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1 dent on host cell Argonaute 2 (AGO2) but not Dicer.
2 zed mechanism by which hypoxia downregulates Dicer.
3 e mosquito Aedes aegypti by interfering with Dicer.
4 r precursors by the ribonucleases Drosha and Dicer.
5  manner independent of its interactions with dicer.
6 -stranded RNA substrates by the endonuclease Dicer.
7 ocessed by two RNase III enzymes, Drosha and Dicer.
8  or GM-CSF strongly up-regulated full-length Dicer.
9 ery of helicase-dependent functions in other Dicers.
10 ORgammat chimera was cleaved and released by Dicers.
11 gest that metamorphosis impairment caused by Dicer-1 and miRNA depletion is due to a deregulation of
12 sely, Loqs-PB alone interacted with mosquito dicer-1 and was essential for full miRNA production.
13 in activator of PKR (PACT), while Drosophila Dicer-1 associates with Loquacious (Loqs).
14 nd give an additive phenotype with belle and Dicer-1 mutants, indicating that IMP functions independe
15                               In Drosophila, Dicer-1 produces approximately 22-24-nt miRNAs from pre-
16        In 2009 we reported that depletion of Dicer-1, the enzyme that catalyzes the final step of miR
17 hich impaired metamorphosis, and by treating Dicer-1-depleted individuals with an miR-2 mimic to allo
18 eral miRNA processing enzymes (DROSHA [95%], DICER [17%], TARBP2 [38%]) showed increased expression p
19 r B2 from Flock House virus or Aedes aegypti dicer-2 (Aedicer-2) using a constitutive heat shock prom
20 SC loading complex (RLC), which contains the Dicer-2 (Dcr-2)-R2D2 complex and recruits duplex siRNA t
21 erved that the helicase domain of Drosophila Dicer-2 (dmDcr-2) governs substrate recognition and clea
22 microscopy to solve structures of Drosophila Dicer-2 alone and in complex with blunt dsRNA.
23 ncreasing expression of either Su(var)3-9 or Dicer-2 also led to an increase in life span.
24 qs-PD enhances the rate of dsRNA cleavage by Dicer-2 and also enables processing of substrates normal
25 -independent, but we find that modulation of Dicer-2 cleavage also requires dsRNA binding by Loqs-PD.
26 , two pathways are proposed, either based on Dicer-2 cleavage to generate 20-nucleotide vsRNAs or bas
27 ion in Ae. albopictus C6/36 cells, which are dicer-2 defective.
28  double-stranded RNA (dsRNA), and Drosophila Dicer-2 distinguishes dsRNA substrates by their termini.
29 ding protein that functions as a cofactor of Dicer-2 in Drosophila.
30                                  Mutation of Dicer-2 led to an increase in DNA double-strand breaks.
31 ely 22-24-nt miRNAs from pre-miRNAs, whereas Dicer-2 makes 21-nt siRNAs from long double-stranded RNA
32 well as increased life span in TE-sensitized Dicer-2 mutants.
33 bstrate by a phosphate-binding pocket in the Dicer-2 PAZ (Piwi, Argonaute, and Zwille/Pinhead) domain
34 hored by the phosphate-binding pocket in the Dicer-2 PAZ domain and the distance between the pocket a
35 tions in the phosphate-binding pocket of the Dicer-2 PAZ domain decreased RNA silencing activity in v
36                                          How Dicer-2 precisely makes 21-nt siRNAs with a remarkably h
37                        Further, we show that Dicer-2 predominantly targets viral dsRNA and produces 2
38 ds light on the molecular mechanism by which Dicer-2 produces 21-nt siRNAs with a remarkably high fid
39 directly interact with the Hel2 subdomain of Dicer-2's helicase domain.
40 ding overexpression of Sir2, Su(var)3-9, and Dicer-2, as well as decreased expression of Adar, mitiga
41 y Adar mutants is suppressed by silencing of Dicer-2, which has a RNA helicase domain similar to MDA5
42 nsect DNA viruses are negatively affected by dicer-2-mediated RNA interference (RNAi).
43 nt, to a considerable degree overlap between Dicer-2-related (19 to 21 nt) and Dicer-2-unrelated vsRN
44 ap between Dicer-2-related (19 to 21 nt) and Dicer-2-unrelated vsRNAs, suggesting a common origin for
45 cruit substrates into the helicase domain of Dicer-2.
46 with His-MDA-7/IL-24 protein, down-regulates DICER, a critical regulator in miRNA processing.
47                           Deleting miRNAs by Dicer ablation (Dicer KO) in thymocytes selectively impa
48                      Phosphorylated Dicer (p-Dicer) accumulates in the nucleus and is recruited to DN
49                   DNA damage-induced nuclear Dicer accumulation is conserved in mammals.
50     In line with this observation, enhancing DICER activity by a small molecule, enoxacin, is benefic
51 epidopteran (Sf9) cells inhibited endogenous dicer activity in a dose-dependent manner, while express
52 2, following heat shock treatment, inhibited dicer activity in all cells tested.
53 ression had little to no ability to suppress dicer activity in cell lysates, but higher expression of
54 er, we utilized an in vitro assay to measure dicer activity in lepidopteran and dipteran cells, combi
55  compound previously demonstrated to augment DICER activity, show stronger DDR signalling and faster
56 loses this interaction and does not suppress Dicer activity.
57 ut of the microRNA (miRNA)-processing enzyme Dicer (ADicerKO), as well as humans with lipodystrophy,
58 e important roles of GW182 and DDX6, but not Dicer, Ago2 and DCP1A, in PB formation, and that Kaposi'
59 sion of this mutant Dicer, but not wild-type Dicer, also resulted in a partial inhibition of Influenz
60 Naumovozyma castellii, which have an unusual Dicer and a conventional Argonaute that are both require
61 but not NiggA led to decreased expression of Dicer and Ago 2, suggesting that NiggV interaction with
62 ess granule formation and re-organization of DICER and AGO2 protein interactions with their partners.
63 ain pre-miRNA processing machinery including Dicer and Argonaute-2, which allow for cell-free pre-miR
64 ouse model with conditional deletion of both Dicer and Bim, to determine the biologic significance of
65 ssociate with the aberrant miRNA profiles in Dicer and Drosha cKO spermatozoa.
66                            Germline-specific Dicer and Drosha conditional knockout (cKO) mice produce
67 e only known miRNA whose processing bypasses Dicer and instead relies on the slicer activity of Argon
68 B to repress its expression independently of Dicer and microRNAs.
69  neurodegeneration and further suggests that DICER and miRNAs affect neuronal integrity and are possi
70     Further processing of precursor miRNA by Dicer and other components generates mature miRNA.
71 nfected cells is mediated by wild-type human Dicer and potently suppressed by both NS1 of IAV as well
72 ted double-knockout human cells lacking both Dicer and protein kinase RNA-activated.
73                 FTX interacted with DHX9 and DICER and regulated A-to-I RNA editing and miRNA express
74                                However, both Dicer and the Argonaute protein family have expanded rol
75 ion of essential miRNA biogenesis components Dicer and TRBP is increased following latent KSHV infect
76 enes, including the well-characterized gene, dicer, and a probable uncharacterized cyclin dependent k
77 tent with reduced microRNA processing enzyme Dicer, and increased expression of Alu element in OIR.
78                         Here, we report that Dicer- and Drosha-dependent diRNAs function as guiding m
79 B core RNAi genes including those coding for Dicer, Argonaute, and double-stranded RNA-binding protei
80 calpain inhibitor prevented loss of platelet dicer as well as the diabetes mellitus-induced decrease
81                                  An in vitro Dicer assay shows that this rG4 inhibits Dicer processin
82        These results demonstrate the role of Dicer-associated RNA binding proteins in maintenance of
83                                        Human Dicer associates with HIV TAR RNA-binding protein (TRBP)
84 with TGF-beta and 1,25diOHvitD3, full-length Dicer became abundant together with varying amounts of ~
85    MicroRNA-451 is refractory to the loss of Dicer because of its Ago2-dependent processing.
86 rains contain capsid mutations that increase Dicer binding affinity and enhance pathogenicity.
87 to contribute to this process, their mode of Dicer binding and their genome-wide effects on miRNA pro
88 sRBPs are reported to homodimerize, with the Dicer-binding region implicated in self-association.
89  sulfonyl fluoride) up-regulated full-length Dicer, both in MM6 cells and in primary human blood mono
90    Remarkably, overexpression of this mutant Dicer, but not wild-type Dicer, also resulted in a parti
91 cin (mTOR) signaling pathway was enhanced in Dicer(-/-) CD4(+) T cells, and its pharmacological inhib
92 ficantly enhanced the induction of iTregs in Dicer(-/-) CD4(+) T cells.
93  interfering RNAs enhanced Treg induction in Dicer(-/-) CD4(+) T cells.
94 bryonic eye morphogenesis appeared normal in Dicer CKO mice.
95                       RNAseq analysis of the Dicer CKO retina revealed altered expression of genes in
96 Dicer(flox/flox) conditional knockout mouse (Dicer CKO) to delete Dicer1 from cone cells, we show tha
97      The most highly upregulated gene in the Dicer-CKOMG MG is the proteoglycan Brevican (Bcan) and o
98 n, we used a conditional deletion of Dicer1 (Dicer-CKOMG) in retinal Muller glia (MG).
99 s, initiates from short introns but bypasses Dicer cleavage.
100 ents that may form substrates for subsequent Dicer cleavage.
101                                 Furthermore, Dicer cleaves all satellite RNAs in conjunction with MIW
102 siRNA biochemistry involving SNAs shows that Dicer cleaves the modified siRNA duplex from the surface
103                                              Dicer controls the biogenesis of microRNAs (miRNAs) and
104 tive 5p miRNAs into Argonaute proteins via a Dicer-coupled 5' monophosphate-dependent strand selectio
105 d suppressors of G0 defects in cells lacking Dicer (dcr1Delta), which mapped to genes involved in chr
106 y assembled genomes, RNaseIII (Drosha and/or Dicer) deficient samples and single cells (at both embry
107                                              Dicer-deficient cancers have poor prognoses, which is li
108                                   Drosha and Dicer-deficient cells, devoid of most miRNAs, are hypers
109  specifically upregulated in Drosha- but not Dicer-deficient ES cells.
110 RBP or PACT was designed and introduced into Dicer-deficient mammalian cells, revealing selective def
111  significance of increased Bim expression in Dicer-deficient nephron progenitors.
112 hotoreceptor cells degenerate and die in the Dicer-deleted retina.
113                                      Using a Dicer-deletion mouse model, our previous studies have de
114 r findings suggest that PIR-1 modulates both Dicer-dependent and Dicer-independent Argonaute pathways
115 o a prolonged G1/S transition via decreasing DICER-dependent biogenesis of miRNA let-7, which increas
116 double-strand breaks (DSBs) in a DROSHA- and DICER-dependent manner has been shown to regulate the DN
117 eads to an increase in p53 accumulation in a Dicer-dependent manner, thus explaining why PARN-defecti
118                      Our studies reveal that DICER-dependent microRNAs are essential for gonadotropin
119                                        Thus, DICER-dependent microRNAs confer a new layer of transcri
120                                      Loss of DICER-dependent microRNAs in gonadotropes resulted in pr
121                    We found that many of the DICER-dependent microRNAs, predicted in silico to bind g
122  is unique to nematodes, the second involves Dicer-dependent RNA-directed DNA methylation, hitherto u
123 el retrotransposable element silenced by the Dicer-dependent RNAi pathway.
124  is required for the maturation of 26G-RNAs, Dicer-dependent small RNAs that regulate thousands of ge
125                                              Dicer depletion causes endogenous DNA damage and delays
126  miR-630 is a promising approach to overcome Dicer deregulation in cancer.
127 ific inactivation of key miRNA pathway genes Dicer, Dgcr8, and the entire Argonaute gene family (Ago1
128  argonaute (AGO1, AGO2) and endoribonuclease dicer (DICER1) transcripts, and endogenous microRNAs wer
129 rm-PAZ domains have been considered the only Dicer domains that bind dsRNA termini, unexpectedly, we
130          However, we found that knockdown of DICER dramatically increased cell resistance to camptoth
131 icited, in part, by the miR-144 targeting of Dicer during erythropoiesis.
132                                          The dicer endonuclease DCL3 cuts resulting duplexes to gener
133 ory effect of HBx protein on activity of the Dicer endoribonuclease.
134  that strong binding and inhibition of human Dicer enzyme by the capsid protein is a potential mechan
135                                              Dicer enzymes function at the core of RNA silencing to d
136 istically impact DU145, wild-type HCT116, or Dicer(Ex5) HCT116 cell proliferation.
137 s were depleted, which was attenuated in the Dicer(Ex5) HCT116 cells (Figure 5B; Tay et al., 2011).
138 tenuated ceRNA effect in microRNA deficient (Dicer(Ex5)) HCT116 cells, we observed increased PTEN pro
139 actor antibody in mice resulted in rescue of Dicer expression and significantly decreased tumor growt
140             Here we describe a regulation of Dicer expression in monocytic cells, based on proteolysi
141                                 However, how dicer expression levels and miRNA biogenesis are regulat
142  that during zebrafish hindbrain development dicer expression levels are controlled by miR-107 to tun
143           MDA-7/IL-24 protein down-regulates DICER expression through canonical IL-20/IL-22 receptors
144 howed that miR-200a overexpression inhibited Dicer expression, in turn, resulted in inhibition of miR
145 ; however, even with the significant loss of Dicer expression, myomiR (miR-1, -133a and -206) express
146 ypoxic conditions, targets and downregulates Dicer expression.
147 d tumor growth and metastasis, and decreased Dicer expression.
148 ously demonstrated that the endoribonuclease DICER facilitates chromatin decondensation during lesion
149 ver a requirement for Argonaute proteins and Dicer, factors involved in small RNA maturation and tran
150                          Using a Chrnb4-cre; Dicer(flox/flox) conditional knockout mouse (Dicer CKO)
151 r eukaryotes, the microRNA biogenesis enzyme Dicer forms a 1:1 association with a dsRNA-binding prote
152             Mass spectrometry identified the Dicer fragments and showed cleavage about 450 residues u
153 er with varying amounts of ~170- and ~50-kDa Dicer fragments.
154 on of the microRNA (miRNA)-processing enzyme Dicer from nephron progenitors results in premature depl
155 calcemia and uremia is dependent upon intact dicer function and miRNAs.
156 o produce pre-microRNA in the nucleus, while DICER generates not only mature microRNA, but also endog
157    Recent findings suggest that noncanonical Dicer generates small noncoding RNA to mediate the DNA d
158                                           PT-Dicer(-/-) glands cultured in low-calcium medium secrete
159 pecific loss of the miRNA-processing enzyme, Dicer, identified intestinal epithelial cells (IEC) and
160 (2020) demonstrate that microRNA-144 targets Dicer in a negative feedback loop, affecting global cano
161 s deficit is overcome when miR-144 represses Dicer in a negative-feedback loop during erythropoiesis.
162 TRBP and PACT show that the proteins bind to Dicer in a similar manner and by mutual exclusion.
163  that aerobic exercise training up-regulates DICER in adipose tissue of mice and humans.
164                              By inactivating Dicer in adult quiescent hepatocytes we avoided the hepa
165                     Stable overexpression of DICER in cancer cells impedes Ad.mda-7 or His-MDA-7/IL-2
166 nadotropin beta subunits in vivo, we deleted Dicer in gonadotropes by a Cre-lox genetic approach.
167                 Furthermore, mutants lacking Dicer in gonadotropes displayed severely reduced fertili
168 ctive depletion of the miR-processing enzyme Dicer in mature myeloid cells blocks angiogenesis and me
169 state cells, whereas Ad.mda-7 down-regulates DICER in multiple cancer cells including glioblastoma mu
170 re, we show that Ago2 is less efficient than Dicer in processing pre-miRNAs, but this deficit is over
171    These results uncover a novel function of DICER in regulating the cell cycle through miRNA biogene
172 ges facilitated by Drosha in the nucleus and Dicer in the cytoplasm.
173 les for RNAi proteins, such as Argonaute and Dicer, in chromosome function.
174 aged WT and KO mice for ~22 months following Dicer inactivation to determine if myomiR expression wou
175 hat PIR-1 modulates both Dicer-dependent and Dicer-independent Argonaute pathways and provide insight
176          The eIF1A-Ago2 assembly facilitates Dicer-independent biogenesis of miR-451, which mediates
177 R-10a maturation by binding pre-miR-10a in a DICER-independent manner.
178  of Microprocessor regulation via studies of Dicer-independent mir-451, which is clustered with canon
179 at the integration of siRNA sequences into a Dicer-independent RNA stem-loop based on pre-miR-451 mic
180 iously that antisense transcription triggers Dicer-independent siRNA (disiRNA) production and disiRNA
181                         Thus, repression via dicer-independent siRNA-mediated facultative heterochrom
182 s PTH secretion, demonstrating that they are dicer-independent.
183 iRNA binding unit connected by a linker to a Dicer inhibiting unit.
184 our studies define a previously unrecognized Dicer interaction interface and suggest that Loqs-PD is
185                         The endoribonuclease Dicer is a key component of the human RNA interference p
186                                              DICER is a key enzyme in microRNA (miRNA) biogenesis.
187 gs show that capsid-dependent suppression of Dicer is a major determinant of ZIKV immune evasion and
188                                              Dicer is a ribonuclease III enzyme in biosynthesis of mi
189                                              Dicer is phosphorylated by the ERK-MAP kinase pathway an
190                     Here, we show that human Dicer is phosphorylated in the platform-Piwi/Argonaute/Z
191           MDA-7/IL-24-mediated regulation of DICER is reactive oxygen species-dependent and mediated
192                                    Adipocyte DICER is required for whole-body metabolic adaptations t
193 e in neural stem cells (NSCs) and found that Dicer is specifically targeted by the capsid from ZIKV,
194                                              DICER is unchanged by Ad.mda-7/IL-24 in normal immortal
195  shown that hypoxia downregulates Drosha and Dicer, key enzymes in miRNA biogenesis, causing a decrea
196 link to rRNA was almost completely lost in a DICER knock-out cell line.
197                           Wild-type (WT) and Dicer knockout (KO) mice were subjected to either synerg
198 rated an inducible, skeletal muscle-specific Dicer knockout mouse to deplete microRNAs in adult skele
199 ferentiation, was found up-regulated in iNKT Dicer KO cells together with enhanced TGF-beta signaling
200  effector differentiation, displayed by iNKT Dicer KO cells.
201 were differentially expressed between WT and Dicer KO iNKT cells at different differentiation stages
202           Deleting miRNAs by Dicer ablation (Dicer KO) in thymocytes selectively impairs iNKT cell su
203   Accordingly, miR-200s are downregulated in Dicer-KO CDs, its direct target genes Zeb1, Zeb2, and Sn
204 ression, we show that a mutant form of human Dicer lacking the amino-terminal helicase domain can pro
205          Loss of miR-107 function stabilizes dicer levels and miR-9 biogenesis across the ventricular
206        We propose that miR-107 modulation of dicer levels in differentiating neuronal cells is requir
207                                              Dicer levels were altered in platelets from diabetic mic
208 mediated RdDM requires PolV and DRM2 but not Dicer like-3 and other PolIV pathway components.
209 s an antiviral defense through the action of DICER-like (DCL) and ARGONAUTE (AGO) proteins.
210              These pathways rely on distinct Dicer-like (DCL) proteins that process double-stranded R
211                    We identified homologs of DICER-LIKE (DCL), ARGONAUTE (AGO), and other genes invol
212 c RNA-directed RNA polymerase (RdR1) and the Dicer-like (DCL3 and DCL4) proteins are recruited during
213                                    A MINIMAL DICER-LIKE (mDCL) gene, which lacks the N-terminal helic
214 ocalization of the Microprocessor components Dicer-like 1 (DCL1) and Hyponastic Leaves 1 (HYL1) with
215  Arabidopsis thaliana, tRFs are processed by Dicer-like 1 and incorporated into Argonaute1 (AGO1), ak
216  and miRNA processing core proteins, such as Dicer-like 1, SERRATE, and HYPONASTIC LEAVES 1, whereas
217 tion in a mutant lacking 22- to 24-nt sRNAs (dicer-like 2, 3, 4 triple mutant).
218 to be processed from double-stranded RNAs by Dicer-like 3 (DCL3) and loaded into the effector Argonau
219 y, FLAG-tagged VIG1 copurifies with AGO3 and Dicer-like 3 (DCL3), consistent with it also being a com
220 ), RNA-dependent RNA polymerase 2 (RDR2) and DICER-like 3 (DCL3).
221 utants from this screen, there were three at Dicer-like 3 that failed to produce both miRNAs and siRN
222 with the most C-terminal dsRBM domain of the Dicer-like 4 (DCL4) proteins.
223 is was shown previously to contribute to the DICER-LIKE 4 (DCL4)-mediated biogenesis of viral small i
224                                              Dicer-like 5 (Dcl5) is proposed to be responsible for pr
225 ubsequently processed into small RNAs by the DICER-LIKE enzymes.
226 in an analysis of data derived from multiple Dicer-like mutants in Arabidopsis.
227 tors are mostly produced by Botrytis cinerea Dicer-like protein 1 (Bc-DCL1) and Bc-DCL2.
228  of vsiRNA sequences reflect different plant Dicer-like proteins and Argonautes involved in vsiRNA bi
229 ate an antagonistic relationship between the Dicer-like proteins at at least some methylation loci.
230 ci in response to loss of one or more of the Dicer-like proteins that indicate an antagonistic relati
231 A processing machinery (i.e., independent of DICER-LIKE proteins).
232 -5s and tRF-3s is not primarily dependent on DICER-LIKE proteins, though they seem to be associated w
233 t family of RNA-acting prim-pol domains with DICER-like proteins.
234 RASE IV, RNA-DEPENDENT RNA POLYMERASE-2, and DICER-LIKE-4.
235  the double-stranded RNA binding protein and DICER-LIKE1 (DCL1) cofactor HYPONASTIC LEAVES1 (HYL1).
236 sion-dependent RdDM, which functions through DICER-LIKE3 (DCL3) but bypasses the requirement of both
237 hese loci depends upon P. patens homologs of DICER-LIKE3 (DCL3), RNA-DEPENDENT RNA POLYMERASE2, and t
238 polymerases RdR1 and RdR2 (but not RdR3) and Dicer-like3 (DCL3, but not DCL2 or DCL4) increased susce
239           These transcripts are processed by DICER-LIKE3 into 24-nucleotide small interfering RNAs (s
240                                        Plant DICER-LIKE4 (DCL4) performs dual functions, acting in an
241  24-nt phasiRNA precursor (24-PHAS) loci and Dicer-like5 (Dcl5) expression, and dcl5-1 mutants unable
242 d primarily transcriptionally >100-fold upon Dicer loss and is resistant to resilencing by complete r
243  strands and with properties consistent with Dicer-mediated cleavage of the dsRNA genome.
244  reveal a novel mechanism in which MIWI- and Dicer-mediated cleavage of the satellite RNAs prevents t
245                                              Dicer-mediated miRNA biogenesis is required for embryoni
246          Furthermore, l-DNA aptamers inhibit Dicer-mediated processing of pre-miRNA-155.
247 mation of a pre-miR-aptamiR complex inhibits Dicer-mediated processing of the pre-miR, which is requi
248                                              Dicer-mediated processing of virus-specific dsRNA into s
249                         Here, we report that DICER mediates the recruitment of the methyltransferase
250 cemia increased serum PTH >4-fold less in PT-Dicer(-/-) mice compared with control mice with no incre
251                           Remarkably, the PT-Dicer(-/-) mice did not increase serum parathyroid hormo
252                          Moreover, uremic PT-Dicer(-/-) mice increased serum PTH and FGF23 significan
253                          In contrast, the PT-Dicer(-/-) mice responded normally to activation of the
254 ted parathyroid-specific Dicer1 knockout (PT-Dicer(-/-) ) mice where parathyroid miRNA maturation is
255    We propose that exercise training-induced DICER-miR-203-3p up-regulation in adipocytes is a key ad
256                              Skeletal muscle Dicer mRNA expression remained significantly decreased b
257               Following tamoxifen treatment, Dicer mRNA expression was significantly decreased by 87%
258  80% in old KO mice and sequencing of cloned Dicer mRNA revealed the complete absence of the floxed e
259 well as an ill-defined boundary phenotype in Dicer mutants.
260 maturation assay, (2) expression levels in a Dicer null cell line, and (3) Ago2 pulldown.
261  miRNA-dependent repression, as confirmed in Dicer-null cells.
262                                Inhibition of Dicer or Ago2 expression revealed that small RNAs are in
263                    In addition, knockdown of DICER or AGO2 using either siRNA or MOE-gapmer chemistri
264                               Phosphorylated Dicer (p-Dicer) accumulates in the nucleus and is recrui
265 NA biogenesis through alteration of the MITF-DICER pathway.
266  to afford a dimeric molecule that binds the Dicer processing site and an adjacent bulge, affording a
267  ligands to target a common structure in the Dicer processing sites of three miRNAs in the cluster, m
268 cted to bind oncogenic pre-miR-155, inhibits Dicer processing under simulated physiological condition
269 tro Dicer assay shows that this rG4 inhibits Dicer processing, supporting the potential role of rG4 s
270 xpression, confirming hPMR1 acts upstream of Dicer processing.
271                                   The enzyme Dicer produces small silencing RNAs such as micro-RNAs (
272 s not affect Pri-miR-221 expression, and the DICER protein, as no changes occur in other miRNA proces
273 onocytes, inhibit an apparently constitutive Dicer proteolysis, allowing for increased formation of m
274 nents of the antiviral RNAi pathway, such as Dicer-related helicase 1 (DRH-1), to display hypersuscep
275        In addition, stable overexpression of DICER renders cancer cells more resistant to Ad.mda-7 in
276                     Loss of miR-144-mediated Dicer repression in zebrafish embryos and human cells le
277 ction studies confirm that overexpression of DICER rescues deregulation of miRNAs by mda-7/IL-24, par
278 ditional phosphorylation of carboxy-terminal Dicer residues (S1728 and S1852).
279                                         This Dicer-resistant epigenetic switch confers tumorigenicity
280                              Together, these Dicer-resistant genes constitute an mRNA expression sign
281 ression of their downstream targets PTEN and Dicer, respectively, suggesting that Rbfox2 indirectly r
282 that the levels and substrate selectivity of DICER result in the preferential biogenesis of specific
283 cule named Targapremir-210 that binds to the Dicer site of the miR-210 hairpin precursor.
284 nical pre-miRNAs is not a general feature of Dicer substrate hairpins.
285 Core lipid nanoparticles (LNP) loaded with a Dicer substrate small interfering RNA targeting catenin
286 omprise a substantial fraction of endogenous Dicer substrates in mammalian genomes.
287 s and enters the miRNA biogenesis pathway as Dicer substrates.
288      Rictor was more abundantly expressed in Dicer(-/-) T cells as was mTOR, and their expression was
289 sed on the structure, a catalytically active Dicer that cannot bind TRBP or PACT was designed and int
290 ed on these findings, we created a bacterial Dicer that is ideally suited for producing heterogeneous
291 entiating MM6 cells up-regulated full-length Dicer, through EP2/EP4 and cAMP.
292                          ADARs interact with Dicer to augment the processing of pre-miR-27a to mature
293                        Invertebrates rely on Dicer to cleave viral double-stranded RNA (dsRNA), and D
294 s localized processing of nuclear dsRNA by p-Dicer to promote DNA repair.
295 We solved the crystal structure of the human Dicer-TRBP interface, revealing the structural basis of
296 ription and cleavage by the DROSHA/DGCR8 and DICER/TRBP/PACT complexes.
297          Further investigation revealed that Dicer was decreased in miR-200a overexpressed BC cells;
298 entiated Mono Mac 6 (MM6) cells, full-length Dicer was undetectable; only an ~50-kDa fragment appeare
299 t progenitors display elevated expression of DICER, which promotes enhanced maturation of a set of ce
300                       Collectively, we place Dicer within the context of the DDR by demonstrating a D

 
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