In Stock Cell Lines
Homo sapiens (Human)
Lung
Adherent
The STAT1 Knockout A549 Cell Line is a CRISPR/Cas9-edited lung adenocarcinoma epithelial cell line with targeted disruption of STAT1, a central transcription factor in interferon signaling. Derived from the A549 human alveolar type II-like model, this cell line abolishes STAT1-dependent responses downstream of receptors such as IFNAR1 and IFNGR1 and kinases including JAK1 and JAK2. Loss of STAT1 impairs transcriptional activation of immune and antiproliferative genes (e.g., IRF1, MX1, PDL1), making this model ideal for studying antiviral innate immunity, JAK-STAT pathway mechanisms, and interferon-mediated tumor suppression. Applications include phospho-STAT1 flow cytometry, interferon-stimulated gene expression analysis, and cancer immunotherapy research.
CNRIP1 Knockout jurkat Polyclonal Cells
Cat. No. ARG13448
KDELR3 Knockout HEK293T Polyclonal Cells
Cat. No. ARG26204
ATP6V1C2 Knockout HGC-27 Polyclonal Cells
Cat. No. ARG29667
ARHGEF17 Knockout A549 Polyclonal Cells
Cat. No. ARG31609
ACSL4 Knockout NCI-H1703 Polyclonal Cells
Cat. No. ARG36534
EIF5A2 Knockout A2780 Polyclonal Cells
Cat. No. ARG41079
The STAT1 Knockout A549 Cell Line is a CRISPR/Cas9-edited lung adenocarcinoma epithelial cell line carrying a targeted disruption of the STAT1 gene. This knockout cell line provides a stable loss-of-function model for studying STAT1-dependent signaling in a well-characterized human alveolar type II-like epithelial background. The gene disruption was achieved using CRISPR/Cas9-mediated genome editing, resulting in abrogation of STAT1 protein expression and its downstream transcriptional activities.
The A549 host cell line was originally established from the lung adenocarcinoma tissue of a 58-year-old Caucasian male. These cells exhibit characteristics of human alveolar type II pneumocytes and are widely employed as a model for lung epithelial biology, including research on non-small cell lung cancer, viral infections, and innate immune responses. Their adherent growth and well-documented transcriptomic profile make A549 cells an ideal platform for generating gene-edited sublines.
STAT1 functions as a pivotal transcription factor downstream of type I (IFNA, IFNB) and type II (IFNG) interferons. Ligand binding to IFNAR1/IFNAR2 or IFNGR1/IFNGR2 receptors activates JAK1, JAK2, and TYK2, which phosphorylate STAT1. Phosphorylated STAT1 dimerizes and forms complexes with STAT2 and IRF9, translocating to the nucleus to regulate genes such as IRF1, MX1, OAS1, ISG15, and CIITA. Additionally, STAT1 interacts with CREBBP and EP300 coactivators, while negative regulators like SOCS1 and PIAS1 modulate its activity. This network governs antiviral innate immunity, apoptosis, and cell cycle control.
In the A549 background, disruption of STAT1 profoundly impairs interferon-mediated cellular responses. Loss of STAT1 attenuates expression of interferon-stimulated genes, compromising antiviral defense and altering the regulation of immune checkpoint molecules such as PDL1. Moreover, STAT1 knockout abrogates the antiproliferative and pro-apoptotic effects typically induced by interferons, making this cell line a valuable tool for dissecting JAK-STAT pathway contributions to tumor cell survival and immune evasion. The model enables precise interrogation of STAT1’s role in lung cancer progression and host-pathogen interactions.
This knockout cell line is suited for a broad range of research applications, including mechanistic studies of interferon signaling, antiviral immunity, and cancer immunotherapy. It facilitates assays such as western blotting for STAT1 and its targets, RT-qPCR analysis of interferon-stimulated gene expression, immunofluorescence to assess transcription factor localization, phospho-STAT1 flow cytometry, and functional antiviral or apoptosis assays. Researchers can employ this model to investigate STAT1-targeted drug candidates or explore interactions between tumor cells and the immune microenvironment. For further information, please contact Ascent Research.
