In Stock Cell Lines
Homo sapiens (Human)
Lung
Adherent
The ATF3 Knockout BEAS-2B Cell Line is a CRISPR/Cas9-edited knockout cell line derived from human bronchial epithelial BEAS-2B cells, with targeted disruption of ATF3, a stress-inducible transcription factor that integrates TNF-??, IL-1??, JNK, and p38 MAPK signals and regulates genes like IL-6 and Bax. This model enables investigation of airway epithelial stress responses, inflammation, and pathologies such as asthma, COPD, and lung cancer, utilizing standard assays like western blotting, RT-qPCR, apoptosis detection, and ELISA.
GID8 Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG16091
Sting1 Knockout RCS Cell Line
Cat. No. ARG44138
FKBP5 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG18122
DNAH5 Knockout Raji Polyclonal Cells
Cat. No. ARG39051
CLDND1 Knockout HEK293T Polyclonal Cells
Cat. No. ARG4447
Rat Intestinal Microvascular Endothelial Cell Medium
Cat. No. ARM0244
The ATF3 Knockout BEAS-2B Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the BEAS-2B human bronchial epithelial cell line, with targeted disruption of the ATF3 gene. This loss-of-function model enables the dissection of ATF3-dependent transcriptional programs in airway biology, providing a defined system for investigating stress-inducible signaling without wild-type ATF3 interference.
BEAS-2B cells are an immortalized human bronchial epithelial line widely used as a model for airway epithelial function, particularly in inflammation, oxidative stress, and oncogenic transformation studies. They retain responsiveness to cytokines and environmental stressors, offering a stable and consistent platform for long-term experiments that are impractical with primary cells.
ATF3 is a stress-inducible bZIP transcription factor that integrates signals from pathways triggered by TNF-??, IL-1??, oxidative stress, and ER stress. Upstream kinases JNK and p38 MAPK, along with regulators c-Jun and p53, control ATF3 expression and activity. ATF3 forms heterodimers with AP-1 partners (c-Jun, JunB, ATF2) and interacts with NF-??B p65, Smad3, and HDAC1. It transcriptionally regulates genes involved in apoptosis (Bax, Bcl-2), cell cycle (Cyclin D1, p21), and inflammation (IL-6, IL-8, MCP-1), as well as ER stress response (CHOP). Key upstream signaling components include MEKK1, MKK4/7, and the JNK/p38 MAPK cascades.
In BEAS-2B cells, ATF3 knockout compromises stress-induced gene expression programs, altering apoptosis, cell cycle regulation, and inflammatory cytokine production. This makes the model highly relevant for studying airway diseases such as asthma, COPD, lung adenocarcinoma, and pulmonary fibrosis, where ATF3 is implicated in modulating NF-??B, p53, and TGF-?? pathway outputs. The knockout allows clear assessment of ATF3??s role in epithelial stress responses and pathological remodeling.
Researchers can apply this cell line in airway epithelial stress response studies, lung cancer research, and inflammation signaling investigations. Standard assays include western blotting, RT-qPCR, apoptosis detection, ELISA for IL-6, luciferase reporter assays, phospho-JNK western blotting, and wound healing assays, facilitating comprehensive mechanistic and functional analyses. For further information, please contact Ascent Research.
