The antibody is versatile across multiple experimental platforms, as summarized below:
| Method | Dilution | Samples |
|---|---|---|
| Western Blot (WB) | 1:5000–1:50,000 | A549, Jurkat, HepG2, HeLa, SH-SY5Y |
| Immunoprecipitation (IP) | 0.5–4.0 µg/mg lysate | HeLa cells |
| IHC | 1:50–1:500 | Human kidney, testis (TE buffer pH 9.0) |
| IF/ICC | 1:50–1:500 | HeLa cells |
| ELISA | N/A (validated) | - |
WB: 41 publications (e.g., tumor suppressor studies in breast, lung cancers) .
IHC: 2 publications (e.g., pancreatic cancer biomarker analysis) .
EIF2AK2 is a serine/threonine kinase activated by:
Antiviral Defense: Phosphorylates eIF2α (Ser51), inhibiting global protein synthesis while upregulating stress-response genes (e.g., ATF4) .
Tumor Suppression: Linked to poor prognosis in cancers (breast, lung, colorectal) when suppressed .
Inflammation: Activates NF-κB and p38 MAPK pathways via interactions with TRAF and MAP2K6 .
A 2023 study identified EIF2AK2 as a potential diagnostic and prognostic biomarker for pancreatic cancer :
Expression: Significantly higher in pancreatic cancer tissues vs. adjacent tissues.
Survival Analysis: High EIF2AK2 levels correlated with improved survival outcomes (Kaplan-Meier, Cox regression) .
Mechanism: Knockdown experiments in PANC-1 cells reduced proliferation and induced apoptosis (CCK-8, wound healing assays) .
EIF2AK2’s dual role in stress response and oncology highlights its therapeutic potential:
Antiviral Strategies: Targeting viral evasion mechanisms (e.g., influenza NS1 protein inhibition) .
Cancer Therapy: Modulating EIF2AK2 activity to enhance tumor suppression or immunotherapy efficacy .
EIF2AK2 is implicated in: