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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 30 Oct 2014.

Eukaryotic translation elongation factor 2

Elongation Factor 2, EF-2, NPR-C, eEF2
This gene encodes a member of the GTP-binding translation elongation factor family. This protein is an essential factor for protein synthesis. It promotes the GTP-dependent translocation of the nascent protein chain from the A-site to the P-site of the ribosome. This protein is completely inactivated by EF-2 kinase phosporylation. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: NPR, CAN, V1a, ACID, mTOR
Papers using Elongation Factor 2 antibodies
Unsaturated fatty acids down-regulate srebp isoforms 1a and 1c by two mechanisms in HEK-293 cells.
Supplier
Khromykh Alexander, In PLoS Pathogens, 2000
... Doms), anti-tubulin (Sigma), and anti-P-AMPK, t-AMPK, P-ACC, t-ACC, P-eEF2, t-eEF2 (Cell Signaling Technology) ...
Papers on Elongation Factor 2
Eukaryotic elongation factor 2 kinase regulates the cold stress response by slowing translation elongation.
New
Willis et al., In Biochem J, 29 Nov 2014
We demonstrate that although there are changes to the factors that control initiation, including phosphorylation of eIF2 on the alpha subunit, the reduction in the global translation rate is mediated by regulation of elongation via phosphorylation of eEF2 by its specific kinase, eEF2K.
The Diphthamide Modification Pathway from Saccharomyces cerevisiae - Revisited.
New
Stark et al., Leicester, United Kingdom. In Mol Microbiol, 29 Nov 2014
UNLABELLED: Diphthamide is a conserved modification in archaeal and eukaryal translation elongation factor 2 (EF2).
Engineering toxin-resistant therapeutic stem cells to treat brain tumors.
New
Shah et al., United States. In Stem Cells, 24 Nov 2014
UNLABELLED: Pseudomonas exotoxin (PE) potently blocks protein synthesis by catalyzing the inactivation of elongation factor-2 (EF-2), and PE-cytotoxins have been used as anti-tumor agents.
Following movement of domain IV of elongation factor G during ribosomal translocation.
New
Ermolenko et al., Rochester, United States. In Proc Natl Acad Sci U S A, 21 Nov 2014
Translocation of mRNA and tRNAs through the ribosome is catalyzed by a universally conserved elongation factor (EF-G in prokaryotes and EF-2 in eukaryotes).
Combined deletion of Pten and p53 in mammary epithelium accelerates triple-negative breast cancer with dependency on eEF2K.
New
Zacksenhaus et al., Toronto, Canada. In Embo Mol Med, 20 Nov 2014
Kinome screens identified eukaryotic elongation factor-2 kinase (eEF2K) inhibitors as more potent than PI3K/AKT/mTOR inhibitors on both mouse and human Pten/p53-deficient TNBC cells.
Ribosomal stress activates eEF2K-eEF2 pathway causing translation elongation inhibition and recruitment of Terminal Oligopyrimidine (TOP) mRNAs on polysomes.
New
Loreni et al., Roma, Italy. In Nucleic Acids Res, 20 Nov 2014
We have identified an additional response to ribosomal stress that includes the activation of eukaryotic translation elongation factor 2 kinase with a consequent inhibition of translation elongation.
Initiation of translation by cricket paralysis virus IRES requires its translocation in the ribosome.
New
Impact
Ramakrishnan et al., Cambridge, United Kingdom. In Cell, Jun 2014
Translocation of the IRES by elongation factor 2 (eEF2) is required to bring the first codon of the mRNA into the A site and to allow the start of translation.
A review of ketamine in affective disorders: current evidence of clinical efficacy, limitations of use and pre-clinical evidence on proposed mechanisms of action.
Review
New
Dinan et al., Cork, Ireland. In J Affect Disord, Mar 2014
Efforts to unravel ketamine's therapeutic mechanism of action have implicated the mammalian target of rapamycin (mTOR)-dependent synapse formation in the rat prefrontal cortex, eukaryotic elongation factor 2 phosphorylation (p-eEF2) and glycogen synthase kinase (GSK-3).
[Ketamine's antidepressant effect: focus on ketamine mechanisms of action].
Review
New
Gaillard et al., Paris, France. In Encephale, Feb 2014
Intracellular signaling pathways such as mTOR, GSK3 or eEF2 seem to play a key role and are associated with an increased synaptic plasticity.
Glutamate receptor antagonists as fast-acting therapeutic alternatives for the treatment of depression: ketamine and other compounds.
Review
New
Impact
Charney et al., Bethesda, United States. In Annu Rev Pharmacol Toxicol, Dec 2013
These clinical findings have been reverse-translated into preclinical models in an effort to elucidate ketamine's antidepressant mechanism of action, and three important targets have been identified: mammalian target of rapamycin (mTOR), eukaryotic elongation factor 2 (eEF2), and glycogen synthase kinase-3 (GSK-3).
Elongation factor-2 phosphorylation in dendrites and the regulation of dendritic mRNA translation in neurons.
Review
New
Sala et al., Milano, Italy. In Front Cell Neurosci, Dec 2013
Worthy of note, there is accumulating evidence that the eukaryotic Elongation Factor 2 Kinase (eEF2K)/eukaryotic Elongation Factor 2 (eEF2) pathway may be strongly involved in this process.
The biosynthesis and biological function of diphthamide.
Review
New
Lin et al., Ithaca, United States. In Crit Rev Biochem Mol Biol, Nov 2013
Eukaryotic and archaeal elongation factor 2 contains a unique post-translationally modified histidine residue, named diphthamide.
The eEF2 kinase confers resistance to nutrient deprivation by blocking translation elongation.
New
Impact
Sorensen et al., Vancouver, Canada. In Cell, Jun 2013
We report that eukaryotic elongation factor 2 kinase (eEF2K), which is activated by AMP-kinase (AMPK), confers cell survival under acute nutrient depletion by blocking translation elongation.
Structures of the human and Drosophila 80S ribosome.
New
Impact
Beckmann et al., München, Germany. In Nature, Jun 2013
Here we present structures of Drosophila melanogaster and Homo sapiens 80S ribosomes in complex with the translation factor eEF2, E-site transfer RNA and Stm1-like proteins, based on high-resolution cryo-electron-microscopy density maps.
Diphthamide modification on eukaryotic elongation factor 2 is needed to assure fidelity of mRNA translation and mouse development.
GeneRIF
Leppla et al., Bethesda, United States. In Proc Natl Acad Sci U S A, 2012
Diphthamide modification on eukaryotic elongation factor 2 is needed to assure fidelity of mRNA translation and mouse development
In vitro and in vivo protection by melatonin against the decline of elongation factor-2 caused by lipid peroxidation: preservation of protein synthesis.
GeneRIF
Ayala et al., Sevilla, Spain. In J Pineal Res, 2012
melatonin prevented the molecular changes in eEF-2 and the decline in protein synthesis rate secondary to lipid peroxidation.
C-type natriuretic peptide and its receptors in atherosclerotic plaques of the carotid artery of clinically asymptomatic patients.
GeneRIF
Eckstein et al., München, Germany. In Eur J Vasc Endovasc Surg, 2012
Report the presence of CNP and its receptors, NPR2/3 in atherosclerotic plaques of human carotid artery, with increased expression of NPR3 in histologically unstable plaques.
Prolyl hydroxylase-dependent modulation of eukaryotic elongation factor 2 activity and protein translation under acute hypoxia.
GeneRIF
Pascual et al., Sevilla, Spain. In J Biol Chem, 2012
PHD2 modulated eEF2 activity and protein translation under acute hypoxia.
Knockdown of natriuretic peptide receptor-A enhances receptor C expression and signalling in vascular smooth muscle cells.
GeneRIF
Anand-Srivastava et al., Montréal, Canada. In Cardiovasc Res, 2012
knockdown of NPR-A up-regulates the expression of NPR-C, Gialpha proteins, and NPR-C-linked adenylyl cyclase signalling and suggests a cross-talk between NPR-A and NPR-C.
NMDA receptor blockade at rest triggers rapid behavioural antidepressant responses.
Impact
Monteggia et al., Dallas, United States. In Nature, 2011
We find that the ketamine-mediated blockade of NMDAR at rest deactivates eukaryotic elongation factor 2 (eEF2) kinase (also called CaMKIII), resulting in reduced eEF2 phosphorylation and de-suppression of translation of brain-derived neurotrophic factor.
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