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Gene silencing studies showed that the suppression of immunoproteasome induction is essentially dependent on protein kinase (show CDK7 ELISA Kits) R (PKR (show PKLR ELISA Kits)). Indeed, the generation of a strictly immunoproteasome-dependent cytotoxic T lymphocyte epitope was impaired in in vitro processing experiments using isolated 20S proteasomes from HCV-infected cells and was restored by the silencing of PKR (show PKLR ELISA Kits) expression.
data provide the first evidence that KSHV ORF57 plays a role in modulating PKR (show PKLR ELISA Kits)/eIF2alpha (show EIF2A ELISA Kits)/SG axis and enhances virus production during virus lytic infection.
The PKR (show PKLR ELISA Kits) is a key constituent of the metaflammasome and interacts directly with several inflammatory kinases, such as inhibitor kappaB (IkappaB) kinase (show CHUK ELISA Kits) (IKK (show CHUK ELISA Kits)) and c-Jun N-terminal kinase (JNK), insulin receptor substrate 1 (IRS1 (show IRS1 ELISA Kits)), and component of the translational machinery such as eIF2alpha (show EIF2A ELISA Kits).
infection with New World arenaviruses JUNV and MACV, but not OW LASV, activated PKR (show PKLR ELISA Kits), concomitant with elevated phosphorylation of the translation initiation factor alpha subunit (show POLG ELISA Kits) of eukaryotic initiation factor (show EIF4G1 ELISA Kits) 2
The stem-loop of noncoding RNA 886 is structural feature not only critical for inhibiting PKR (show PKLR ELISA Kits) autophosphorylation, but also the phosphorylation of its cellular substrate, EIF-2alpha (show EIF2S1 ELISA Kits).
Protein kinase (show CDK7 ELISA Kits) R (PKR (show PKLR ELISA Kits)) was required for induction of stress granules (SGs (show FBN1 ELISA Kits)) by mumps virus (MuV) infection and regulated type III IFN (IFN-lambda1) mRNA stability.
data establish a model in which the Influenza A virus NS1 (show PTPN11 ELISA Kits) N-terminal domain engages in a binding interaction to inhibit activation of PKR (show PKLR ELISA Kits) and ensure efficient viral propagation and virulence
It was established in this report that interactions between PACT (show RBBP6 ELISA Kits), ADAR1 (show ADAR ELISA Kits) and HIV-1-encoded Tat (show TAT ELISA Kits) protein diminish the activation of PKR (show PKLR ELISA Kits) in response to HIV-1 infection.
In insulitic islets from living patients with recent-onset T1D, most of the overexpressed ISGs, including GBP1 (show GBP1 ELISA Kits), TLR3 (show TLR3 ELISA Kits), OAS1 (show OAS1 ELISA Kits), EIF2AK2, HLA-E (show HLAE ELISA Kits), IFI6 (show IFI6 ELISA Kits), and STAT1 (show STAT1 ELISA Kits), showed higher expression in the islet core compared with the peri (show PLIN1 ELISA Kits)-islet area containing the surrounding immune cells
NF90 (show MMP4 ELISA Kits) exerts its antiviral activity by antagonizing the inhibitory role of NS1 (show PTPN11 ELISA Kits) on PKR (show PKLR ELISA Kits) phosphorylation
PKR activation is an essential part of the molecular switch from adaptation to inflammation in response to hyperosmotic stress.
We therefore concluded that in osteoblasts, P. gingivalis activated PKR, which in turn increased NLRP3 (show NLRP3 ELISA Kits) expression by activating NF-kappaB (show NFKB1 ELISA Kits). Our results suggest that PKR modulates inflammation by regulating the expression of the NLRP3 (show NLRP3 ELISA Kits) inflammasome through the NF-kappaB (show NFKB1 ELISA Kits) pathway in periodontal diseases.
identify iNOS (show NOS2 ELISA Kits)/NO as an integral component of IFN-beta (show IFNB1 ELISA Kits) production in response to dsRNA in hepatocytes in a pathway that involves the coordinated activities of TLR3 (show TLR3 ELISA Kits)/Trif (show RNF138 ELISA Kits) and PKR
The data predicts that PKR diminishes inflammasome activity by controlling protein translation to repress the induction of factors that are critical for the activity of the cryopyrin (show NLRP3 ELISA Kits) inflammasome.
This study provides insight into the molecular pathology of Cornelia de Lange syndrome by establishing a relationship between NIPBL (show NIPBL ELISA Kits) and HDAC8 (show HDAC8 ELISA Kits) mutations and PKR activation.
Deletion of PKR does not affect HFD-induced obesity, hepatic steatosis or glucose metabolism, and only modestly affects adipose tissue inflammation.
results show that ceramide acts at two distinct levels of the insulin (show INS ELISA Kits) signaling pathway (IRS1 (show IRS1 ELISA Kits) and Akt (show AKT1 ELISA Kits)). PKR, which is induced by both inflammation signals and ceramide, could play a major role in the development of insulin (show INS ELISA Kits) resistance in muscle cells.
Data (including data from studies in transgenic/knockout mice) suggest that PACT/RAX (protein activator of protein kinase (show CDK7 ELISA Kits) R) functions as negative regulator of PKR/Eif2ak2 (protein kinase (show CDK7 ELISA Kits) R) in development of postnatal anterior pituitary tissue.
Data indicate increasing expression of PKR during TNF-a (show TNF ELISA Kits)-induced osteoclast formation. Its inhibition prevents TNF-a (show TNF ELISA Kits)-induced bone destruction in vivo and can be then considered as new therapeutic target for bone disease.
The authors show that Murine cytomegalovirus m142 and m143 knockout mutants attain organ titers equivalent to those attained by wild-type virus in Pkr knockout mice.
The protein encoded by this gene is a serine/threonine protein kinase that is activated by autophosphorylation after binding to dsRNA. The activated form of the encoded protein can phosphorylate translation initiation factor EIF2S1, which in turn inhibits protein synthesis. This protein is also activated by manganese ions and heparin. Three transcript variants encoding two different isoforms have been found for this gene.
double-stranded RNA-activated protein kinase
, interferon-induced, double-stranded RNA-activated protein kinase
, p68 kinase
, P1/eIF-2A protein kinase
, interferon-inducible RNA-dependent protein kinase
, IFN-stimulated dsRNA-activated eIF2-alpha kinase 2
, double-stranded RNA activated protein kinase
, eukaryotic translation initiation factor 2-alpha kinase 2
, double stranded RNA activated protein kinase
, eIF-2A protein kinase 2
, interferon-inducible elF2alpha kinase
, protein kinase, interferon-inducible double stranded RNA dependent
, tyrosine-protein kinase EIF2AK2
, IFN- type I-induced and dsRNA-activated kinase
, IFN-induced and double-stranded RNA-activated kinase
, T-cell viral integration site
, dsRNA-activated kinase
, eIF-2 alpha
, eukaryotic translation initiation factor 2 alpha kinase 2
, protein kinase RNA-activated
, protein kinase, interferon inducible double stranded RNA dependent
, serine/threonine-protein kinase TIK
, Protein kinase, interferon-inducible double stranded RNA dependent