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Atg7 (显示 ATG7 蛋白) ablation mainly induced the PERK-ATF4 (显示 ATF4 蛋白)-CHOP (显示 DDIT3 蛋白) axis of the endoplasmic reticulum (ER) stress response in growth plate chondrocytes.
heme-regulated inhibitor (HRI (显示 EIF2AK1 蛋白)), protein kinase (显示 CDK7 蛋白) R (PKR (显示 EIF2AK2 蛋白)), PKR (显示 EIF2AK2 蛋白)-like endoplasmic reticulum kinase, (PERK) and general control non-depressible 2 (GCN2 (显示 EIF2AK4 蛋白)) are sufficient for the integrated stress response; there are no additional eIF2alpha (显示 EIF2A 蛋白) kinases in vertebrates
these findings reveal a new crucial combined effect of the silencing of PERK and ATF4 (显示 ATF4 蛋白) in modulating ER stressmediated apoptosis during chondrocyte differentiation and proliferation.
Activation of the ER stress execution proteins, PERK and CHOP10 (显示 DDIT3 蛋白), was evaluated to determine whether this process was involved in 15d-PMJ2 cell death. 15d-PMJ2 increased the phosphorylation of PERK and expression of CHOP10 (显示 DDIT3 蛋白) in tumorigenic but not nontumorigenic cells
In response to endoplasmic reticulum stress, activation of PERK coordinates the integrated stress response by phosphorylating eIF2alpha (显示 EIF2A 蛋白), which is then quickly dephosphorylated by the GADD34 (显示 PPP1R15A 蛋白) complex. Data imply dual role of the ISR in promoting and inhibiting medulloblastoma tumorigenesis.
These findings identify DLK as a central regulator of not only JNK but also PERK stress signaling in neurons, with both pathways contributing to neurodegeneration.
PERK has a role in mediating the internal ribosome entry site-dependent translational activation of mRNAs encoding angiogenic growth factors after ischemic stress
NDRG2 is a novel ERS-responsive protein and acts as PERK co-factor to facilitate PERK branch, thereby contributing to ERS-induced apoptosis.
the impaired working memory in forebrain-specific Perk knockout mice may stem from altered Gq protein-coupled intracellular Ca(2 (显示 CA2 蛋白)+) dynamics in cortical pyramidal neurons.
Overall, these data demonstrate that hypoxia can suppress adiponectin expression and activate the PERK and IRE1 signaling pathways in differentiated adipocytes, and this two pathways are involved in the suppression of adiponectin expression induced by hypoxia.
Three branches of the Unfolded Protein Response (UPR) have been described, including the activation of the inositol-requiring enzyme 1 (IRE1 (显示 ERN1 蛋白)), the pancreatic ER kinase (PKR (显示 PKLR 蛋白))-like ER kinase (PERK), and the activating transcription factor 6 (ATF6 (显示 ATF6 蛋白)).
Our work demonstrates for the first time that the adaptation to endoplasmic reticulum(ER) stress in cancer cells produces a MDR phenotype. The PERK/Nrf2 (显示 GABPA 蛋白)/MRP1 (显示 MDM4 蛋白) axis is responsible for the resistance to ER stress and chemotherapy, and may represent a good therapeutic target in aggressive and resistant tumors.
miR-204 Targets PERK and Regulates UPR Signaling and beta-Cell Apoptosis
novel findings suggest that HMGB1 (显示 HMGB1 蛋白) triggered EPC (显示 TCF21 蛋白) apoptosis in a manner of RAGE (显示 AGER 蛋白)-mediated activation of the PERK/eIF2alpha (显示 EIF2A 蛋白) pathway.
The present study is the first to uncover a key prosurvival modulator, Yip1A, which coordinates IRE1 signaling with PERK signaling to support the survival of HeLa and CaSki cervical cancer cells.
To illustrate the mechanism by which the PERK luminal domain interacts with misfolded proteins, the crystal structure of the human PERK luminal domain was determined to 3.2 A resolution. Two dimers of the PERK luminal domain constitute a tetramer in the asymmetric unit.
These results indicated that dual targeting of PI3K and PERK pathways might improve clinical prognosis and enhance the treatment of ESCC patients.
The role of neutrophil elastase (显示 ELANE 蛋白) in the activation of unfolded protein response effector molecules via PERK and CHOP (显示 DDIT3 蛋白) is reported.
The protein encoded by this gene phosphorylates the alpha subunit of eukaryotic translation-initiation factor 2 (EIF2), leading to its inactivation, and thus to a rapid reduction of translational initiation and repression of global protein synthesis. It is a type I membrane protein located in the endoplasmic reticulum (ER), where it is induced by ER stress caused by malfolded proteins. Mutations in this gene are associated with Wolcott-Rallison syndrome.
eukaryotic translation initiation factor 2-alpha kinase 3
, eukaryotic translation initiation factor 2-alpha kinase 3-like
, PRKR-like endoplasmic reticulum kinase
, pancreatic eIF2-alpha kinase
, eukaryotic translation initiation factor 2 alpha kinase 3
, pancreatic EIF2-alpha kinase