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Cat. No. ARG39054

DNAH5 Knockout jurkat Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Blood (peripheral blood)

  • Disease:

    Acute lymphoblastic leukemia (ALL)

The DNAH5 Knockout Jurkat Polyclonal Cells comprise a CRISPR/Cas9-edited T-lymphocyte population with targeted DNAH5 disruption. Derived from the Jurkat T-ALL line, these non-ciliated cells serve as a loss-of-function model for studying axonemal dynein heavy chain biology in a cilia-na?ve context. DNAH5 is regulated by FOXJ1 and RFX2/3, and its disruption abrogates ciliary motility in ciliated systems. Applications include off-target screening, antibody validation, and genomic integrity assays. The polyclonal knockout pool is ideal as a non-ciliary control for ciliary functional studies, enabling researchers to discriminate cilia-specific effects. Standard assays such as PCR, western blot, and cell viability testing can be performed. Contact Ascent Research for additional details.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    Jurkat

    Cell Type

    T cell line

    Sex of Donor

    Male

    Age

    14 years

    Derived From Site

    In situ; Peripheral blood

    Gene Name

    DNAH5

    Gene Identifier

    NCBI Gene ID 1767

    Growth Mode

    Suspension

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640

    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 DNAH5 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited human T-lymphocyte population featuring targeted disruption of the DNAH5 gene. This polyclonal pool contains a heterogeneous array of editing events, offering a robust loss-of-function model without clonal isolation. Derived from the Jurkat E6-1 acute lymphoblastic leukemia line, these cells provide a versatile platform for studying DNAH5 in a non-ciliated background.

Jurkat cells are an immortalized T-cell leukemia model extensively used to investigate T-cell receptor signaling, apoptosis, and immune cell function. As these cells lack motile cilia, DNAH5 knockout does not induce ciliary dyskinesia. Instead, the model serves as an ideal ciliary-negative control or a system to explore non-ciliary roles of the axonemal dynein heavy chain.

DNAH5 encodes an outer dynein arm heavy chain that functions as an ATPase motor driving ciliary beat. In ciliated cells, its expression is regulated by transcription factors FOXJ1, RFX2, RFX3, and MCIDAS, with negative input from NOTCH signaling. The protein interacts with DNAI1, DNAI2, DNAH11, CCDC114, and ARMC4 to form the outer dynein arm complex. Loss of DNAH5 results in immotile cilia, defective mucociliary clearance, and left-right axis disruption. In Jurkat cells, this knockout reconstructs a loss-of-function context for studying dynein heavy chain biology independent of ciliary structures.

The absence of cilia in Jurkat cells repositions the DNAH5 knockout model toward applications in off-target screening, antibody validation, and genomic integrity studies. The polyclonal nature minimizes clonal bias and provides a heterogeneous population suitable for bulk analyses. It also serves as a critical non-ciliary control for experiments requiring ciliary-negative backgrounds, such as compound screening or pathway analyses where ciliary effects must be excluded.

Investigators can utilize these cells in viability, apoptosis, and proliferation assays to assess DNAH5 targeting effects. Genomic PCR and Sanger sequencing confirm editing at the DNAH5 locus, while RT-qPCR and western blot enable quantification of transcript and protein levels. Immunocytochemistry can monitor the localization of dynein components. This product is well-suited for antibody validation, off-target analysis, and as a negative control in ciliary motility studies. For further technical specifications or custom inquiries, please contact Ascent Research.

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