The ATE1 Knockout A-549 Polyclonal Cells product comprises a live polyclonal population of human A-549 lung adenocarcinoma cells featuring CRISPR/Cas9-mediated disruption of the ATE1 gene. This polyclonal knockout pool circumvents the clonal artifacts often associated with single-cell-derived lines, providing a more representative model for studying ATE1 loss-of-function. The cells are supplied as a heterogeneous population ready for expansion, enabling robust functional interrogation of protein arginylation pathways in a cancer-relevant cellular context.
The A-549 parental line originates from a human lung adenocarcinoma and exhibits characteristic epithelial morphology. Widely adopted as an in vitro model for non-small cell lung carcinoma (NSCLC), A-549 cells recapitulate key oncogenic features such as KRAS mutation and deregulation of proliferative, survival, and stress pathways. This well-characterized system is instrumental for investigating tumor cell biology including migration, invasion, drug resistance, and metastatic potential, making it an ideal host for ATE1 knockout studies.
ATE1 encodes the arginyltransferase enzyme that catalyzes post-translational arginylation, a modification that targets proteins for N-end rule-mediated degradation or regulates their function. ATE1 activity is modulated by upstream factors such as the transcription factor Sp1 and cellular stress signals (oxidative stress, heat shock, nitric oxide). Substrates include cytoskeletal proteins (beta-actin, myosin), signaling regulators (RGS proteins, alpha-synuclein), and chaperones (calreticulin). Arginylated proteins are recognized by E3 ubiquitin ligases like UBR1 and UBR2, which promote ubiquitination and proteasomal turnover. ATE1 interacts with the ubiquitin-proteasome system and chaperones such as Hsp70, linking arginylation to protein quality control and cellular homeostasis.
In A-549 cells, ATE1 knockout eliminates arginylation, thereby disrupting actin cytoskeleton dynamics, cell migration, and stress responses ?? processes tightly linked to lung adenocarcinoma aggressiveness and metastasis. This model facilitates dissection of the N-end rule pathway’s contribution to tumorigenic properties and provides a platform to evaluate therapeutic strategies targeting arginylation. The polyclonal design ensures that observed phenotypes are robust and not skewed by clonal selection.
Researchers can employ this knockout model for western blot analysis of arginylated proteins, fluorescence-based actin dynamics assays, scratch wound and transwell migration/invasion experiments, and immunoprecipitation of arginylated substrates. It is also compatible with mass spectrometry for identifying arginylation sites, as well as drug sensitivity and proliferation assays. This polyclonal ATE1 knockout population is a versatile resource for mechanistic studies and drug discovery in cancer, neurodegeneration, and related fields. For product inquiries and technical support, please contact Ascent Research.
