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CO-stimulated PERK activation and enhanced the levels of FGF21 via the eIF2alpha-ATF4 signaling pathway. The induction of FGF21 by CO attenuated endoreticulum stress- or diet-induced, obesity-dependent hepatic steatosis.
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Data suggest that endoplasmic reticulum stress-induced CHOP/Ddit3 inhibits expression of Bip/Grp78 and Atf4; ATF4, in turn, plays critical role in CHOP-mediated regulation of B-cell receptor-controlled murine gammaherpesvirus-68 lytic replication. (CHOP/Ddit3 = DNA-damage inducible transcript-3; Bip/Grp78 = chaperone BiP 78 kDa; Atf4 = activating transcription factor-4)
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The results suggest that ATF4 may serve a protective role in the mouse liver.
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Golgi stress response elicited by monensin stimulates CSE by acting via ATF4 with characteristics distinguishable from the endoplasmic reticulum stress response
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established Neuro2a cells with edited GADD34 and ATF4/GADD34 genes and found that ATF4 acts as a proapoptotic factor, but GADD34 depletion did not attenuate the expression of cleaved caspase-3 induced by tunicamycin treatment.
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Atg7 ablation mainly induced the PERK-ATF4-CHOP axis of the endoplasmic reticulum (ER) stress response in growth plate chondrocytes.
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under nutrient-limiting conditions that stimulate ATF4 activity, TRIB3 is implicated in the regulation of metabolic adaptation by restraining the transcription of Fgf21.
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these findings reveal a new crucial combined effect of the silencing of PERK and ATF4 in modulating ER stressmediated apoptosis during chondrocyte differentiation and proliferation.
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Sirt1 reduced endoplasmic reticulum stress and apoptosis of brown adipocytes in vivo/in vitro by inhibiting Smad3/ATF4 signaling pathway.
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These findings indicate that the aggregation of S-opsin induced by exposure to blue -emitting diode light causes endoplasmic reticulum stress, and ATF4 activation in particular.
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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 and the ISR even in the absence of GCN2 or eIF2alpha kinase activity.
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BTG1 has a role in regulating hepatic lipid metabolism and in preventing ATF4 and SCD1 from inducing liver steatosis
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Transcriptional profiling reveals that mouse neuroblastoma sphere-forming cells acquire a metabolic program characterized by transcriptional activation of the cholesterol and serine-glycine synthesis pathways, primarily as a result of increased expression of sterol regulatory element binding factors and Atf4, respectively
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MIF-2/D-DT is an early response cytokine in the I/R injury repair of the proximal tubule, enhancing regeneration through SLPI- and ATF4-dependent mechanisms.
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ATF4 has a role in gene expression during basal conditions, with 385 genes altered by the loss of ATF4 in the absence of apparent stress. Deletion of ATF4 alters genes that are required for the conversion of cholesterol to bile acid (CYP7A1), esterification of cholesterol (SOAT2), and transport from the hepatocyte (ABCA1); when ATF4 loss is coupled with ER stress, results in increase in free cholesterol within hepatocyte
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ATF4 pathway is activated in vivo upon mitochondrial stress.
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Data, including data from studies using cells from knockout mice, suggest that gasotransmitter H(2)S up-regulates eIF2a phosphorylation by inhibiting PPP1CA via persulfidation, which in turn leads to transient suppression of global translation and activation of Atf4 expression. (eIF2a = eukaryotic initiation factor-2alpha; PPP1CA = protein phosphatase 1 catalytic subunit alpha; Atf4 = activating transcription factor 4)
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Results identify the beneficial role of hypothalamic ATF4/ATG5 axis in the regulation of energy expenditure, obesity, and obesity-related metabolic disorders.
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SLC30A10 has a protective role in 1-methyl-4-phenylpyridinium-induced toxicity via PERK-ATF4 pathway.
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ER stress-induced increase in ATF4 and CHOP expression is initiated by an increase in Atf4 and Chop mRNA, which is also dependent upon eIF2alpha phosphorylation.
