EC Number   |
General Information |
Reference |
|---|
   2.7.11.20 | evolution |
eEF2K is a calcium/calmodulin dependent kinase that belongs to the alpha kinase family, which has negligible sequence identity to the conventional protein kinase family |
740281 |
| 2.7.11.20 | evolution |
eukaryotic elongation factor 2 kinase (eEF2K) is a member of the small group of atypical alpha-kinases, eEF2K is not a member of the main kinase superfamily. alpha-Kinases show no sequence similarity to the main protein kinase superfamily, although they do display limited three-dimensional structural similarity |
739828 |
| 2.7.11.20 | evolution |
eukaryotic elongation factor 2 kinase is a member of the atypical alpha-kinase family |
741450 |
| 2.7.11.20 | malfunction |
eEF2K gene knockdown on TNF-alpha-induced inflammatory responses in HUVECs |
739836 |
| 2.7.11.20 | malfunction |
eEF2K-knockout mice are viable and fertile under standard vivarium conditions. mGluR-induced long-term depression (LTD), but not LTD induced by other stimuli, is impaired in eEF2K knockout mice. The memory deficits in eEF2K knock-in mice are due to sleep-related alterations. Fear-conditioning responses in mice are deficient in eEF2K activity |
739828 |
| 2.7.11.20 | malfunction |
enzyme deficiency leads to impaired mGluR-long term potentiation, higher miniature inhibitory postsynaptic current frequency and amplitude in hippocampal granule cells, higher tonic inhibition measured in the in granule cells of the dentate gyrus, and impaired AMPAR-endocytosis following mGluR activation. The heterozygous deletion of the enzyme in mice models of Alzheimer's disease rescue cognitive, morphological and electrophysiological alterations associated to Alzheimer's disease |
762016 |
| 2.7.11.20 | malfunction |
enzyme gene knockdown significantly augments glucose deprivation-induced cleavage of caspase-3 and apoptotic nuclear condensation. In contrast, enzyme gene knockdown significantly inhibits glucose deprivation-induced increase of microtubule-associated protein 1 light chain 3-II to -I ratio and autophagosome formation. Enzyme gene knockdown significantly inhibits GD-induced phosphorylation of adenosine monophosphate-activated protein kinase alpha and its downstream substrate, unc-51 like autophagy activating kinase 1 |
760364 |
| 2.7.11.20 | malfunction |
enzyme silencing blunts autophagic responses, but promotes doxorubicin-induced pyroptotic cell death in melanoma cells. Enzyme suppressionresults in inhibiting autophagy and augmenting pyroptosis, thus modulating the sensitivity of melanoma cells to doxorubicin |
760309 |
| 2.7.11.20 | malfunction |
enzyme silencing with eEF2K siRNA inhibits phosphorylation of JNK and NF-kappaB p65 as well as reactive oxygen species (ROS) production by TNF-alpha. In vascular smooth muscle cells, eEF2K siRNA also inhibits VCAM-1 induction and phosphorylation of JNK and NF-kappaB by TNF-alpha. In vascular endothelial cells, siRNA against eEF2K inhibited induction of VCAM-1 and endothelial-selectin as well as monocyte adhesion by TNF-alpha. Phenotypes, overview |
-, 739836 |
| 2.7.11.20 | malfunction |
in vivo studies with Gcn2 knockout mice show increased susceptibility to both acute or chronic liver damage induced by CCl4, as shown by higher alanine aminotransferase and aspartate aminotransferase activities, increased necrosis and higher inflammatory infiltrates compared with wild-type mice. Chronic CCl4 treatment increases deposition of interstitial collagen type I. Col1a1 and col1a2 mRNA levels also increase in CCl4-treated Gcn2-/- mice compared with wild-type mice |
723079 |
