AGTRAP 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, featuring targeted disruption of the AGTRAP gene. This loss-of-function model provides a versatile tool for studying AGTRAP functions in a standardized cellular context. The polyclonal nature preserves genetic heterogeneity while ensuring robust gene disruption, and cells are supplied as a proliferating pool ready for experimental use.
A-549 cells are a widely used human lung adenocarcinoma epithelial line with features of alveolar type II epithelium, serving as a key model for respiratory and cancer research. Their cancerous origin and epithelial phenotype make them particularly relevant for investigating oncogenic and fibrotic signaling networks in a lung cancer context.
AGTRAP negatively modulates angiotensin II type 1 receptor (AT1R) signaling by binding to the receptor’s activated C-terminal tail and facilitating receptor internalization in cooperation with beta-arrestin. This complex dampens angiotensin II-induced MAPK and NF-kB cascade activation, leading to reduced transcription of pro-fibrotic and hypertensive genes. AGTRAP also influences TGF-beta signaling and epithelial sodium channel (ENaC) activity, connecting AT1R to sodium homeostasis and fibrosis. In the absence of AGTRAP, angiotensin II stimulation results in exaggerated ERK phosphorylation, enhanced NF-kB activity, and upregulation of TGF-beta and collagen expression.
In A-549 cells, AGTRAP knockout enables dissection of AT1R-dependent pathways in a cancerous epithelial system where renin-angiotensin components are expressed. Loss of AGTRAP-mediated negative regulation sensitizes cells to angiotensin II, boosting MAPK and NF-kB responses and TGF-beta-driven fibrotic programs, a phenotype useful for studying lung adenocarcinoma progression and epithelial-mesenchymal transition. Endogenous expression of angiotensinogen and ACE further establishes a self-contained model for autocrine/paracrine angiotensin II signaling studies.
This product supports diverse assays: western blotting for AGTRAP, AT1R, and phospho-ERK; RT-qPCR for AGTRAP, TGF-beta, and collagen; angiotensin II phospho-signaling analysis; migration assays; and AT1R immunofluorescence. Applications include AT1R regulatory mechanism studies, hypertension and fibrosis modeling, drug screening, and renin-angiotensin system investigations in lung cancer. For inquiries, contact Ascent Research.
