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Pref-1 (show DLK1 Proteins) 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 (show IFNA Proteins) but rather correlates with adequate levels of basal Oas (show SMOC1 Proteins) gene expression, maintained by basal interferon (show IFNA Proteins) 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
Results reported in the present study suggest a sex-specific interaction between miR (show MLXIP Proteins)-146a and RNASEL genes in melanoma skin cancer susceptibility.
These results demonstrate that ablation of RNase L activity promotes survival of ADAR1 (show ADAR Proteins) deficient cells even in the presence of MDA5 (show IFIH1 Proteins) and MAVS (show MAVS Proteins), 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 (show DHX58 Proteins) pathway, RNase L cleavage products can also activate the NLRP3 (show NLRP3 Proteins)-inflammasome pathway, which requires DHX33 (show DHX33 Proteins) (DExD/H-box helicase) and the mitochondrial adaptor protein MAVS (show MAVS Proteins).
This study provides the evidence that germline variations in RNASEL are associated with fatal PCa (show FLVCR1 Proteins) in men (Gleason score >7 for rs486907 and RNASEL underexpressed [P = 0.007] in patients with PCa (show FLVCR1 Proteins)).
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.
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 (show TMPRSS5 Proteins)-PNP (show NP Proteins) 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