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Leishmania infection results in phosphorylation and activation of host PERK enzyme and increased transcription of genes of inhibitor of apoptosis gene family (cIAP) mRNA.
These results suggest that the translational control mediated by PERK is a critical determinant of extracellular matrix secretion in chondrocytes.
PERK regulates oligodendrocyte survival during differentiation.
Data suggest the activation of PERK is part of a protective response to mutant rhodopsin that ultimately limits photoreceptor cell death.
Atg7 ablation mainly induced the PERK-ATF4-CHOP axis of the endoplasmic reticulum (ER) stress response in growth plate chondrocytes.
heme-regulated inhibitor (HRI), protein kinase R (PKR), PKR-like endoplasmic reticulum kinase, (PERK) and general control non-depressible 2 (GCN2) are sufficient for the integrated stress response; there are no additional eIF2alpha kinases in vertebrates
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.
Activation of the ER stress execution proteins, PERK and CHOP10, 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 in tumorigenic but not nontumorigenic cells
In response to endoplasmic reticulum stress, activation of PERK coordinates the integrated stress response by phosphorylating eIF2alpha, which is then quickly dephosphorylated by the GADD34 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+) 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.
Free CNPY2 then engages protein kinase R-like endoplasmic reticulum kinase (PERK) to induce expression of the transcription factor C/EBP homologous protein (CHOP), thereby initiating the unfolded protein response.
Therefore, our study suggests that CREB and PSD95 are novel substrates of PERK, so inhibition of PERK phosphorylation using GSK2656157 would be beneficial against memory impairment after TBI.
regulates both Ca2+ -dependent working memory and protein synthesis-dependent memory flexibility
SLC30A10 has a protective role in 1-methyl-4-phenylpyridinium-induced toxicity via PERK-ATF4 pathway.
In many endoplasmic reticulum (ER) stress-related disorders, activation of the unfolded protein sensor protein kinase RNA-like ER kinase (PERK) kinase is beneficial. Nonetheless, in Charcot-Marie-Tooth 1B neuropathy mice, we show that activation of PERK in Schwann cells, but not in neurons, is detrimental for myelination. PERK may interfere with myelination, independent of its role in ER stress.
ER-stressed astrocytes can drive an inflammatory M1-like phenotype in microglia, and this can be attenuated with inhibition of PERK. Importantly, targeting PERK neither disrupted normal cytokine signaling in astrocytes or microglia nor impaired macrophage phagocytosis or T cell polarization.
phosphorylated PERK and ATF4 would be upregulated in Orexin neurons in Sudden Infant Death Syndrome (SIDS) compared to non-SIDS.
In this paper, we evaluate the clinical features of the patients having W522X mutation and we compare this group with other patients reported to date. Except the characteristic features as diabetes mellitus and epiphyseal dysplasia, all the WRS patients, including patients with W522X mutation, show extensive phenotypic variability that correlates poorly to genotype.
PERK is a master-regulator dictating pancreatic beta cell homoeostasis in development and in diabetes. (Review)
Three branches of the Unfolded Protein Response (UPR) have been described, including the activation of the inositol-requiring enzyme 1 (IRE1), the pancreatic ER kinase (PKR)-like ER kinase (PERK), and the activating transcription factor 6 (ATF6).
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/MRP1 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 triggered EPC apoptosis in a manner of RAGE-mediated activation of the PERK/eIF2alpha 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 in the activation of unfolded protein response effector molecules via PERK and CHOP is reported.
High PERK expression is associated with gastrointestinal neuroendocrine tumors.
The PERK-eIF2alpha-ATF4-CHOP signaling pathway has a critical role in tumor progression during endoplasmic reticulum stress. (Review)
Results unveil a new aspect of PERK function and previously unknown roles for Claspin and Chk1 as negative regulators of DNA replication in the absence of genotoxic stress.
These data indicate that PERK regulates radioresistance in oropharyngeal carcinoma through NF-kB activation-mediated phosphorylation of eIF2alpha
The actin regulator FLNA interacts with the endoplasmic reticulum stress kinase PERK and this interaction is required for the efficient formation of ER-plasma membrane contact sites.
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