The HAVCR1 Knockout A-549 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population with targeted disruption of the HAVCR1 gene (TIM-1). The polyclonal nature yields a heterogeneous pool of loss-of-function alleles, which mimics a natural knockout population and avoids the biases of clonal selection. This format is ideally suited for bulk functional assays that require population-level readouts, enabling robust dissection of TIM-1-dependent processes, including viral entry, immune modulation, and phosphatidylserine-mediated phagocytosis, in a human lung epithelial context.
The parental A-549 cell line is a well-characterized human lung adenocarcinoma model established from a 58-year-old Caucasian male. Its type II pneumocyte phenotype provides a relevant alveolar epithelial background for studying respiratory host?Cpathogen interactions and inflammatory signaling. This consistent genetic background supports reproducible experimentation for functional analysis of TIM-1 in airway biology.
HAVCR1 encodes TIM-1, a type I transmembrane glycoprotein that functions as a phosphatidylserine receptor and hepatitis A virus entry factor. Engagement by phosphatidylserine or its ligand TIM-4 triggers downstream signaling via the PI3K/AKT pathway through interaction with PIK3R1, and activates NF-??B (NFKB1) to promote transcription of IL-4 and IL-5. TIM-1 also associates with integrins ITGAL and ITGAM, linking apoptotic cell recognition to immune cell adhesion and migration. These signaling events position TIM-1 as a key node at the intersection of viral pathogenesis, phagocytosis, and T-cell costimulation.
In A-549 cells, knockout of HAVCR1 ablates the primary receptor for hepatitis A virus, creating a defined model for viral entry studies. Loss of TIM-1 also eliminates phosphatidylserine-dependent clearance of apoptotic cells, enabling dissection of epithelial phagocytic function with relevance to asthma and chronic lung inflammation. Moreover, the knockout allows analysis of the impact on PI3K/AKT and NF-??B pathway activity, providing insight into how lung epithelial cells contribute to local cytokine production and innate immune responses.
Researchers can utilize HAVCR1 Knockout A-549 Polyclonal Cells in hepatitis A virus infectivity assays, TIM-4 binding studies by flow cytometry, IL-4/IL-5 ELISA, and quantitative phagocytosis assays. Western blotting and RT-qPCR confirmation of pathway component expression and proliferation/apoptosis assays complement these applications. This product supports therapeutic target screening for asthma, allergic diseases, and acute kidney injury, and is a versatile tool for viral immunology and drug discovery. For technical support or custom engineering, please contact Ascent Research.
