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1                                              RNase E and RNase G are homologous endonucleases that pl
2                                              RNase E/enolase distribution changes from membrane-assoc
3                                              RNase H enzymes sense the presence of ribonucleotides in
4                                              RNase II, a 3' to 5' processive exoribonuclease, is the
5                                              RNase III enzyme Drosha interacts with DGCR8 to form the
6                                              RNase P is a universal enzyme that removes 5' leader seq
7                                              RNase P is an essential tRNA-processing enzyme in all do
8                                              RNase P is primarily responsible for the 5 maturation of
9                                              RNase P represents a unique example of an enzyme that ca
10 ering hyaluronic acid (HA)-modified RNase A (RNase A-HA) in nanocomplex with cationic lipid-like mole
11 lls (LSEC) which line the sinusoids activate RNase L in response to NS2(H126R) These data suggest tha
12 2',5'-oligoadenylates (2-5A), which activate RNase L.
13          Infection with ns2(H126R) activated RNase L in Ifih1(-/-) BMM to a similar extent as in wild
14  in the formation of an enzymatically active RNase-S protein.
15 by residual platelets in plasma or by adding RNase inhibitors to serum to reduce degradation.
16         The unique presence of an additional RNase HII domain raises an important question regarding
17                                Additionally, RNase H2 can remove single ribonucleotides misincorporat
18 nto low-molecular-weight (LMW) species after RNase A treatment.
19                 CsrA stabilizes CsrB against RNase E cleavage by binding to two canonical sites adjac
20              The antimicrobial peptide (AMP) RNase 7 is constitutively expressed in the epidermis of
21 n with an HIV-1-derived vector containing an RNase H-deficient reverse transcriptase (RT).
22                For this study, we created an RNase III null mutant of Streptococcus pyogenes and its
23 n analysis of R-loops in vivo, we develop an RNase-H-based approach; this reveals predominant R-loop
24 he domain responsible is reported to have an RNase H-like fold.
25 A (like RnhC characterized previously) is an RNase H1-type magnesium-dependent endonuclease with stri
26                                 DICER1 is an RNase III endoribonuclease central to miRNA biogenesis,
27    We created a knock-in mouse model with an RNase H2 AGS mutation in a highly conserved residue of t
28 ) possesses both DNA polymerase activity and RNase H activity that act in concert to convert single-s
29 s, electrophoretic mobility shift assay, and RNase A footprinting.
30 ligomerization, stress granule assembly, and RNase activity intrinsic to G3BP1.
31 actor SAMHD1, a dNTP hydrolase (dNTPase) and RNase, on HBV replication.
32                                  RNase E and RNase G are homologous endonucleases that play important
33       In the absence of RNase E, RNase G and RNase Z are weakly able to process the proK and proM tra
34 winged-helix (WH) motif and the helicase and RNase D C-terminal (HRDC) domain play important but dist
35          Single nucleotide incorporation and RNase H cleavage were examined using presteady-state kin
36                       Microarray mapping and RNase H cleavage identified accessible sites for oligonu
37 endent regulation, because both rbn mRNA and RNase BN protein are at their highest levels in early ex
38 ytes express undetectable levels of OASs and RNase L, which likely explains the lack of RNase L activ
39  proK and proM transcripts, while PNPase and RNase P are utilized in the processing of proL The termi
40  for a strong interaction between PNPase and RNase Y.
41 urifies with RNA as an inactive protein, and RNase A treatment enables strong DNA deaminase activity.
42 , thereby attaining what has eluded RNAi and RNase H experiments: elimination of MRP RNA in the major
43 oncoding RNAs that are resistant to RNAi and RNase H-based degradation.
44                    We conclude that Top1 and RNase H1 are partially functionally redundant in mammali
45 ported that the absence of Topoisomerase and RNase H activity in Escherichia coli or Saccharomyces ce
46  Specifically designed BC200 truncations and RNase footprinting assays demonstrate that RHAU binds to
47  structurally distinct RNPs, telomerase, and RNases P/MRP from unrelated progenitor RNAs.
48 s, encode 2',5'-PDEs capable of antagonizing RNase L.
49 PDE) that cleaves 2-5A, thereby antagonizing RNase L activation.
50                          Homologs of Aquifex RNase P (HARP) were identified in many Archaea and some
51                                     Archaeal RNase P is a ribonucleoprotein made up of one catalytic
52 e number and location of K-turns in archaeal RNase P RNAs (RPRs) are unclear.
53 ex self-amplifying RNA vaccines (RepRNA) are RNase-sensitivity and inefficient translation in dendrit
54 he Ribonuclease A superfamily (also known as RNase 5) are known to be associated with Amyotrophic Lat
55 ues consistently inhibited HIV RT-associated RNase H in the low micromolar range in the absence of si
56 on of phage transcripts by CRISPR-associated RNases ensures robust immunity in situations that lead t
57 However, the strict specificity of bacterial RNase HII for RNA-DNA junctions indicates that R-lesions
58 uctural and biophysical studies of bacterial RNase P propose direct coordination of metal ions by the
59 y common substrate between the two bacterial RNase H enzymes.
60 a and most Bacteria also encode an RNA-based RNase P; activity of both RNase P forms from the same ba
61 n to access the evolutionary history between RNases H from mesophilic and thermophilic bacteria.
62 eases (RNase T, RNase PH, RNase D, RNase BN, RNase II and polynucleotide phosphorylase [PNPase]) to g
63 ncode an RNA-based RNase P; activity of both RNase P forms from the same bacterium or archaeon could
64                               We used bovine RNase B, human transferrin, and bovine fetuin as models
65 ished by uridine-->adenosine mutation and by RNase pretreatment.
66 nockdown and hepatotoxicity is attenuated by RNase H1 knockdown, and that this effect can be generali
67 SpSpRp, that promotes target RNA cleavage by RNase H1 in vitro and provides a more durable response i
68 ate triggers 5' end-dependent degradation by RNase E.
69                         dsRNA elimination by RNase III treatment prior to DRIPc-seq allowed the genom
70 nstraints are overcome when fragmentation by RNase I is efficient and when a broad cDNA size range is
71             However, reducing IgV R-loops by RNase HI overexpression in wild-type cells does not affe
72 cells - effects that can be recapitulated by RNase treatment or RNA polymerase inhibition - and cause
73 e replicative polymerases are not removed by RNase H2.
74  replication defects that were suppressed by RNase H1 overexpression.
75                   The well-studied catalytic RNase P RNA uses a specificity module to recognize the p
76                      One of the two cellular RNases H may assist in this process.
77                             Escherichia coli RNase E is an essential enzyme that forms multicomponent
78  cleaves target RNA, and exhibits collateral RNase activity.
79  complexes consist of four major components: RNase E, PNPase, RhlB RNA helicase, and enolase.
80                                 In contrast, RNase H1 acts to prevent LOH within a small region of ch
81 ular framework for sRNA turnover by the CsrD-RNase E pathway.
82 5' exonucleases (RNase T, RNase PH, RNase D, RNase BN, RNase II and polynucleotide phosphorylase [PNP
83 nctional group modifications of U51 decrease RNase P-catalyzed phosphodiester bond cleavage 16- to 23
84 that strains containing a helicase-deficient RNase R due to mutations in its ATP-binding Walker motif
85 regulating RNase E subcellular distribution, RNase E enzymatic activity, and the stability of the sRN
86                   In the absence of RNase E, RNase G and RNase Z are weakly able to process the proK
87 deliver payloads of cytotoxic protein (i.e., RNase A) to the cells without a loss in its biological f
88                        Escherichia coli (Ec) RNase III catalytic activity is known to increase during
89                               Loss of either RNase H1 or Top1 caused R-loop accumulation, and the acc
90 tive IRE1alpha, inhibits both its kinase end RNase activities, and protects cells from apoptosis both
91 mals, consists of 12 Mg(2+)-dependent 3'-end RNases with substrate specificity that is mostly unknown
92 A and non-coding RNA) targeted by endogenous RNase H1.
93 for a functional NS2 protein, the endogenous RNase L antagonist.
94 ant role of the low-specificity endonuclease RNase E in shaping the transcriptome of a bacterial path
95 und the major decay-initiating endonuclease, RNase Y, and there is ample evidence for a strong intera
96 e products of the essential endoribonuclease RNase E in Salmonella enterica.
97                         The endoribonuclease RNase III cleaves double stranded RNAs, which can be for
98 , inhibits both kinase and endoribonuclease (RNase) activities of the stress sensor, and protects cel
99  enzyme 1alpha (IRE1alpha) endoribonuclease (RNase), a key mediator of the UPR, cleaves Xbp1 mRNA to
100     Many sRNAs recruit the endoribonuclease, RNase E, to facilitate processing of mRNAs.
101                             When the enolase-RNase E/degradosome interaction is disrupted, the anaero
102 eins, but are typified by mutually exclusive RNase III endonucleases with distinct cleavage specifici
103 volve any of the six 3' --> 5' exonucleases (RNase T, RNase PH, RNase D, RNase BN, RNase II and polyn
104 rated a transgenic mouse that over-expressed RNase H1, an enzyme that cleaves the RNA of RNA/DNA hybr
105 a key recognition determinant that may favor RNase E catalysis.
106                                     Finally, RNase H-based fragmentation analysis and 3-sequence anal
107  Asp-10, Arg-13, and Thr-36 are critical for RNase activity and likely catalyze the proton-relay mech
108 s cerevisiae strains that were defective for RNase H1, H2, or both.
109 cleic acid conformation that is required for RNase H cleavage.
110                             Thus, a role for RNase MRP in human pre-rRNA processing is established.
111 s (ASOs) designed to serve as substrates for RNase H1 were inactive in the hepatocytes from the RNase
112 tate upon association with S-protein to form RNase-S and is an excellent model system to study couple
113         Mycobacterium smegmatis encodes four RNase H enzymes: RnhA, RnhB, RnhC and RnhD.
114 pitulating this process in vitro, Hfq guides RNase E cleavage of a representative small-RNA precursor
115 of ancestral proteins of the ribonuclease H (RNase H) family using ancestral sequence reconstruction
116 ranscriptase (RT) associated ribonuclease H (RNase H) remains an unvalidated antiviral target.
117 ranscriptase (RT)-associated ribonuclease H (RNase H) remains the only virally encoded enzymatic func
118 de-modified RNA-DNA with Bacillus halodurans RNase H1.
119                              The protein has RNase P activity in vitro and rescued the growth of Esch
120  favorable binding to the active site of HIV RNase H, providing a basis for the design of more potent
121 ossible challenges may be that targeting HIV RNase H is confronted with a steep substrate barrier.
122 o develop a detailed model that explains how RNase R digests structured RNA and how this differs from
123 inal nucleotides for such cleavage; however, RNase G is impeded more than RNase E when fewer than fou
124                 The card also includes human RNase P as a nucleic acid extraction control and an inte
125  EGSs that are more robust in inducing human RNase P to cleave their targeted mRNAs.
126                      Here we show that human RNase H2 is unable to process an abasic rNMP (rAP site)
127        The salient conclusions are that: (i) RNase H1 activity is essential for mycobacterial growth
128 -activity relationship (SAR) for identifying RNase H inhibitors with antiviral activity.
129                 Our study also shows that if RNase does not efficiently cut within the binding sites,
130                         These data implicate RNase III recognition of viral RNA as an antiviral defen
131 C5 position that led to drastically improved RNase H inhibition and significant antiviral activity.
132 explaining why R-tracts do not accumulate in RNase H-deficient cells, while double-strand breaks do.
133 e that one residue, Lys501, is acetylated in RNase II.
134 p1 is covalently linked to the end of DNA in RNase H2-deficient yeast cells, supporting this model.
135 subtilisresidues predicted to be involved in RNase Y binding showed a loss of PNPase-RNase Y interact
136 y stall, so the failure of R-loop removal in RNase H-deficient bacteria becomes lethal.
137  repair (NER) as a backup pathway for RER in RNase HII-deficient cells and the known mutagenic profil
138 se 7 and a recombinant ribonuclease-inactive RNase 7 mutant.
139 al nucleotide-processing proteins, including RNase H2.
140                                      Indeed, RNase H-deficient cells have increased chromosomal rearr
141 bone marrow-derived macrophages, and inhibit RNase L-mediated rRNA degradation in these cells.
142 type that potently and selectively inhibited RNase H without inhibiting HIV in cell culture.
143 e SOX has been shown to possess an intrinsic RNase activity and a potential consensus sequence for en
144 of highly pure circRNA populations involving RNase R treatment followed by Polyadenylation and poly(A
145 lix transcription factor ID1 as an IRE1alpha RNase target.
146                           In fact, IRE1alpha RNase processes a subset of microRNAs (miRs), including
147 nce through hyperactivation of the IRE1alpha RNase.
148 via cleavage of precursor miRNAs through its RNase domain.
149 s with the C-terminal domain of eRF1 via its RNase H domain to sterically occlude the binding of pept
150  endonuclease activity is inhibited by known RNase H inhibitors.
151  mutational profiling of B. subtilis lacking RNase HII, the enzyme that incises at single rNMP residu
152               Here, we report that mammalian RNase H1 enriches in nucleoli and co-localizes with R-lo
153 ty to DNA antisense oligonucleotide-mediated RNase H digestion.
154 haracterized to date adopt similar microbial RNase architectures despite possessing low sequence iden
155 bserved in cells deficient for mitochondrial RNase P.
156 f protein folding and unfolding; both modern RNases H evolved to be more kinetically stable than thei
157 his delivering hyaluronic acid (HA)-modified RNase A (RNase A-HA) in nanocomplex with cationic lipid-
158           Promotion of read-through by MoMLV RNase H prevents nonsense-mediated mRNA decay (NMD) of m
159 nary DRIPc-seq experiments identified mostly RNase H-resistant but exosome-sensitive RNAs that mapped
160 to the division of labor among mycobacterial RNases H by deleting the rnhA, rnhB, rnhC and rnhD genes
161 olarized TH2 cells using skin-derived native RNase 7 and a recombinant ribonuclease-inactive RNase 7
162 n which it can provide organellar or nuclear RNase P activities.
163          The oligoadenylate synthetase (OAS)-RNase L pathway is a potent antiviral activity.
164 s antagonize the oligoadenylate-RNase L (OAS-RNase L) pathway.
165 nown to encode antagonists of the potent OAS-RNase L antiviral pathway, highlighting its importance i
166 ch the wild-type virus blocks the potent OAS-RNase L antiviral pathway.
167 terases (2',5'-PDEs) that antagonize the OAS-RNase L pathway, and we report here that these proteins
168 ient nsp15, activated MDA5, PKR, and the OAS/RNase L system, resulting in an early, robust induction
169      Our result demonstrate that ablation of RNase L activity promotes survival of ADAR1 deficient ce
170                            In the absence of RNase E, RNase G and RNase Z are weakly able to process
171  negatively correlated with the abundance of RNase H1.
172                            The activation of RNase L by NS2(H126R) is cell type dependent and correla
173                                Activation of RNase L during murine coronavirus (mouse hepatitis virus
174 pare the nuclease and helicase activities of RNase R.
175 gests that the genome-protection activity of RNase H1 is regulated at a step after hybrid recognition
176 and thus decreases the catalytic activity of RNase II.
177 mpairs the 5'-3' exoribonuclease activity of RNase J1, increasing the half-life of the primary transc
178 9 modestly decrease the cleavage activity of RNase P, suggesting outer-sphere coordination of O6 on G
179 e motion is achieved through the addition of RNase H, which selectively hydrolyses the hybridized RNA
180  been combined with a structural analysis of RNase R, based on its homology to RNase II, whose struct
181                  The chemical conjugation of RNase A with HA both increased the supramolecular intera
182                    CPV resolvase is dimer of RNase H superfamily domains related to Escherichia coli
183 ficant differences between the disruption of RNase Hs and Top1 in regards to the orientation-specific
184            We found that the distribution of RNase H1 and Top1 along rDNA coincided at sites where R-
185 ITM1 and IFITM2 and suppressed expression of RNase L and SAMHD1.
186 ted frequency of Rad52 foci, inactivation of RNase H2 and RAD52 led to synthetic lethality, and combi
187 d RNase L, which likely explains the lack of RNase L activation during NS2(H126R) infection.
188 y be explained by the undetectable levels of RNase L as well as by the OASs expressed in hepatocytes.
189 to synthetic lethality, and combined loss of RNase H2 and RAD51 induced slow growth and replication s
190 vels were altered by in vivo manipulation of RNase H levels did not form detectable R-loops, suggesti
191                              Co-migration of RNase H1 and R-loops from nucleoli to perinucleolar ring
192 significantly reduced with overexpression of RNase H1.
193 ranscription is performed in the presence of RNase H, which specifically digests the RNA strands with
194                       Limited proteolysis of RNase-A yields a short N-terminal S-peptide segment and
195                          This restriction of RNase H1 activity to a subset of hybrids is not the resu
196 ce, the steady-state level of target RNAs of RNase II may be altered in the cells.
197 r to a protein-binding domain in the RNAs of RNase P/MRP.
198  that dictate the potency and selectivity of RNase H inhibition as well as the observed antiviral act
199  responsible for the cleavage specificity of RNase E at the 3' terminus.
200 trans-acting sRNAs that can be substrates of RNase III.
201 nt evidence for cytoplasmic translocation of RNase III nucleases in response to virus in diverse euka
202 ed coronavirus antagonize the oligoadenylate-RNase L (OAS-RNase L) pathway.
203 tter form of the enzyme, called protein-only RNase P (PRORP), is widespread in eukaryotes in which it
204 NA complex that illustrates how protein-only RNase P enzymes specifically bind tRNA and highlights th
205 e identified an unknown type of protein-only RNase P in the hyperthermophilic bacterium Aquifex aeoli
206 adopts the same fold as angiogenin and other RNase A paralogs, but the toxin does not share sequence
207 NA and recruit intracellular ribonuclease P (RNase P), a tRNA processing enzyme, to degrade target mR
208  of conserved nucleobases in ribonuclease P (RNase P).
209 ulatory effects of the antimicrobial peptide RNase 7 on activated T cells.
210 x 3' --> 5' exonucleases (RNase T, RNase PH, RNase D, RNase BN, RNase II and polynucleotide phosphory
211 d in RNase Y binding showed a loss of PNPase-RNase Y interaction.
212                       The role of the PNPase-RNase Y interaction in the exonucleolytic function of PN
213 structural homology, CdiA-CTYkris has potent RNase activity in vitro and in vivo.
214 larly, the recently discovered proteinaceous RNase P (PRORP) possesses two domains - pentatricopeptid
215 ition by Prp17, Cef1 and the reoriented Prp8 RNase H-like domain.
216 ote exon ligation, bind together to the Prp8 RNase H-like domain.
217                                      Rather, RNase E is primarily responsible for the endonucleolytic
218 nts with a ribonuclease-inactive recombinant RNase 7 mutant showed that RNase 7 ribonuclease activity
219 ently stabilized nucleolar R-loops recruited RNase H1 to the nucleoli.
220 rm in response to anaerobiosis by regulating RNase E subcellular distribution, RNase E enzymatic acti
221  Here we demonstrate that Drosha and related RNase III ribonucleases from all three domains of life a
222 small RNA GlmZ to the essential ribonuclease RNase E for inactivation.
223 he kinase activity of PERK and ribonuclease (RNase) of IRE1alpha mediated the upregulation of hexokin
224                          Human ribonuclease (RNase) H2 is the principal enzyme able to cleave rNMPs i
225 Angiogenin (ANG) is a secreted ribonuclease (RNase) with cell-type- and context-specific roles in gro
226 plex and larger endogenous ribonucleoprotein RNase P.
227          Mutations in the long noncoding RNA RNase component of the mitochondrial RNA processing endo
228  Human calmodulin and bovine ribonuclease S (RNase S) were screened against the library.
229 e implicated in both S-RNase-dependent and S-RNase-independent pollen rejection.
230   Thus, HT proteins are implicated in both S-RNase-dependent and S-RNase-independent pollen rejection
231 anum arcanum LA2157, which lack functional S-RNase expression.
232                                   However, S-RNase-independent IRBs also clearly contribute to reject
233 RNAi to test whether they also function in S-RNase-independent pollen rejection.
234                            We investigated S-RNase-independent rejection of Solanum lycopersicum poll
235 n range margin were accompanied by loss of S-RNase, smaller flowers, and weakened (or absent) intersp
236  S-specific interaction between the pistil S-RNase and the pollen S-Locus F-box protein controls self
237        For example, the pistil SI proteins S-RNase and HT protein function in a pistil-side IRB that
238 known to function only in conjunction with S-RNase, and then used RNAi to test whether they also func
239  a novel mechanism by which a niche-secreted RNase, angiogenin (ANG), distinctively alters the functi
240 ously connected to HSPC biology-the secreted RNase angiogenin, the cytokine IL18, and the adhesion mo
241 ypes carefully designed to achieve selective RNase H inhibition.
242 tary elements that rely on the PPT sequence: RNase H sequence preference and incompatibility of the p
243        Our findings highlight RnhC, the sole RNase H1 in pathogenic mycobacteria, as a candidate drug
244  interference by functioning as a standalone RNase that degrades invader RNA transcripts, but the mec
245  of the six 3' --> 5' exonucleases (RNase T, RNase PH, RNase D, RNase BN, RNase II and polynucleotide
246 n occur as a result of unintended off-target RNase H1 dependent RNA degradation.
247 avage; however, RNase G is impeded more than RNase E when fewer than four unpaired nucleotides are pr
248 nockout mice and in vivo, demonstrating that RNase H1 is necessary for the activity of DNA-like ASOs.
249                       Our data indicate that RNase 7 has immunomodulatory functions on TH2 cells and
250                   Therefore, we propose that RNase H-deficient mutants convert some R-loops into R-tr
251                           Here, we show that RNase BN itself is subject to growth phase-dependent reg
252                                 We show that RNase H2-deficient yeast cells displayed elevated freque
253 ctive recombinant RNase 7 mutant showed that RNase 7 ribonuclease activity is dispensable for the obs
254              These observations suggest that RNase A-like toxins are commonly deployed in inter-bacte
255                                          The RNase H structural fold defines a large family of nuclei
256                                          The RNase P-mediated endonucleolytic cleavage plays a crucia
257 lls in the adipose tissue is mediated by the RNase activity of omega1; however, the ability of omega1
258 gions whose expression was influenced by the RNase III gene deletion.
259 iated expression of IRE1alpha but not by the RNase-inactive IRE1alpha or the activated X-box binding
260  by Microprocessor, a complex containing the RNase Drosha and its partner protein, DGCR8.
261                  I have closely examined the RNase H domain of Prp8 in each of the structures.
262 H1 were inactive in the hepatocytes from the RNase H1 knockout mice and in vivo, demonstrating that R
263 be provided by either RnhC or RnhA; (ii) the RNase H2 enzymes RnhB and RnhD are dispensable for growt
264          However, the role of enolase in the RNase E/degradosome is not understood.
265 e, we report that presence of enolase in the RNase E/degradosome under anaerobic conditions regulates
266                                       In the RNase-S complex, the N-terminal helix of S-peptide unfol
267 tic site and either decrease or increase the RNase activity affect neuronal survival.
268                           Interestingly, the RNase H domain has different and unexpected roles in eac
269 associates with two RNA binding sites of the RNase E component of the Pseudomonas aeruginosa RNA degr
270 tic metals differs from other members of the RNase H family.
271 it is most similar to the RuvC family of the RNase H-like endonucleases.
272 s of the RNASEL gene or by expression of the RNase L antagonist, murine coronavirus NS2 accessory pro
273 de analysis indicates a decomposition of the RNase tertiary structure into spatially distributed yet
274  non-vertebrate protein found to possess the RNase A superfamily fold, and homologs of this toxin are
275 icinal chemistry data also revealed that the RNase H biochemical inhibition largely correlated the an
276 esence of MDA5 and MAVS, suggesting that the RNase L system is the primary sensor pathway for endogen
277 MCPIP1 promotes Gata3 mRNA decay through the RNase domain.
278 r anaerobic conditions, enolase bound to the RNase E/degradosome stabilizes the small RNA (sRNA) DicF
279 inhibit miR-21 maturation, linking it to the RNase inhibitor 1 forms the bifunctional conjugate 7A, w
280     To better understand the dynamics of the RNases-S complex and its isolated partners, comparative
281            The activity of the 4-thiouridine RNase P is partially rescued by addition of Cd(II) or Mn
282 ion by site-specific cleavage of RNA through RNase H1.
283 psoriasis (PSO) might be directly exposed to RNase 7.
284 nalysis of RNase R, based on its homology to RNase II, whose structure has been determined, to develo
285 asal IFN signaling, and virus-induced IFN to RNase L activation.
286 fected DBR1 knockdown cells was resistant to RNase R that degrades linear RNAs but not RNAs in circul
287 unced downregulation of IL-13 in response to RNase 7 compared to healthy control.
288 of genuine R-loops that responded in vivo to RNase H levels and displayed classical features associat
289 AB mutant Escherichia coli, deficient in two RNase H enzymes that remove both R-loops and incorporate
290                                      The two RNase activities of C2c2 enable multiplexed processing a
291  show that bacterial C2c2 possesses a unique RNase activity responsible for CRISPR RNA maturation tha
292                                   Here using RNase T and CRN-4 as the model systems, we identify pote
293 an inhibitor of human immunodeficiency virus RNase H, inhibited pUL89 endonuclease activity at low-mi
294                 Biogenesis of CoV svRNAs was RNase III, cell type, and host species independent, but
295  for bacterial regulatory small RNAs whereby RNase E acts together with the RNA chaperone Hfq to libe
296                                      Whether RNase H2 may process abasic or oxidized rNMPs incorporat
297 aired sRNA-mRNA duplexes in association with RNase E, allowing proximity-dependent ligation and seque
298 tivated human CD4+T cells and TH2 cells with RNase 7 selectively reduced the expression of TH2 cytoki
299  diminished upon cultivation of T cells with RNase 7.
300 lated human CD3+T cells were stimulated with RNase 7 and screened for possible effects by mRNA microa
301                    Subsequent treatment with RNase H releases RNA-templated ligation products into so

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