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established Neuro2a cells with edited GADD34 and ATF4 (Montrer ATF4 Protéines)/GADD34 genes and found that ATF4 (Montrer ATF4 Protéines) acts as a proapoptotic factor, but GADD34 depletion did not attenuate the expression of cleaved caspase-3 (Montrer CASP3 Protéines) induced by tunicamycin treatment.
In response to endoplasmic reticulum stress, activation of PERK (Montrer EIF2AK3 Protéines) coordinates the integrated stress response by phosphorylating eIF2alpha (Montrer EIF2A Protéines), 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 (Montrer MAVS Protéines) activation to amplify TBK1 (Montrer TBK1 Protéines) signaling and IFN-beta (Montrer IFNB1 Protéines) mRNA transcription, while GADD34-dependent protein synthesis recovery contributes to the heterogeneous expression of interferon (Montrer IFNA Protéines) observed in dsRNA-activated cells.
Results highlighted the essential roles played by GADD34 and CReP (Montrer PPP1R15B Protéines) 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 (Montrer ZNF384 Protéines) 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 (Montrer INS Protéines) 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 (Montrer TLR4 Protéines) combined with amino acid deprivation through regulation of mTOR (Montrer FRAP1 Protéines) signaling pathway in macrophages.
Loss of GADD34 cause vanishing white matter disease due to translation defects.
Compared with normal controls, the wild type TT and allele T of rs611251 of PPP1R15A showed higher frequency in gastric carcinoma, nasopharyngeal carcinomas and lymphomas.
Inhibition of IRE1 (Montrer ERN1 Protéines) modifies the hypoxic regulation of GADD34 family gene expression in cultured glioma cells.
GADD34 constitutes a mechanistic link between endoplasmic reticulum stress and mTOR (Montrer FRAP1 Protéines) 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 (Montrer ANXA11 Protéines) 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 (Montrer EIF2S1 Protéines) by GADD34 plays an important role in doxorubicin resistance of MCF-7/ADR (Montrer AKR1B1 Protéines) cells.
The reactive oxygen species-generating NADPH oxidase-4 (Nox4 (Montrer NOX4 Protéines)) is induced downstream of ATF4 (Montrer ATF4 Protéines), binds to a PP1 (Montrer PPA1 Protéines)-targeting subunit GADD34 at the endoplasmic reticulum, and inhibits PP1 (Montrer PPA1 Protéines) activity to increase eIF2alpha (Montrer EIF2A Protéines) phosphorylation and ATF4 (Montrer ATF4 Protéines) 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
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