In Stock Cell Lines
Homo sapiens (Human)
Lung
Adherent
The MED19 Knockout A549 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the human A549 lung adenocarcinoma epithelial cell line. It provides a loss-of-function model for MED19, a subunit of the Mediator complex that bridges transcription factors and RNA polymerase II. MED19 functions downstream of TP53 and MYC, coactivating targets such as CCND1 and BCL2, which regulate proliferation and apoptosis. This knockout model is valuable for studying Mediator complex-dependent transcription in lung cancer, functional genomics, and drug target validation, and supports assays like Western blotting, RT-qPCR, RNA-seq, and phenotypic profiling of proliferation and migration.
FBN2 Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG15672
CSNK1D Knockout Hela Polyclonal Cells
Cat. No. ARG8436
IFIT2 Knockout AGS Polyclonal Cells
Cat. No. ARG27008
ACBD5 Knockout A549 Polyclonal Cells
Cat. No. ARG31163
ACACA Knockout HAP1 Polyclonal Cells
Cat. No. ARG34937
TRPV1 Knockout HEK293T Cell Line
Cat. No. ARG0321
The MED19 Knockout A549 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the human A549 lung adenocarcinoma epithelial cell line. This product provides a stable loss-of-function model for the MED19 gene (Homo sapiens), enabling investigation of its role in Mediator complex-dependent transcription. Through CRISPR/Cas9-mediated gene disruption, MED19 expression is ablated, making this cell line suitable for a range of biochemical and functional assays without the need for transient knockdown approaches.
The parental A549 cell line originates from a 58-year-old male with lung adenocarcinoma and serves as a widely used model of type II pulmonary epithelial cells. A549 cells retain characteristics of alveolar epithelium and are well-characterized for lung cancer research, drug discovery, and toxicology studies. Their robust growth and genetic tractability make them an appropriate host for gene editing, offering a clinically relevant system for studying lung adenocarcinoma and non-small cell lung carcinoma.
MED19 encodes a subunit of the Mediator complex, a multi-protein assembly that bridges transcription factors and RNA polymerase II to regulate gene expression. Mechanistically, MED19 interacts with core Mediator subunits such as MED1, MED17, and MED26, and with the CDK8 module, facilitating complex assembly and function. It acts downstream of transcription factors like TP53 and MYC, integrating signaling inputs to coactivate target genes. Knockout of MED19 disrupts Mediator complex integrity, impairing transcriptional activation of downstream targets including CCND1, BCL2, and CDH1, which govern cell proliferation, apoptosis, and adhesion.
In the A549 lung adenocarcinoma background, disruption of MED19 provides a valuable tool to dissect the Mediator complex’s role in oncogenic signaling. Since A549 cells display dysregulated growth and survival pathways, MED19 knockout is expected to attenuate the transcription of pro-proliferative and anti-apoptotic genes, thereby impairing tumorigenic phenotypes. This model facilitates exploration of how transcriptional coactivation via the Mediator complex sustains lung cancer cell proliferation and migration, making it highly relevant for non-small cell lung carcinoma studies and target validation.
Researchers can utilize this knockout cell line in applications such as functional genomics to map MED19-dependent transcriptional networks, drug target validation for Mediator complex inhibitors, and phenotypic assays to evaluate proliferation, colony formation, migration, and apoptosis. Representative techniques include Western blotting and RT-qPCR for knockout confirmation, RNA-seq for transcriptome analysis, ChIP-qPCR for Mediator and RNA polymerase II occupancy, and various cell-based assays. The line also supports drug sensitivity screening. For additional information, contact Ascent Research.
