This model is an essential tool for researchers aiming to de-orphanize C17orf75 and explore its potential involvement in cellular processes.

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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

    C17orf75

    Gene Identifier

    NCBI Gene ID 64149

    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 C17orf75 Knockout HAP1 Polyclonal Cells product comprises a population of HAP1 cells that have been modified by CRISPR/Cas9-mediated gene disruption to introduce a loss-of-function mutation in the C17orf75 gene. This polyclonal knockout cell pool contains a heterogeneous mixture of edited alleles, providing a robust model for studying the functional consequences of C17orf75 deficiency. As a pooled knockout population, it avoids clonal selection and captures the diversity of editing outcomes, making it suitable for population-based assays and screens that require representing a broad spectrum of genetic modifications.

HAP1 is a near-haploid human cell line originally derived from the KBM-7 chronic myeloid leukemia cell line. Its haploid karyotype simplifies genetic manipulation and knockout validation because only a single allele needs to be disrupted to achieve functional loss of the target gene. HAP1 cells are widely employed in functional genomics, CRISPR-based screens, and knockout studies due to their ease of culture and the ability to perform high-throughput phenotypic analyses. The chronic myeloid leukemia origin of HAP1 cells also provides a context for studying cancer-related pathways, although the primary utility lies in its haploid nature.

C17orf75 is an uncharacterized open reading frame on chromosome 17, and its biological function remains largely unknown. No definitive molecular interactions, upstream regulators, downstream targets, or associated signaling pathways have been identified for the C17orf75 protein. The absence of characterized functional domains or homologs in model organisms adds to the challenge of predicting its role. Knockout of this gene in HAP1 cells provides a foundational tool for functional characterization studies aimed at elucidating its cellular function, including potential roles in proliferation, survival, or differentiation.

The haploid background of HAP1 cells offers a distinct advantage for studying uncharacterized genes such as C17orf75, as disruption of the single allele can immediately reveal loss-of-function phenotypes without the confounding effects of a second intact allele. The polyclonal nature of this knockout product further enhances robustness by minimizing clonal variability that can arise from single-cell-derived lines. This model is therefore well-suited for initial exploratory screens where rapid assessment of knockout phenotypes can guide more detailed mechanistic investigations. It enables researchers to bypass the time-consuming process of generating clonal lines while still obtaining biologically relevant insights.

Applications of these C17orf75 Knockout HAP1 Polyclonal Cells span multiple areas of basic and translational research. They can be used in functional genomics screens to identify phenotypic consequences of C17orf75 loss, in pooled CRISPR dropout screens to assess cellular fitness, and in complementation assays with wild-type or mutant C17orf75 constructs. Representative assays include RT-qPCR for verifying transcript loss, western blotting for protein absence (if antibodies are available), DNA sequencing to confirm editing at the target locus, and various functional assays such as proliferation, apoptosis, or cell cycle analysis. This knockout model serves as a versatile platform for the de-orphanization of C17orf75. For further information or technical support, please contact Ascent Research.

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