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In response to endoplasmic reticulum stress, activation of PERK (show EIF2AK3 Proteins) coordinates the integrated stress response by phosphorylating eIF2alpha (show EIF2A Proteins), which is then quickly dephosphorylated by the GADD34 complex. Data imply dual role of the ISR in promoting and inhibiting medulloblastoma tumorigenesis.
GADD34 suppresses lipopolysaccharide-induced sepsis and tissue injury through the regulation of macrophage activation.
Translation arrest is further demonstrated to be key for anti-viral response by acting synergistically with MAVS (show MAVS Proteins) activation to amplify TBK1 (show TBK1 Proteins) signaling and IFN-beta (show IFNB1 Proteins) mRNA transcription, while GADD34-dependent protein synthesis recovery contributes to the heterogeneous expression of interferon (show IFNA Proteins) observed in dsRNA-activated cells.
Results highlighted the essential roles played by GADD34 and CReP (show PPP1R15B Proteins) in regulating mRNA translation during unstressed conditions and following endoplasmic reticulum stress.
Sustained protein synthesis sensitized cells to pharmacological induction of the Unfolded Protein Response (UPR), and the observed decrease in cell viability was restored upon inhibition of GADD34 activity. We conclude that NMP4 (show ZNF384 Proteins) is a key regulator of ribosome biogenesis and the UPR, which together play a central role in determining cell viability during endoplasmic reticulum stress.
Through aging or a high fat diet, insulin (show INS Proteins) signaling in GADD34-deficient liver converted to be down regulated compared with WT mice.
Results show that GADD34 plays a vital role in promoting cell death following proteasome inhibition via enhancing protein synthesis involved in endoplasmic reticulum stress, reactive oxygen species production and autophagy formation.
avidity for the substrate plays an important role in imparting specificity on the PPP1R15B-PP1G-actin ternary complex.
GADD34 enhances autophagy and suppresses apoptosis stimulated by LPS (show TLR4 Proteins) combined with amino acid deprivation through regulation of mTOR (show FRAP1 Proteins) signaling pathway in macrophages.
GADD34 upregulated pro-inflammatory mediator.
Inhibition of IRE1 (show ERN1 Proteins) modifies the hypoxic regulation of GADD34 family gene expression in cultured glioma cells.
GADD34 constitutes a mechanistic link between endoplasmic reticulum stress and mTOR (show FRAP1 Proteins) inactivation, therefore promotes cell survival during endoplasmic reticulum stress.
reduction of GADD34 expression significantly suppressed tumor, and resulted in decreased accumulation of MDSCs and T-cells, and inhibition of GADD34 reduced secretion of vascular epithelial growth factor alpha and transforming growth factor beta by MDSCs
ANXA11 (show ANXA11 Proteins) rs1049550 and PPP1R15A rs557806 may improve the identification of mCRC patients sensitive to bevacizumab regimens, and further validation is required in large cohorts
Data of this study strengthen the evidence of an unfolded protein response during the course of RA and provide an insight of the potential interest in GADD34 as a relevant marker for RA.
The results suggest that dephosphorylation of eIF2a (show EIF2S1 Proteins) by GADD34 plays an important role in doxorubicin resistance of MCF-7/ADR (show AKR1B1 Proteins) cells.
The reactive oxygen species-generating NADPH oxidase-4 (Nox4 (show NOX4 Proteins)) is induced downstream of ATF4 (show ATF4 Proteins), binds to a PP1 (show PPA1 Proteins)-targeting subunit GADD34 at the endoplasmic reticulum, and inhibits PP1 (show PPA1 Proteins) activity to increase eIF2alpha (show EIF2A Proteins) phosphorylation and ATF4 (show ATF4 Proteins) levels.
stress pathways lead to the induction of the protein GADD34, which appears to provide protection against the toxic effects of the secreted virulence factors in Pseudomonas aeruginosa infection
The data highlight independent interactions of PP1 (show PPA1 Proteins) and eIF2alpha (show EIF2A Proteins) with GADD34, demonstrating that GADD34 functions as a scaffold both in vitro and in cells
GADD34 may play a neuroprotective role against amyloid-beta toxicity.
This gene is a member of a group of genes whose transcript levels are increased following stressful growth arrest conditions and treatment with DNA-damaging agents. The induction of this gene by ionizing radiation occurs in certain cell lines regardless of p53 status, and its protein response is correlated with apoptosis following ionizing radiation.
protein phosphatase 1, regulatory (inhibitor) subunit 15A
, growth arrest and DNA damage-inducible protein GADD34
, growth arrest and DNA-damage-inducible 34
, myeloid differentiation primary response gene 116
, myeloid differentiation primary response protein MyD116
, protein phosphatase 1 regulatory subunit 15A
, myeloid differentiation primary response protein MyD116 homolog
, progression elevated gene 3 protein