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Cat. No. ARG31919

BAZ2B Knockout A549 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Lung

  • Disease:

    Lung adenocarcinoma

BAZ2B Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma line. This model disrupts BAZ2B, a chromatin remodeler that silences ribosomal RNA genes via recruitment of HDAC1 and DNMT1, and interacts with SNF2H and BAZ2A. In the A-549 cancer background, BAZ2B knockout permits investigation of epigenetic silencing, rRNA biology, and proliferation control. Applications range from western blotting and RT-qPCR to ChIP and proliferation assays, supporting research into lung cancer and chromatin remodeling.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    A549

    Sex of Donor

    Male

    Age

    58 years

    Derived From Site

    Lung

    Gene Name

    BAZ2B

    Gene Identifier

    NCBI Gene ID 29994

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    MEM

    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 BAZ2B Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung carcinoma line, providing a loss-of-function model for the BAZ2B gene. BAZ2B encodes a chromatin remodeling factor involved in epigenetic silencing and transcriptional regulation. The polyclonal format offers a heterogeneous mixture of mutant cells without clonal isolation, suitable for robust functional studies. This tool is designed for research into chromatin organization, rRNA gene silencing, and cancer biology.

The A-549 cell line is a hypotriploid human lung carcinoma epithelial line from a 58-year-old male, widely used as a model for lung adenocarcinoma. These adherent cells are well characterized for oncogenic signaling and drug response studies, offering a cancer-relevant background to examine BAZ2B disruption. The line??s pulmonary origin makes it particularly apt for probing epigenetic mechanisms linked to lung tumor biology.

BAZ2B functions in chromatin remodeling complexes to silence ribosomal RNA genes. It binds rDNA loci and recruits histone deacetylase HDAC1 and DNA methyltransferase DNMT1, establishing repressive heterochromatin through histone deacetylation and DNA methylation. BAZ2B interacts with the chromatin remodeler SNF2H and the paralog BAZ2A to form multi-subunit complexes. Downstream targets include rRNA genes, heterochromatic loci, and cell proliferation genes, while upstream regulation may involve growth factor signaling. The pathway integrates BAZ2B, SNF2H, histone deacetylases, and DNA methyltransferases to exert transcriptional repression.

In A-549 lung adenocarcinoma cells, BAZ2B-mediated silencing of rDNA is thought to regulate ribosome biogenesis and cell growth. CRISPR/Cas9-mediated disruption of BAZ2B can derepress rRNA transcription, potentially altering nucleolar integrity and protein synthesis. This knockout model thus enables dissection of epigenetic control over cancer cell proliferation and may reveal sensitivities to therapies targeting ribosomal machinery or chromatin modifiers.

Applications span investigation of epigenetic silencing mechanisms, functional lung cancer studies, ribosomal RNA biology, and high-throughput screening for chromatin remodeling modulators. Assays include Western blotting for BAZ2B and rRNA markers, RT-qPCR for pre-rRNA, ChIP-qPCR for histone modifications at rDNA, immunofluorescence for nucleolar structure, proliferation assays (MTT/BrdU), and RNA-seq transcriptome profiling. These polyclonal knockout cells support both mechanistic and translational research. For further information, contact Ascent Research.

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