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Pref-1 mRNA is a novel substrate of RNase-L.
RNAse L stimulates fibroblast migration.
Thus, activation of RNase L does not require mouse hepatitis virus virus-induced interferon but rather correlates with adequate levels of basal Oas gene expression, maintained by basal interferon signaling.
Thus, RNA cleavage events catalyzed by RNase L are required for optimal inflammasome activation during viral infections.
cellular functions of RNase L through protein-protein interactions in the spleen for immune response in mammals
Data indicate that deficiency of 2-5A-dependent RNase L (RNase L) in resulted in a significant delay of diabetes onset.
RNase L contributes to innate immunity through regulating macrophage functions.
By targeting the effector enzyme of this antiviral pathway, L* potently inhibits RNase L, underscoring the importance of this enzyme in innate immunity against Theiler's virus.
RNase-L deficiency exacerbates experimental colitis and colitis-associated cancer.
These studies highlight novel roles of RNase L in cigarette smoke plus virus induced inflammation, tissue remodeling, apoptosis, and cytokine elaboration
RNase L activation during mouse hepatitis virus infection is cell type specific and correlates with relatively high levels of expression of oligoadenylate synthetase genes, which are necessary for an effective RNase L antiviral response.
The results suggest that RNase L is not an evolutionarily-conserved host defense mechanism to counteract retroviruses in vivo.
These findings highlight RNase L as an essential regulator of adipogenesis via the regulation of CHOP10 mRNA.
RNase L induces autophagy via c-Jun N-terminal kinase and double-stranded RNA-dependent protein kinase signaling pathways
results indicate a novel function of RNase L as an inducer of autophagy that affects viral yields
Mouse hepatitis virus Ns2 cleaves 2',5'-oligoadenylate, the product of 2',5'-oligoadenylate synthetase, to prevent activation of the cellular endoribonuclease RNase L and consequently block viral RNA degradation.
sunitinib treatments prevent antiviral innate immune responses mediated by RNase L and PKR.
Endoribonuclease L (RNase L) regulates the myogenic and adipogenic potential of myogenic cells
JNK and RNase L function in an integrated signaling pathway during the IFN response that leads to elimination of virus-infected cells through apoptosis
results indicate that the RNase-L-dependent decrease in mtDNA-encoded mRNA transcript levels occurs through a decrease in the half-life of mt-mRNA, and that RNase-L may play a role in the stability of mt-mRNA
Mitochondrial C11orf83 is a potent antiviral protein independent of interferon production; and knockdown of either OAS3 or RNase L impaired the antiviral capability of C11orf83.
Our study suggests that RNASEL:p.Glu265* may be a genetic modifier of risk for early-onset breast cancer predisposition in carriers of high-risk mutations.
Results reported in the present study suggest a sex-specific interaction between miR-146a and RNASEL genes in melanoma skin cancer susceptibility.
These results demonstrate that ablation of RNase L activity promotes survival of ADAR1 deficient cells even in the presence of MDA5 and MAVS, suggesting that the RNase L system is the primary sensor pathway for endogenous dsRNA that leads to cell death.
Mutations in the genes glucokinase regulatory protein (GCKR), RNase L (RNASEL), leukocyte immunoglobulin-like receptor 3 (LILRA3), and dynein axonemal heavy chain 10 (DNAH10) segregated with elevated HDLc levels in families, while no mutations associated with low HDLc.
findings suggest that beside the RLR pathway, RNase L cleavage products can also activate the NLRP3-inflammasome pathway, which requires DHX33 (DExD/H-box helicase) and the mitochondrial adaptor protein MAVS.
This study provides the evidence that germline variations in RNASEL are associated with fatal PCa in men (Gleason score >7 for rs486907 and RNASEL underexpressed [P = 0.007] in patients with PCa).
By sequencing abundant RNA fragments generated by RNase L in cell lines, we identify site-specific cleavage of two groups of noncoding RNAs: Y-RNAs, whose function is poorly understood, and cytosolic tRNAs, which are essential for translation.
RNASEL rs3738579 genotype was significantly related to severe necroinflammatory activity (NIA) grade of chronic hepatitis C patients.
Serum RNase-L levels were inversely associated with metabolic syndrome and age.
We show that mutations in RNase L found in HPC patients may promote prostate cancer by increasing expression of AR-responsive genes and cell motility and identify novel roles of RNase L as a prostate cancer susceptibility gene.
Suggest that naturally occurring mutations in the RNase L gene might promote enhanced prostate cancer cell migration and metastasis.
This review outlines the role of RNase-L in antimicrobial immunity and the cytoskeleton-associated innate response. [review]
Data show that RNA decay by ribonuclease L (RNase L) has an important role in homeostasis and serves as a suppressor of cell adhesion.
Single Nucleotide Polymorphisms in RNASEL involved in the immune response are generally not associated with intraprostatic inflammation in men without a Prostate cancer diagnosis.
OAS3 displayed a higher affinity for dsRNA in intact cells than either OAS1 or OAS2, consistent with its dominant role in RNase L activation.
Tanslation of vaccinia virus A27L and B5R genes is independent of PKR activation, but their expression is dependent on the RNase L activity.
Our results demonstrate a novel role of RNase L generated small RNAs in cross-talk between autophagy and apoptosis that impacts the fate of cells during viral infections and cancer.
Among 794 RNASEL Ssingle nucleotide polymorphism (SNPs) entries 124 SNPs were found nonsynonymous (ns) from which SIFT predicted 13 nsSNPs as nontolerable whereas PolyPhen-2 predicted 28.
Virus infection and RNase L activation disrupt its association with Filamin A and release RNase L to mediate its canonical nuclease-dependent antiviral activities.
A 2.5 A and 3.25 A X-ray crystal and small-angle X-ray scattering structure of RNase L bound to a natural 2-5A activator with and without ADP or the nonhydrolysable ATP mimetic AMP-PNP is functionally characterized.
This gene encodes a component of the interferon-regulated 2-5A system that functions in the antiviral and antiproliferative roles of interferons. Mutations in this gene have been associated with predisposition to prostate cancer and this gene is a candidate for the hereditary prostate cancer 1 (HPC1) allele.
, 2-5A-dependent RNase
, 2-5A-dependent ribonuclease
, RNase L
, ribonuclease 4
, 2',5'-oligoisoadenylate synthetase-dependent
, interferon-induced 2-5A-dependent RNase