ライフサイエンスコーパス: Drosha

1 .283+A, which prevents pri-miRNA cleavage by Drosha.

2 RNA-binding partner protein of the nuclease Drosha.

3 g, producing RNAi effectors not processed by Drosha.

4 by expression of a dominant negative form of Drosha.

5 NAs by facilitating the cleavage reaction by Drosha.

6 NAs) in connection with the RNase III enzyme Drosha.

7 olved in miRNA biogenesis and interacts with Drosha.

8 i-miRNA processing is the main function of c-Drosha.

9 ve nuclear localization signal, generating c-Drosha.

10 mature miRs in the presence of phospho-mimic Drosha.

11 insights into the ever-evolving functions of Drosha.

12 binding protein DGCR8 and the type III RNase DROSHA.

13 ly validated in cell lines expressing mutant DROSHA.

14 ssary and sufficient ubiquitin E3 ligase for Drosha.

15 transcripts by the nuclear RNase III enzyme Drosha.

16 croRNA processing genes (miRNAPGs) DGCR8 and DROSHA (15% of 534 tumors).

17 t signals and faithfully indicates DGCR8 and Drosha activities.

18 S(300) and/or S(302); confirmed by enhanced Drosha activity and association with cofactors, and incr

19 Conversely, GSK3beta activation increases Drosha activity and mature miR accumulation.

20 Thus, surprisingly, KSHV modulates Drosha activity differentially depending on the mode of

21 implies that tying viral gene expression to Drosha activity is advantageous for viruses.

22 Repression of GSK3beta activity reduces Drosha activity toward pri-miRs, leading to accumulation

23 identify the mechanism for GSK3beta-enhanced Drosha activity, which requires GSK3beta nuclear localis

24 icate the existence of cytoplasmic Drosha (c-Drosha) activity.

25 ckdown, real-time polymerase chain reaction, Drosha-activity, microRNA array, proliferation, differen

26 n miRNA biogenesis and function (i.e. Dicer, Drosha, Ago1 and Ago2).

27 Though this microRNA is processed by Drosha (also known as Rnasen), its maturation does not r

28 Here, we show that Drosha, an endoribonuclease best known for its role in t

29 n of menin does not affect the expression of Drosha and CBP80, but substantially impairs the processi

30 cript, leads to enhanced miRNA processing by Drosha and consequently enhanced functional miR-100 both

31 imary-microRNAs and the expression levels of Drosha and DGCR8 (both mRNA and protein) were increased

32 ract with the core microprocessor components Drosha and DGCR8 and the associated regulatory proteins

33 chinery, and interferes with the assembly of Drosha and DGCR8 complex.

34 DROSHA and DGCR8 mutations strongly altered miRNA expres

35 of the microprocessor complex, consisting of Drosha and DGCR8, are both necessary and sufficient for

36 esis requires the Microprocessor components, Drosha and DGCR8, to generate precursor-miRNA, and Dicer

37 cterized by pervasive interaction with DGCR8/Drosha and DGCR8/Drosha-regulated mRNA stability control

38 Together, these results suggest that Drosha and Dicer are implicated in rRNA biogenesis.

39 Both Drosha and Dicer cKO males were infertile due to disrupt

40 was similar at morphological levels between Drosha and Dicer cKO males, but Drosha cKO testes appear

41 that KSRP also serves as a component of both Drosha and Dicer complexes and regulates the biogenesis

42 nd then to mature miRNAs by the multiprotein Drosha and Dicer complexes, respectively, remain largely

43 lain the nonoverlapping phenotypes caused by Drosha and Dicer deficiency.

44 Although Drosha and Dicer each possess independent non-miRNA-rela

45 of sequential endonucleolytic processing by Drosha and Dicer from longer RNA polymerase II (RNAP II)

46 d effect of hypoxia in the downregulation of Drosha and Dicer in cancer cells that leads to dysregula

47 eting the essential miRNA biogenesis enzymes Drosha and Dicer in mouse skin epithelial cells at succe

48 These data reveal multiple functions for Drosha and Dicer in suppressing DNA damage in rapidly pr

49 Inhibition of de novo synthesis of Drosha and Dicer in the embryo led to consistent develop

50 suppression of the miRNA-processing enzymes Drosha and Dicer increased Bim levels, in support of the

51 ity in phenotypes of the inducible epidermal Drosha and Dicer mutants indicates that these defects re

52 tial cleavage of precursor substrates by the Drosha and Dicer RNase III enzymes.

53 esis pathway driven by the RNase III enzymes Drosha and Dicer, an unexpected variety of alternative m

54 tudies have shown that hypoxia downregulates Drosha and Dicer, key enzymes in miRNA biogenesis, causi

55 ilencing of the microRNA processing enzymes, Drosha and Dicer, led to an increase in FOXO1 expression

56 quentially cleaved by the RNase III enzymes, Drosha and Dicer, which generate 5' monophosphate ends t

57 Drosha and Dicer-deficient cells, devoid of most miRNAs,

58 nesis pathway requires two RNaseIII enzymes: Drosha and Dicer.

59 ng of longer precursors by the ribonucleases Drosha and Dicer.

60 CombinedPf4-cre-mediated deletion of Drosha and Dicer1 did not significantly exacerbate pheno

61 ains its capacity to promote self-renewal in Drosha and Dicer1 knockout NSCs.

62 Both DROSHA and DICER1 mutations impair expression of tumour-

63 s in the microRNA (miRNA)-processing enzymes DROSHA and DICER1, and novel mutations in MYCN, SMARCA4

64 nded RNA-binding protein that interacts with Drosha and facilitates microRNA (miRNA) maturation.

65 al genome-wide co-localization of HP1BP3 and Drosha and HP1BP3-dependent Drosha binding to actively t

66 This work increases the known functions of Drosha and implies that tying viral gene expression to D

67 ress engages p38 MAPK pathway to destabilize Drosha and inhibit Drosha-mediated cellular survival.

68 Cleavage of microRNAs and mRNAs by Drosha and its cofactor Pasha/DGCR8 is required for anim

69 croprocessor, a complex containing the RNase Drosha and its partner protein, DGCR8.

70 ciated with enhanced processing of miRNAs by Drosha and more efficient formation of RNA-induced silen

71 report clear phenotypic differences between drosha and pasha/dgcr8 null alleles in two postembryonic

72 Simtrons are bound by Drosha and processed in vitro in a Drosha-dependent mann

73 Here we demonstrate that Drosha and related RNase III ribonucleases from all thre

74 sor, which consists of the nuclear RNase III Drosha and the double-stranded RNA-binding domain protei

75 ucleus and becomes associated with RNase III DROSHA and the RNA helicase p68.

76 luated where Drosha functions in cells using Drosha and/or DGCR8 knock out (KO) cells and cleavage re

77 ies with poorly assembled genomes, RNaseIII (Drosha and/or Dicer) deficient samples and single cells

78 es TGFbeta/BMP-induced recruitment of Smads, Drosha, and DGCR8 to pri-T/B-miRs and impairs their proc

79 the key microRNA processing enzymes: Dicer, Drosha, and DGCR8/Pasha, were significantly reduced at b

80 y the Microprocessor, a complex of DGCR8 and Drosha, and the second by a complex of TRBP and Dicer.

81 revealed transcriptomic differences between Drosha- and Dicer-null pachytene spermatocytes or round

82 ies exhibited increased disorder, suggesting DROSHA- and DICER1-dependent microRNA processing variabi

83 al Region 8 (DGCR8) and its partner nuclease Drosha are essential for processing of microRNA (miRNA)

84 screen, we identify Microprocessor component DROSHA as a novel DNMT1-interactor.

85 Our results highlight DROSHA as a novel regulator of mammalian DNA methylation

86 er of complexity to the molecular anatomy of Drosha as it relates to miRNA biogenesis.

87 der stress, p38 MAPK directly phosphorylates Drosha at its N terminus.

88 nuclear localisation, as phosphorylation of Drosha at S(300) and/or S(302); confirmed by enhanced Dr

89 In contrast, increase in Drosha attenuates stress-induced death.

90 regulated by glucose through the mTORC1-MDM2-DROSHA axis.

91 on of HP1BP3 and Drosha and HP1BP3-dependent Drosha binding to actively transcribed miRNA loci.

92 bear a 5' tRNA moiety, are not processed by Drosha but instead by cellular tRNase Z, which cleaves 3

93 -dependent pri-miRs fail to properly recruit Drosha, but heme-bound DGCR8 can correct erroneous bindi

94 scripts that are specifically upregulated in Drosha- but not Dicer-deficient ES cells.

95 Rescue of Drosha by siRNAs targeting ETS1/ELK1 in vivo results in

96 esults indicate the existence of cytoplasmic Drosha (c-Drosha) activity.

97 more, the N-terminal, but not the C-terminal Drosha can be acetylated by multiple acetyl transferases

98 The nuclear RNase III Drosha catalyzes the first processing step together with

99 obvious developmental delay was observed in Drosha cKO embryos.

100 ker CD31 were significantly downregulated in Drosha cKO mice compared to controls.

101 ith the aberrant miRNA profiles in Dicer and Drosha cKO spermatozoa.

102 vels between Drosha and Dicer cKO males, but Drosha cKO testes appeared to be more severe in spermato

103 integrin rescues maturation and migration of Drosha (cKO) hematopoietic stem and progenitor cells to

104 dothelium-specific deletion of mouse Drosha (Drosha (cKO)), an enzyme essential for microRNA biogenes

105 icient and control vascular endothelium, but Drosha (cKO)-derived hematopoietic stem and progenitor c

106 As derived from hairpins generated either by Drosha cleavage (canonical substrates) or by splicing an

107 d the primary miR-7 transcript to facilitate Drosha cleavage and is independent of SF2/ASF's function

108 plicing machinery to bypass the necessity of Drosha cleavage for their biogenesis.

109 he dominant off-set sequence suggesting that Drosha cleavage generates most miRNA reads without termi

110 Herein we report that Drosha cleavage of LTIII BHRF1 RNA and cis-acting splici

111 first step in miRNA biogenesis, but how the Drosha cleavage site is determined has been unclear.

112 o detects 3'-end processing of pre-miRNAs on Drosha cleavage site that correlates with miRNA-offset R

113 re, using miRNA-offset RNAs to determine the Drosha cleavage site, we show that the Microprocessor me

114 d cleavage, and KapB transcripts lacking the Drosha cleavage sites express higher levels of KapB, res

115 Evidence shown here supports the view that Drosha cleavage to generate mature miRNAs and cis-acting

116 miRNA biogenesis enzyme Drosha cleaves double-stranded primary miRNA by interact

117 GSK3beta achieves this through promoting Drosha:cofactor and Drosha:pri-miR interactions: it bind

118 Acetylation of Drosha competes with its ubquitination, inhibiting the d

119 -miRNA) transcripts are processed by nuclear Drosha complex into ~70-nucleotide stem-loop precursor m

120 8 that was mutually exclusive with the DGCR8-Drosha complex that processes pri-miRNAs in the nucleus.

121 iRNA biogenesis through interacting with the DROSHA complex.

122 We generated Drosha conditional knockout (cKO) mice by crossing VSMC-

123 Germline-specific Dicer and Drosha conditional knockout (cKO) mice produce gametes (

124 Using a series of truncated Drosha constructs, we narrowed down the segment responsi

125 Defects in morphogenesis caused by loss of Drosha could be rescued with four miRNAs.

126 ciated with biallelic mutations in DICER1 or DROSHA, crucial for miRNA biogenesis.

127 oietic stem and progenitor cells emerge from Drosha-deficient and control vascular endothelium, but D

128 Drosha-deficient embryonic stem (ES) cells display genom

129 Knockdown of NFIB in Drosha-deficient hippocampal NSCs restores neurogenesis,

130 onal profiles that were shared in Dicer- and Drosha-deficient mice confirmed the requirement for both

131 1, caused a broad reduction in miRNAs due to Drosha degradation.

132 the E3 ubiquitin ligase Mdm2, which promotes Drosha degradation.

133 se the cellular response to virus infection, Drosha deletion resulted in a significant increase in vi

134 MCM4:MCM6 interaction, triggers a Dicer1 and Drosha-dependent approximately 40% reduction in Mcm2-7 m

135 Here, we report that Dicer- and Drosha-dependent diRNAs function as guiding molecules to

136 bound by Drosha and processed in vitro in a Drosha-dependent manner.

137 Within this class, we identify a cohort of Drosha-dependent mRNA cleavage events that functionally

138 licated in Wilms tumors (WT1, CTNNB1, AMER1, DROSHA, DGCR8, XPO5, DICER1, SIX1, SIX2, MLLT1, MYCN, an

139 Microprocessor [Drosha-DGCR8 (DiGeorge syndrome critical region gene 8)

140 ed that canonical microRNAs dependent on the DROSHA-DGCR8 complex are required for uterine developmen

141 Previous models proposed that the Drosha-DGCR8 complex measures either ~22 nt from the upp

142 ent studies suggest that the microprocessor (Drosha-DGCR8) complex can be recruited to chromatin to c

143 croRNA domains are suboptimal substrates for Drosha-DGCR8, and therefore resistant to microprocessing

144 following transcription and cleavage by the DROSHA/DGCR8 and DICER/TRBP/PACT complexes.

145 trated significant SNP-associated changes in Drosha/DGCR8 and/or Dicer processing.

146 (18.1% of blastemal cases); mutations in the DROSHA/DGCR8 microprocessor genes (18.2% of blastemal ca

147 onstituents act cooperatively and facilitate Drosha/DGCR8 recruitment and pri-miRNA processing to boo

148 identity by enhancing both transcription and Drosha/DGCR8-mediated primary miRNA (pri-miRNA) processi

149 d pri-miRNA processing by the Microprocessor Drosha/DGCR8.

150 Iron may have mediated Drosha/DGCR8/heme-mediated processing of microRNAs.

151 re microRNA expression levels, (ii) in vitro Drosha/Dicer processing, and (iii) RNA-induced silencing

152 We further find that Drosha directly targets NFIB to repress its expression i

153 cular endothelium-specific deletion of mouse Drosha (Drosha (cKO)), an enzyme essential for microRNA

154 miRNA features, including dependence on the Drosha endonuclease for processing.

155 RNA polymerase II and then processed by the Drosha endonuclease to generate approximately 60 nt pre-

156 cogenic Ras(V12) were dependent on increased Drosha expression as Drosha knockdown was sufficient to

157 Enhanced Drosha expression did not alter global miRNA production

158 The comparison of normalized Dicer and Drosha expression in ex vivo and in vitro condition reve

159 with advanced tumor stage (P=0.007), and low Drosha expression with suboptimal surgical cytoreduction

160 Interestingly, while repressing Drosha expression, as reported earlier, we found that EW

161 the meta-analysis replicated 6 SNPs from the DROSHA, FMR1, LIN28, and LIN28B genes, including rs12194

162 hanism mediates stress-induced inhibition of Drosha function.

163 ntly possess multilineage potential but that Drosha functions as a molecular barrier preventing oligo

164 mical analyses reveal that, in this context, Drosha functions as an antiviral clamp, conferring steri

165 Here, we re-evaluated where Drosha functions in cells using Drosha and/or DGCR8 knoc

166 rtron hairpins are substantially longer than Drosha-generated pre-miRNAs, indicating that the charact

167 function and knockdown studies indicate that Drosha generates a short pre-mir-451 hairpin that is dir

168 e canonical animal microRNA (miRNA) pathway, Drosha generates approximately 60- to 70-nucleotide pre-

169 The RNA binding and enzymatic domains of Drosha have been characterized and are on its C-terminus

170 ing is likely facilitated by preformed DGCR8-Drosha heterodimers that can discriminate between authen

171 ular structure was absent in the yolk sac of Drosha homozygotes at E14.5.

172 e cytoplasm together with a small isoform of Drosha, implying the existence of a different miRNA proc

173 Here, we report that deletion of Drosha in adult dentate gyrus NSCs activates oligodendro

174 the host miRNA machinery proteins Dicer and Drosha in exosomes from infected cells.

175 rase II transcripts by the RNase III enzymes Drosha in the nucleus and Dicer in the cytoplasm.

176 ial endonucleolytic cleavages facilitated by Drosha in the nucleus and Dicer in the cytoplasm.

177 nucleolin directly interacts with DGCR8 and Drosha in the nucleus.

178 The role of Drosha in vascular smooth muscle cells (VSMCs) has not b

179 Disruption of Drosha in VSMCs of mice leads to the dysregulation of mi

180 Disruption of Drosha in VSMCs resulted in embryonic lethality at E14.5

181 iogenesis of these testicular endo-siRNAs is DROSHA independent, but DICER dependent.

182 We review here the many Drosha-independent and Dicer-independent microRNA biogen

183 iated gene knockdown was splicing-dependent, Drosha-independent and had variable dependence on RNAi p

184 orge syndrome critical region gene 8 (Dgcr8)/Drosha-independent but Dicer-dependent manner.

185 These data therefore identify a general Drosha-independent DGCR8/Pasha pathway that promotes pro

186 of miRNAs generated by a Dicer-dependent but Drosha-independent mechanism.

187 The RNase III enzyme Drosha initiates microRNA (miRNA) biogenesis in the nucl

188 hypoxia-inducible factors (HIFs) through HIF-Drosha interaction.

189 RNase III enzyme Drosha interacts with DGCR8 to form the Microprocessor,

190 re enzymatically processed in the nucleus by Drosha into hairpin intermediate miRs (pre-miRs) and fur

191 DROSHA is a nuclear RNase III enzyme responsible for cle

192 show that hypoxia-mediated downregulation of Drosha is dependent on ETS1/ELK1 transcription factors.

193 the biogenesis of several small RNA species, DROSHA is essential mainly for the canonical miRNA produ

194 However, little is known whether Drosha is regulated.

195 Our data demonstrated that Drosha is required for VSMC survival by targeting multip

196 Here, we show that Drosha is targeted by stress.

197 The Microprocessor complex (DGCR8/Drosha) is required for microRNA (miRNA) biogenesis but

198 Further analysis indicated that the c-Drosha isoform is abundant in multiple cell lines, drama

199 We identified two novel in-frame Drosha isoforms generated by alternative splicing in bot

200 We demonstrated that DROSHA knockdown enhanced cell migration and invasion, w

201 s further defined by examining the impact of DROSHA knockdown on cell behaviors.

202 om an orthotopic xenograft model showed that DROSHA knockdown resulted in reduced growth of primary t

203 dependent on increased Drosha expression as Drosha knockdown was sufficient to inhibit Ras-dependent

204 omal cells and derived vesicles but not with Drosha-knockdown cells and vesicles.

205 Drosha-knockdown cells produced extracellular vesicles t

206 phologic and functional recovery in AKI, the Drosha-knockdown counterparts were ineffective.

207 ar vesicles but not after treatment with the Drosha-knockdown counterparts.

208 i-miRNAs become enriched in the cytoplasm of Drosha KO cells, it remains unclear whether pri-miRNA pr

209 stingly, simultaneous depletion of Dicer and Drosha led to a different processing defect, causing slo

210 n transcriptional mechanisms, differences in Drosha levels contribute to low levels of KapB expressio

211 ssing VSMC-specific Cre mice, SM22-Cre, with Drosha (loxp/loxp) mice.

212 PK pathway to destabilize Drosha and inhibit Drosha-mediated cellular survival.

213 This regulation is dependent on Drosha-mediated cleavage, and KapB transcripts lacking t

214 inly for the canonical miRNA production, and DROSHA-mediated miRNA production is essential for normal

215 t that this genetic variant directly affects Drosha-mediated processing of pri-mir-30c-1 in vitro and

216 ammalian DNA methylation and we propose that DROSHA-mediated processing of RNA is necessary to ensure

217 Knockdown of TRAIL-R2 increased Drosha-mediated processing of the let-7 microRNA precurs

218 ibited at the early miRNA biogenesis step of Drosha-mediated processing.

219 ain of p53 augments its association with the Drosha microprocessor and promotes nuclear primary miRNA

220 ays a critical role in the regulation of the Drosha microprocessor and that post-transcriptional regu

221 p68 (also known as DDX5), a component of the DROSHA microprocessor complex.

222 ns, as expected, but also with components of Drosha microprocessor complexes, consistent with roles f

223 n of AGS cells has no significant effects on Drosha mRNA levels.

224 This induction did not involve Drosha mRNA transcription or protein stability but rathe

225 Thus, we propose that ARF regulates Drosha mRNA translation to prevent aberrant cell prolife

226 ied on the increased translation of existing Drosha mRNAs.

227 Interestingly, a truncated Drosha mutant located exclusively in the cytoplasm cleav

228 e which is phenocopied in dicer-1, pasha and drosha mutants.

229 in human cells demonstrates that DICER1 and DROSHA mutations influence miRNA processing through dist

230 s restores neurogenesis, suggesting that the Drosha/NFIB mechanism robustly prevents oligodendrocyte

231 gcr8 leads to defects that are not shared by drosha null mutations in the morphology of gamma neurons

232 SS is validated with a specifically designed Drosha-null/conditional-null mouse model, generated usin

233 y forming a nuclear complex with hnRNPA1 and Drosha on pri-miRs.

234 production in spermatogenesis, we generated Drosha or Dicer conditional knock-out (cKO) mouse lines

235 However, deficiency in Drosha or Dicer did not always result in identical pheno

236 Deletion of either Drosha or Dicer during an established growth phase (anag

237 knock-out (cKO) mouse lines by inactivating Drosha or Dicer exclusively in spermatogenic cells in po

238 Deletion of Drosha or Dicer in resting phase follicles did not affec

239 Specific deletion of either Drosha or Dicer phenocopies mice lacking a functional Fo

240 In cells depleted of Drosha or Dicer, different precursors to 5.8S rRNA stron

241 y 70% of the AGO2-IP mRNAs were increased by DROSHA or DICER1 knockdown.

242 structured precursors through the action of Drosha-Pasha and Dicer-1-Loquacious complexes.

243 Taken together, our data reveal an mTOR-Mdm2-Drosha pathway in mammalian cells that broadly regulates

244 The RNaseIII enzyme Drosha plays a pivotal role in microRNA (miRNA) biogenes

245 ulated in multiple tumors, suggesting that c-Drosha plays a unique role in gene regulation.

246 After initial processing in the nucleus by Drosha, precursor microRNAs (pre-miRNAs) are transported

247 ds endogenous pri-miRNAs and facilitates the Drosha/pri-miRNA association in vivo.

248 s this through promoting Drosha:cofactor and Drosha:pri-miR interactions: it binds to DGCR8 and p72 i

249 Drosha-processed microRNAs (miRNAs) have been shown to b

250 Using an elucidated relationship between Drosha processing and the single-stranded nature of the

251 uction and provides a new tool for detecting Drosha processing events and predicting pre-miRNA proces

252 at restrain the terminal loop region inhibit Drosha processing of primary microRNA transcripts as wel

253 A-to-I editing can affect Drosha processing or directly alter the microRNA (miRNA)

254 ules that bound RNA motifs nearby and in the Drosha processing site.

255 rated into the miRNA basal segments inhibits Drosha processing, resulting in titratable control over

256 ipts that give rise to miRNAs independent of Drosha processing.

257 structures are critical to the precision of Drosha processing.

258 ssing and stability via association with the DROSHA-processing complex during genotoxic stress.

259 t that chronic or acute loss of Arf enhanced Drosha protein expression.

260 atin A (TSA) and nicotinamide (NIA) increase Drosha protein level as measured by western blot but hav

261 that ubiquitination and acetylation regulate Drosha protein levels oppositely.

262 Elevated Drosha protein levels were required to maintain the incr

263 uitin-proteasome pathway, thereby increasing Drosha protein levels.

264 some inhibitors MG132 or Omuralide increases Drosha protein levels.

265 leads to the ubiquitination and reduction of Drosha protein levels.

266 DGCR8 and Drosha recognize and cleave primary transcripts of micro

267 We found that, in early-stage thymocytes, Drosha recognizes and directly cleaves many protein-codi

268 ments of the pri-miRNA stem-loop followed by Drosha recruitment and pri-miRNA cleavage.

269 ntial model of DGCR8 recognition followed by Drosha recruitment is unlikely.

270 Loss of Drosha reduced VSMC proliferation in vitro and in vivo.

271 sive interaction with DGCR8/Drosha and DGCR8/Drosha-regulated mRNA stability control, suggesting uniq

272 This adds to the DROSHA repertoire of non-miRNA dependent functions as we

273 Taken together, we propose that Drosha represents a unique and conserved arm of the cell

274 NA-seq in cells expressing dominant-negative DROSHA resulted in much greater coverage of pri-miRNA tr

275 Finally, we show that the Drosha RNA endonuclease, which functions upstream of Dic

276 in Dicer RNase IIIa and IIIb domains and in Drosha RNase IIIb domains, has the potential to particip

277 from the 5'-arm of pre-miRNA hairpins, while DROSHA RNase IIIB mutations globally inhibit miRNA bioge

278 Insertion of Dicer and Drosha RNase processing sites within the shRNA allows ge

279 by modulating the enzymatic function of the Drosha (RNase type III) complex through its physical ass

280 DROSHA:rs6886834 variant A allele (HR, 6.38; 95% CI, 2.4

281 Reduction of Drosha sensitizes cells to stress and increases death.

282 ar RNA (snoRNA) transcripts independently of Drosha, suggesting the existence of alternative DGCR8 co

283 If the distances are not optimal, Drosha tends to cleave at multiple sites, which can, in

284 cleavage sites suggested higher fidelity of Drosha than Dicer.

285 ntified recessive gain-of-function allele in drosha that probably interferes with the microRNA indepe

286 Drosha, the catalytic core of the microprocessor complex

287 GAM downregulates Drosha, the main effector of miRNA maturation in the nuc

288 to be associated with aberrant expression of Drosha, the molecular mechanisms that regulate its prote

289 vity in the presence and absence of Dicer or Drosha, the RNase III nucleases responsible for generati

290 erated mesenchymal stromal cells depleted of Drosha to alter microRNA expression.

291 t EWS was able to enhance the recruitment of Drosha to chromatin.

292 Pri-mir-17-92 is immediately cleaved by DROSHA to pre-miR-18a, indicating that its regulation oc

293 s an RNA-binding protein that interacts with DROSHA to produce pre-microRNA in the nucleus, while DIC

294 imary transcripts that undergo processing by Drosha to produce ~65-nucleotide precursors that are the

295 ation at either site is sufficient to locate Drosha to the nucleus.

296 ses trigger exportin 1 (XPO1/CRM1)-dependent Drosha translocation into the cytoplasm in a manner inde

297 Drosha was induced by nutrient and energy deprivation an

298 increased virus infection in the absence of Drosha was not due to a loss of viral small RNAs but, in

299 hairpin by DGCR8 followed by recruitment of DROSHA, which cleaves the RNA duplex to yield the pre-mi

300 efficient processing by the endoribonuclease DROSHA, which initiates miRNA biogenesis.