| Popis: |
Abstract Eukaryotic Elongation Factor 2 Kinase (eEF2K), a member of the α-kinase family, services as a crucial negative regulator of protein synthesis, particularly under conditions of cellular stress. A pan-cancer analysis of eEF2K expression, genetic variants, and clinical relevance across multiple tumor types was performed using data from the Cancer Genome Atlas (TCGA) and GEO. Our findings suggest that eEF2K has dual roles in cancer progression, with its expression correlating with patient prognosis. Significant phosphorylation of eEF2 at T57, Y434, and T59 was observed, which may regulate protein synthesis during stress. The elevated T59 phosphorylation in COAD, despite the low eEF2K expression, indicates that this may be regulated by alternative kinases, such as AMPK or mTOR. This suggests that compensatory mechanisms may be involved. In addition to modulating eEF2 phosphorylation, eEF2K is involved in a number of other processes, including peptidyl-serine phosphorylation, the G2/M transition, and the MAPK cascade. The protein products of eEF2K are capable of localizing to the nucleus, cytoplasm, and cytosol, where they bind to a range of proteins, including ATP and calcium ions. These findings provide novel insights into the role of eEF2K in cancer biology and suggest that the targeting of eEF2K and eEF2 phosphorylation may offer promising therapeutic strategies. |
Full text from SpringerLink