The EIF2AK2 Knockout HGC-27 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HGC-27 gastric carcinoma cell line, featuring targeted disruption of the EIF2AK2 gene. This polyclonal knockout model provides a pooled population of HGC-27 cells with heterogeneous genetic modifications at the EIF2AK2 locus, generated via CRISPR/Cas9-mediated gene disruption. The product is designed as a loss-of-function tool for studying the roles of EIF2AK2 in gastric cancer biology, stress signaling, and innate immunity without the selection of a single clonal isolate.
The parental HGC-27 cell line is a widely used epithelial model established from the lymph node metastasis of a gastric carcinoma patient. As a metastatic gastric cancer cell line, HGC-27 retains key malignant characteristics, including anchorage-independent growth and invasive potential, making it a relevant system for investigating molecular mechanisms of gastric cancer progression and metastasis. The cells are maintained in standard culture conditions and exhibit typical epithelial morphology, providing a robust platform for functional genomics studies.
EIF2AK2 encodes the serine/threonine kinase PKR, which is activated by dsRNA, interferons, TNF-??, and the stress-sensor PACT (PRKRA) under conditions of ER stress and oxidative damage. Upon activation, PKR phosphorylates eIF2?? (EIF2S1) at Ser51, blocking general translation while permitting translation of ATF4, which induces the pro-apoptotic factor DDIT3 (CHOP). PKR also signals through NF-??B and p53, and it interacts with TRBP (TARBP2), ADAR1, and the inhibitory chaperone p58IPK (DNAJC3). In the interferon pathway, PKR operates downstream of the IFNAR1?CJAK1?CTYK2 receptor complex and contributes to STAT1-dependent gene expression, thereby linking innate immune recognition to translational repression and cell death.
In the context of HGC-27 gastric carcinoma cells, EIF2AK2-mediated signaling has been implicated in tumor-suppressive functions. PKR-dependent phosphorylation of eIF2?? can suppress tumor cell proliferation and promote apoptosis in response to oncogenic stress, while its crosstalk with NF-??B and PI3K-AKT pathways modulates survival signaling. Disruption of EIF2AK2 in this metastatic background enables researchers to dissect the kinase’s contributions to gastric cancer cell growth, stress resilience, and immune evasion. The polyclonal knockout population allows the study of these processes in a heterogeneous pool, reflecting a more physiologically relevant gene disruption scenario.
This polyclonal knockout product is suitable for gastric cancer studies, antiviral immunity research, and stress signaling analyses. Key applications include Western blotting for PKR and downstream targets (e.g., phospho-eIF2??, ATF4, CHOP); RT-qPCR for stress gene transcripts; viral infection assays; Annexin V apoptosis assays; cell proliferation or colony formation tests; and co-immunoprecipitation to explore PKR interactions. The model also supports RNA-seq for transcriptome-wide insights into translational control. For further information, contact Ascent Research.
