Gene-specific regulation by general translation factors.
By T. Dever. Cell, 2002
746 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/2c6eae375d2669d1fd9da540b4ba8b35acc2de28
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Citations in the corpus
- Autophagy Is Activated for Cell Survival after Endoplasmic ReticulumStress (2006, background): “There are four eIF2 kinases (GCN2, PKR, PERK, and HRI) which are activated by amino acid starvation, viral infection, ER stress, and heme depletion, respectively (6).”
- Translational control of long-lasting synaptic plasticity and memory. (2009, neutral): “Neurons would probably never experience such insults, except under pathological conditions such as hypoxia and stroke (DeGracia et al., 1997), but weak levels of kinase activation are likely to be the rule (Dever, 2002).”
- Impact of Protein Kinase PKR in Cell Biology: from Antiviral to Antiproliferative Action (2006, background): “Phosphorylation of eIF-2 limits the number of active 43S complexes, promoting reinitiation from GCN4 and ATF-4 ORFs.”
- Global Subcellular Characterization of Protein Degradation Using Quantitative Proteomics (2012, neutral): “Within our total data set, many of the proteins that significantly increase in abundance after MG132 treatment are associated with induction of the unfolded protein response (UPR), including ATF3, SERPINH1, HSF2, and HSP90AB1 (Fig.”
- Translation reinitiation at alternative open reading frames regulates gene expression in an integrated stress response (2004, background): “The crucial event is the paradoxically increased translation of the GCN4 mRNA, triggered by yeast’s only eIF2 kinase, Gcn2p, which is activated by amino acid deprivation (Hinnebusch, 2000; Dever, 2002).”
- Regulation of translation via mRNA structure in prokaryotes and eukaryotes. (2005, background): “All rights reserved. doi:10.1016/j.gene.2005.06.037 functions of these proteins (Dever, 2002; Kapp and Lorsch, 2004; Laursen et al., 2005; von der Haar et al., 2004).”
- The ERK1/2 mitogen-activated protein kinase pathway as a master regulator of the G1- to S-phase transition (2007, background): “The current view is that phosphorylation of eIF4E does not lead to a global increase in mRNA Oncogene translation but rather enhances translation of specific mRNAs with extensive 50UTR structure (Dever, 2002; Mamane et al., 2004).”
- Pushing the limits of the scanning mechanism for initiation of translation (2002, neutral): “Initiation factor eIF2 plays a key role in translational control (Clemens, 2001; Dever, 2002) and mutations that perturb regulation of eIF2 have profound pathological consequences (Delépine et al., 2000; Han et al., 2001; Harding et al., 2001; Van der Knaap et al., 2002) .”
- Molecular mechanisms of translational control (2004, background): “A number of kinases that are activated under different conditions can phosphorylate eIF2α at Ser51 (REFS 17, 18) .”
- ER stress (PERK/eIF2α phosphorylation) mediates the polyglutamine-induced LC3 conversion, an essential step for autophagy formation (2007, background): “In mammals, there are at least four eIF2a kinases including GCN2, PKR, PERK, and HRI, which are activated by amino acid starvation, viral infection, ER stress, and heme depletion, respectively.(32)”
- Structural Characterization of the Human Eukaryotic Initiation Factor 3 Protein Complex by Mass Spectrometry*S (2007, background): “Most other initiation factors are phosphoproteins (28, 29), and phosphorylation has been shown to function as a general mechanism for the regulation of initiation (29).”
- A Novel Function of eIF2α Kinases as Inducers of the Phosphoinositide-3 Kinase Signaling Pathway (2007, background): “To date, there are four distinct eIF2 kinases with unique ability to respond to various stress conditions (Dever, 2002).”
- Translational control in the endoplasmic reticulum stress response. (2002, background): “Thus, phosphorylation of eIF2α turns out to be a convenient means to control translation initiation, and specific eIF2α kinases have evolved to couple upstream signals to this pivotal event (8, 9).”