ATF3 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical adenocarcinoma cell line, designed for loss-of-function studies of the ATF3 gene. This product provides a mixed population of cells carrying CRISPR/Cas9-mediated gene disruptions at the ATF3 locus, enabling robust interrogation of ATF3-dependent biological processes without clonal selection. The polyclonal format mitigates clonal artifacts and ensures representation of diverse editing outcomes, making it suitable for population-level functional assays.
The HeLa cell line, originating from cervical adenocarcinoma of Henrietta Lacks, is a widely used model in cancer biology. HeLa cells harbor HPV-18 DNA, express telomerase, and exhibit a p53-deficient, highly proliferative epithelial phenotype. These characteristics make HeLa particularly useful for studying transcription factor function, cell cycle regulation, and stress responses in a cervical cancer context.
ATF3 encodes a stress-responsive basic leucine zipper (bZIP) transcription factor that acts as a hub in multiple signaling networks, including MAPK, Toll-like receptor (TLR), unfolded protein response (UPR), and TGF-?? pathways. ATF3 is rapidly induced by diverse stressors such as ER stress, oxidative stress, DNA damage, and pro-inflammatory cytokines including TNF-?? and IL-1?? through upstream kinases like JNK and p38 MAPK. Upon activation, ATF3 forms homodimers or heterodimers with other bZIP proteins such as c-Jun and CREB to regulate transcription, either repressing or activating target genes such as CCND1, CDKN1A (p21), BCL2, BIM, ID1, and CHOP (DDIT3) in a context-dependent manner. ATF3 also interacts with NF-??B, HDAC1, and CBP/p300 to modulate inflammatory and survival programs.
In the HeLa background, ATF3 knockout allows dissection of its dual roles in apoptosis and proliferation. Given the p53-null status of HeLa cells, ATF3-mediated stress responses may rely on alternative pathways, making this model particularly valuable for exploring p53-independent transcriptional control of cell fate. Disruption of ATF3 in this context can unmask compensatory mechanisms and reveal how ATF3 integrates signals from ER stress sensors (IRE1, PERK) and MAPKs (JNK, p38, ERK1/2) to influence cancer cell survival, migration, or drug sensitivity.
Typical applications include analyzing ATF3-dependent gene regulation via RT-qPCR, ChIP-qPCR, or luciferase reporter assays; assessing apoptotic responses under chemotherapeutic or ER stress challenge using flow cytometry (Annexin V) or caspase activation assays; and investigating cell cycle alterations after genotoxic insults. This polyclonal knockout population also supports high-throughput screening for modulators of stress signaling and validation of ATF3 target engagement in cancer and inflammation models. For additional details or to order, please contact Ascent Research.
