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Cat. No. ARG39359

DNAL1 Knockout NCI-H1299 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Carcinoma

This product consists of CRISPR/Cas9-edited polyclonal knockout NCI-H1299 cells with targeted disruption of DNAL1, a gene encoding an axonemal dynein light chain required for ciliary motility and ciliogenesis. The knockout population is generated in a p53-null, KRAS wild-type human lung adenocarcinoma cell line, providing a physiologically relevant NSCLC model for studying cilia-dependent processes. DNAL1 functions downstream of FOXJ1 and RFX3, interacts with DNAH5/DNAH11 outer dynein arm components, and modulates Hedgehog signaling via GLI transcription factors and cell cycle regulators Cyclin D1/CDK4. Applications include investigating ciliary signaling in lung cancer, proliferation and metastasis assays, primary ciliary dyskinesia research, and drug sensitivity studies.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    NCI-H1299

    Sex of Donor

    Male

    Age

    43 years

    Gene Name

    DNAL1

    Gene Identifier

    NCBI Gene ID 83544

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    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 DNAL1 Knockout NCI-H1299 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the NCI-H1299 human lung carcinoma cell line, designed to disrupt expression of the DNAL1 gene. As a heterogeneous pool, this product avoids clonal selection artifacts and provides a versatile loss-of-function model for investigating DNAL1-dependent biological processes.

The host NCI-H1299 line was established from a lymph node metastasis of a lung adenocarcinoma and is widely employed as a model for non-small cell lung cancer (NSCLC) with high metastatic potential. This cell line is p53-null and KRAS wild-type, offering a specific genetic background for studying tumor progression and signaling mechanisms independent of p53-mediated regulation.

DNAL1 encodes an axonemal dynein light chain essential for outer dynein arm assembly and ciliary motility. It is transcriptionally regulated by FOXJ1 and RFX3, and functionally interacts with dynein heavy chains DNAH5 and DNAH11. Disruption of DNAL1 impairs ciliogenesis, thereby attenuating cilia-dependent Hedgehog signaling, as evidenced by reduced GLI1 and GLI2 transcriptional activity. In parallel, DNAL1 influences cell cycle progression through modulation of Cyclin D1 and CDK4, linking ciliary function to proliferative control.

In the NCI-H1299 background, DNAL1 knockout is anticipated to compromise ciliary function, potentially altering Hedgehog-driven transcriptional programs and cell cycle regulation. Given the metastatic origin of this line, the loss of DNAL1 may also affect invasive and migratory properties, offering a physiologically relevant system to dissect the interplay between ciliary dynamics and NSCLC malignancy.

This polyclonal knockout pool supports a broad range of experimental applications, including the study of cilia-dependent signaling pathways in NSCLC, functional analysis of DNAL1 in cell proliferation and metastasis, disease modeling of primary ciliary dyskinesia, and evaluation of drug responses. Researchers can validate knockout effects via Western blotting for DNAL1 and ciliary markers, RT?qPCR for GLI1 and CCND1, immunofluorescence staining of acetylated tubulin and ???tubulin, cell proliferation and migration assays, flow cytometry for cell cycle analysis, and transcriptome profiling by RNA?seq. For further technical details or custom solutions, please contact Ascent Research.

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