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ABC50 (显示 ABCF1 蛋白) N-terminal region interacts with eukaryotic initiation factor (显示 EIF4G1 蛋白) eIF2 and is a target for regulatory phosphorylation by CK2 (显示 CSNK2A1 蛋白)
hypusine-eIF5A (显示 EIF5 蛋白)-facilitated translation elongation promotes arsenite-induced polysome disassembly and stress granule assembly in cells subjected to adverse environmental conditions
analysis of the ER stress response in immunogenic cell death and the potential value of eIF2alpha (显示 EIF2A 蛋白) phosphorylation as a biomarker for this clinically relevant variant of apoptosis [review]
The data highlight independent interactions of PP1 (显示 PPA1 蛋白) and eIF2alpha (显示 EIF2A 蛋白) with GADD34 (显示 PPP1R15A 蛋白), demonstrating that GADD34 (显示 PPP1R15A 蛋白) functions as a scaffold both in vitro and in cells
These experiments connect embryonic stem cell growth factors to eIF2alpha (显示 EIF2A 蛋白) phosphorylation.
We identified EIF2A phosphorylation as a novel early molecular event occurring in response to NAMPT (显示 NAMPT 蛋白) inhibition and mediating protein synthesis arrest.
The results suggest that dephosphorylation of eIF2a by GADD34 (显示 PPP1R15A 蛋白) plays an important role in doxorubicin resistance of MCF-7/ADR (显示 AKR1B1 蛋白) cells.
The Newcastle disease virus-induced translation shutoff at late infection times was attributed to sustaining phosphorylation of eIF2a, which is mediated by continual activation of PKR and degradation of PP1.
GHRH (显示 GHRH 蛋白) and GHRH-R (显示 GHRHR 蛋白) loops are involved in placental choriocarcinoma cell line viability and apoptosis through Akt (显示 AKT1 蛋白) and eIF2a pathways.
These findings suggest that phosphorylated-eIF2alpha (显示 EIF2A 蛋白) regulates synaptic actions of nicotine in both mice and humans, and that reduced phosphorylated-eIF2alpha (显示 EIF2A 蛋白) may enhance susceptibility to nicotine (and other drugs of abuse) during adolescence.
Caspase (显示 CASP3 蛋白)(s)-dependent proteolysis of molecular chaperones and eIF2alpha (显示 EIF2A 蛋白) may be novel signaling pathways of apoptosis.
EIF2alpha (显示 EIF2A 蛋白) regulates oligodendrocyte survival during differentiation.
We hypothesize that the essential role of methionine-charged initiator tRNA in forming ternary complex is responsible for the robust ability of methionine deficiency to induce ATF4 (显示 ATF4 蛋白) and the ISR even in the absence of GCN2 (显示 EIF2AK4 蛋白) or eIF2alpha (显示 EIF2A 蛋白) kinase activity.
ER stress-induced increase in ATF4 (显示 ATF4 蛋白) and CHOP (显示 DDIT3 蛋白) expression is initiated by an increase in Atf4 (显示 ATF4 蛋白) and Chop (显示 DDIT3 蛋白) mRNA, which is also dependent upon eIF2alpha (显示 EIF2A 蛋白) phosphorylation.
Data indicate that 5xFAD-related pathologies do not necessarily require hyperphosphorylation of eIF2alpha (显示 EIF2A 蛋白) to emerge.
Endoplasmic reticulum stress suppressed CReP (显示 PPP1R15B 蛋白) expression in an IRE1 alpha (显示 ERN1 蛋白)-dependent manner, which increased eIF2alpha (显示 EIF2A 蛋白) phosphorylation and consequently attenuated protein synthesis.
eIF2alphaP acts as a molecular switch that dictates either cell survival or death by activated Akt (显示 AKT1 蛋白) in response to oxidative stress.
aberrant phosphorylation of eukaryotic initiation factor (显示 EIF4G1 蛋白)-2a (eIF2a (显示 EIF2A 蛋白)) may induce synaptic failure and neurodegeneration through persistent translational inhibition of global protein synthesis.
Alteration of protein homeostasis and eIF2alpha (显示 EIF2A 蛋白) phosphorylation status by pathogenic huntingtin (显示 HTT 蛋白) appears to be an important cause of striatal cell death.
Data indicate that prolonged endoplasmic reticulum stress inhibits protein synthesis independently of translation initiation factor (显示 TIF1 蛋白) eIF2alpha (显示 EIF2A 蛋白)-P.
This study demonistrated that Genetic deletion of eIF2alpha (显示 EIF2A 蛋白) kinase PERK (显示 EIF2AK3 蛋白) prevented enhanced phosphorylation of eIF2alpha (显示 EIF2A 蛋白) and deficits in protein synthesis, synaptic plasticity and spatial memory in animal disease model of Alzheimer's disease.
In conclusion, the immediate-early (显示 JUN 蛋白) IE180 protein of pseudorabies virus has the previously uncharacterized ability to suppress phosphorylation levels of the eukaryotic translation initiation factor (显示 EIF2A 蛋白) eIF2alpha (显示 EIF2A 蛋白).
Therapeutic modulation of eIF2alpha phosphorylation rescues TDP-43 (显示 TARDBP 蛋白) toxicity in amyotrophic lateral sclerosis disease models.
The translation initiation factor EIF2 catalyzes the first regulated step of protein synthesis initiation, promoting the binding of the initiator tRNA to 40S ribosomal subunits. Binding occurs as a ternary complex of methionyl-tRNA, EIF2, and GTP. EIF2 is composed of 3 nonidentical subunits, the 36-kD EIF2-alpha subunit (EIF2S1), the 38-kD EIF2-beta subunit (EIF2S2\; MIM 603908), and the 52-kD EIF2-gamma subunit (EIF2S3\; MIM 300161). The rate of formation of the ternary complex is modulated by the phosphorylation state of EIF2-alpha (Ernst et al., 1987
, eukaryotic translation initiation factor 2 subunit 1
, eukaryotic translation initiation factor 2 subunit alpha
, eukaryotic translation initiation factor 2A
, eukaryotic translation initiation factor 2 alpha subunit
, Eukaryotic translation initiation factor 2 subunit 1
, eukaryotic translation initiation factor 2, subunit 1 alpha, 35kDa
, eukaryotic translation initiation factor 2, subunit 1 (alpha )
, eukaryotic initiation factor 2alpha
, eukaryotic translation initiation factor 2
, eukaryotic translation initiation factor 2alpha
, minute (1) 14C