TRIM24 Knockout A549 Cell Line

Product Type:
In Stock Cell Lines
Species:
Homo sapiens (Human)
Tissue Source:
Lung
Disease:
Carcinoma
Host Cell:
A-549
Gene Name:
TRIM24
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The TRIM24 Knockout A549 Cell Line is a CRISPR/Cas9-edited human cell line that disrupts TRIM24 expression, a gene encoding an E3 ubiquitin ligase involved in p53 degradation and nuclear receptor coactivation. In lung adenocarcinoma, TRIM24 interacts with ESR1, THRA, and MDM2 to modulate transcription and suppress apoptosis. This knockout model is valuable for studying p53-dependent cell cycle arrest, AKT pathway activity, and hormone receptor-driven oncogenesis. Researchers can perform Western blotting, RT-qPCR, ChIP-qPCR, proliferation assays, and drug screening to characterize TRIM24 function and its therapeutic potential in lung cancer.

Shipping Info: Cryopreserved in vials and shipped on dry ice

Disclaimer: For Research Use Only
Host CellA-549
Sex of DonorMale
Age58 years
Gene NameTRIM24
Gene IdentifierNCBI Gene ID 8805
MorphologyEpithelial-like
Growth ModeAdherent
StorageLiquid nitrogen (LN2)
Temperature37°C
Atmosphere5% CO₂
Sterility testingThe bacterial, yeast, and fungi are not detected in these cells by daily monitor.
Mycoplasma testingNegative for mycoplasma through PCR analysis

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.

By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use.

This product is provided "AS IS". For Research Use Only. Not for human or animal therapeutic use.

Description

The TRIM24 Knockout A549 Cell Line is a CRISPR/Cas9-edited human cell line designed to ablate TRIM24 gene expression, providing a stable loss-of-function model for lung adenocarcinoma research. This cell line is derived from the A549 parental line and is supplied as an adherent culture, ensuring a consistent genetic background for reproducible experiments. The knockout model allows for definitive functional studies of TRIM24 without the limitations of transient silencing approaches.

The host A549 cell line originates from human lung adenocarcinoma epithelial cells of a 58-year-old male. These cells exhibit characteristics of alveolar type II pneumocytes and adhere in monolayer culture, making them a standard model for respiratory disease, drug metabolism, and toxicity investigations. Their lung adenocarcinoma origin provides a pathologically relevant system for probing oncogenic mechanisms.

TRIM24 functions as an E3 ubiquitin ligase that targets TP53 for ubiquitin-mediated degradation, repressing p53-dependent apoptosis and cell cycle arrest. It also serves as a transcriptional coactivator for nuclear receptors including estrogen receptor alpha (ESR1) and thyroid hormone receptor alpha (THRA), upregulating genes such as MYC and CCND1. TRIM24 is phosphorylated by AKT1 and forms complexes with MDM2 and histone deacetylases, linking growth factor signaling to chromatin remodeling and oncogenic transcription. Upstream transcription factor SP1 further modulates TRIM24 expression.

In A549 cells, TRIM24 overexpression enhances proliferation by suppressing p53 and activating AKT-driven pathways. CRISPR/Cas9-mediated disruption of TRIM24 restores p53 activity and attenuates AKT signaling, thereby reducing cell growth and promoting apoptosis. This knockout cell line is therefore a critical tool for elucidating the interplay between p53 tumor suppression and PI3K/AKT oncogenic signaling in lung adenocarcinoma, as well as for assessing TRIM24??s role in nuclear receptor-coactivated transcription.

The TRIM24 Knockout A549 Cell Line supports a wide array of assays, including Western blotting and RT-qPCR for knockout validation and target gene analysis, RNA-seq for transcriptome profiling, and ChIP-qPCR for chromatin association studies. Functional experiments such as MTS/MTT proliferation, colony formation, and migration assays can evaluate growth and metastatic potential, while flow cytometry enables apoptosis and cell cycle assessment. Co-immunoprecipitation experiments probe interactions with ESR1 or MDM2, and luciferase reporter assays measure transcriptional responses. Additionally, this model is suitable for drug screening to identify compounds with TRIM24-specific effects. For technical assistance, please contact Ascent Research.