The BRI3BP Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung adenocarcinoma epithelial cell line, targeting the BRI3BP gene. This product provides a heterogeneous pool of cells harboring various CRISPR-mediated mutations at the BRI3BP locus, enabling loss-of-function studies without clonal selection. The polyclonal format preserves genetic diversity and is well suited for investigating gene function in a physiologically relevant mixed population, avoiding clonal artifacts.
The A-549 cell line, originating from a 58-year-old Caucasian male lung adenocarcinoma, serves as a model for alveolar type II pneumocytes. These adherent epithelial cells are used in cancer biology, toxicology, and drug metabolism research. Their robust growth and well-characterized signaling make them ideal for studying mitochondrial apoptosis and stress responses in lung adenocarcinoma. The parental line retains key alveolar features, including surfactant production and xenobiotic metabolism, critical for respiratory disease modeling.
BRI3BP encodes a mitochondrial protein that interacts with BRI3 and the stress kinases JNK1 and JNK2, scaffolding apoptotic signaling. Under apoptotic stimuli, DNA damage, or oxidative stress, BRI3BP promotes JNK activation, phosphorylating c-Jun and transcriptionally regulating pro-apoptotic genes. This cascade induces mitochondrial outer membrane permeabilization, cytochrome c release, and caspase-9 and -3 cleavage, executing cell death. The BRI3BP interactome integrates upstream damage signals with the core apoptotic machinery, a critical node in JNK-mediated apoptosis.
BRI3BP ablation in A-549 cells perturbs stress-induced apoptosis and JNK signaling, offering a model to dissect mitochondrial adaptor roles in lung adenocarcinoma cell death. Since A-549 cells exhibit both intrinsic and extrinsic apoptotic pathways, the polyclonal knockout population enables evaluation of BRI3BP??s function across diverse genetic backgrounds. This model is relevant for studying apoptosis evasion in lung cancer and crosstalk between JNK signaling and mitochondrial integrity in alveolar epithelial cells.
The polyclonal knockout cells suit applications in apoptosis research, cancer biology, Alzheimer??s disease modeling, drug screening, and mitochondrial dysfunction. Representative assays include Western blotting for BRI3BP, phospho-JNK, and cleaved caspase-3; RT-qPCR for BRI3BP mRNA; flow cytometry for Annexin V/PI apoptosis; immunofluorescence for mitochondrial morphology; JC-1 assay for membrane potential; co-immunoprecipitation of BRI3-JNK; and MTT cell viability. These tools enable study of BRI3BP-dependent signaling in lung adenocarcinoma and related fields. For further information, please contact Ascent Research.
