|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The UPR signaling pathways initiated by double-stranded RNA-activated protein kinase (PKR) like ER kinase (PERK), inositol requiring enzyme 1 α (IRE1α), and activating transcription factor 6 (ATF6) are vital for tumor growth, aggressiveness, microenvironment remodeling, and resistance to cancer therapeutics.
|
30159133 |
2018 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Growing evidence indicates that PKR and eIF2α play pivotal roles in the stimulation of stress granule formation as well as in the subsequent translation modulation in response to stressful conditions; however, little is known about whether MSI1 is involved in this PKR/eIF2α cancer stem cell-enhancing machinery.
|
29486283 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The UPR signaling pathways initiated by double-stranded RNA-activated protein kinase (PKR) like ER kinase (PERK), inositol requiring enzyme 1 α (IRE1α), and activating transcription factor 6 (ATF6) are vital for tumor growth, aggressiveness, microenvironment remodeling, and resistance to cancer therapeutics.
|
30159133 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Binding of eEF1A2 to the RNA-dependent protein kinase PKR modulates its activity and promotes tumour cell survival.
|
30420615 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Anti-Bv8/PROK2 antibodies or small molecule PKR inhibitors ameliorate pain arising from tissue injury and inhibit angiogenesis and inflammation associated with tumors or some autoimmune disorders.
|
29537336 |
2018 |
|
Adolescent idiopathic scoliosis
|
0.100 |
GeneticVariation
|
disease |
GWASCAT |
The coexistence of copy number variations (CNVs) and single nucleotide polymorphisms (SNPs) at a locus can result in distorted calculations of the significance in associating SNPs to disease.
|
30019117 |
2018 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Growing evidence indicates that PKR and eIF2α play pivotal roles in the stimulation of stress granule formation as well as in the subsequent translation modulation in response to stressful conditions; however, little is known about whether MSI1 is involved in this PKR/eIF2α cancer stem cell-enhancing machinery.
|
29486283 |
2018 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The UPR signaling pathways initiated by double-stranded RNA-activated protein kinase (PKR) like ER kinase (PERK), inositol requiring enzyme 1 α (IRE1α), and activating transcription factor 6 (ATF6) are vital for tumor growth, aggressiveness, microenvironment remodeling, and resistance to cancer therapeutics.
|
30159133 |
2018 |
|
SCOLIOSIS, ISOLATED, SUSCEPTIBILITY TO, 3
|
0.100 |
GeneticVariation
|
disease |
GWASCAT |
The coexistence of copy number variations (CNVs) and single nucleotide polymorphisms (SNPs) at a locus can result in distorted calculations of the significance in associating SNPs to disease.
|
30019117 |
2018 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
This review highlights the major findings linking PKR and abnormal brain metabolism associated with AD lesions.
|
28982375 |
2017 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this study, we examined whether PKR inhibition can rescue synaptic and learning deficits in two different AD mouse models; 5XFAD transgenic and Aβ<sub>1-42</sub>-injected mice.
|
29233183 |
2017 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Kisspeptin was revealed to inhibit the migratory and invasive abilities of highly metastatic breast SK‑BR‑3, prostatic PC‑3 and colorectal adenocarcinoma LoVo human cancer cell lines, whereas its inhibitory effects were abolished following the silencing of EIF2AK2 expression using RNA interference.
|
28944853 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Finally, we discuss the impact that the recent knowledge regarding PKR involvement in metabolism has in our understanding of the complex processes of cancer and metabolism pathologies, highlighting the translational research establishing the clinical and therapeutic potential of this pleiotropic kinase.
|
28724458 |
2017 |
|
Hepatitis C
|
0.100 |
Biomarker
|
disease |
BEFREE |
We propose that modulation of autophosphorylation of PKR by p48 isoform is an important mechanism whereby the HCV virus escapes innate antiviral immune responses by circumventing p42-mediated inhibition of its replication.
|
27770702 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Higher MHC-II expression in tumor cells was associated with the absence of lymphovascular invasion (p = 0.042); larger amounts of TILs (p < 0.001); frequent formations of tertiary lymphoid structures (p < 0.001); higher expression of myxovirus resistance gene A, one of the main mediators of the interferon signaling pathway (p < 0.001); and higher expression of double-stranded RNA-activated protein kinase, which can be induced by interferons (p = 0.008).
|
28817603 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Kisspeptin was revealed to inhibit the migratory and invasive abilities of highly metastatic breast SK‑BR‑3, prostatic PC‑3 and colorectal adenocarcinoma LoVo human cancer cell lines, whereas its inhibitory effects were abolished following the silencing of EIF2AK2 expression using RNA interference.
|
28944853 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Finally, we discuss the impact that the recent knowledge regarding PKR involvement in metabolism has in our understanding of the complex processes of cancer and metabolism pathologies, highlighting the translational research establishing the clinical and therapeutic potential of this pleiotropic kinase.
|
28724458 |
2017 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
nc886 is a recently identified cellular non-coding RNA and its depletion leads to acute cell death via PKR (Protein Kinase RNA-activated) activation. nc886 expression is increased in some malignancies, but silenced in others.
|
27612419 |
2016 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In fact, activation of pathogen sensors induces the expression of CSR32/EGOT RIG-I and the RNA-activated kinase PKR sense HCV RNA, activate NF-κB and upregulate EGOT EGOT is increased in the liver of patients infected with HCV and after infection with influenza or Semliki Forest virus (SFV).
|
27283940 |
2016 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Treatment with IFN-α increases expression of IFN-stimulated genes (ISGs) such as double-stranded RNA-activated protein kinase (PKR) and decreases viral RNA and protein levels in HCV-infected Huh-7.5 human hepatoma cells.
|
27929099 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
However, the precise role of nc886/PKR is controversial: is it a tumor suppressor or an oncogene?
|
27612419 |
2016 |
|
Alzheimer's Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
A genetic alteration in the EIF2AK2 gene has previously been shown to be associated with Alzheimer's disease.
|
25607115 |
2015 |
|
Alzheimer's Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The results propose a new mechanism by which ApoE4 affects brain function and further suggest that inhibition of PKR is a way to restore ATF4 overexpression and memory impairment in early stages of sporadic AD.
|
26400930 |
2015 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Several studies have reported that pre-miR-886 plays a tumor-suppressive role in a wide range of cancer cells through its activity as a cellular protein kinase RNA-activated (PKR) ligand and repressor.
|
26318295 |
2015 |
|
Hepatitis C
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Finally, we show that NS5A from GBV-C but not from GBV-B down-regulates HCV IRES activity in the absence or the presence of PKR over expression.
|
24815730 |
2014 |