ライフサイエンスコーパス: Drosha

1 ly validated in cell lines expressing mutant DROSHA.

2 ssary and sufficient ubiquitin E3 ligase for Drosha.

3 transcripts by the nuclear RNase III enzyme Drosha.

4 enhanced processing of the primary miRNA by Drosha.

5 .283+A, which prevents pri-miRNA cleavage by Drosha.

6 n the WT myoblasts due to SUN1 inhibition of Drosha.

7 RNA-binding partner protein of the nuclease Drosha.

8 by expression of a dominant negative form of Drosha.

9 NAs by facilitating the cleavage reaction by Drosha.

10 g, producing RNAi effectors not processed by Drosha.

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

12 ve nuclear localization signal, generating c-Drosha.

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

14 insights into the ever-evolving functions of Drosha.

15 binding protein DGCR8 and the type III RNase DROSHA.

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

17 ificantly, several miRNA processing enzymes (DROSHA [95%], DICER [17%], TARBP2 [38%]) showed increase

18 e isoform specifically binds to and inhibits Drosha, a key component of the microprocessor complex re

19 t signals and faithfully indicates DGCR8 and Drosha activities.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

36 DROSHA and DGCR8 mutations strongly altered miRNA expres

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

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

39 teps initiated by Microprocessor, comprising Drosha and DGCR8.

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

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

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

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

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

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

57 entially processed by two RNase III enzymes, Drosha and Dicer.

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

59 nesis pathway requires two RNaseIII enzymes: 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 icroprocessor, comprised of RNase III enzyme Drosha and its cofactor DGCR8.

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

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

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

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

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

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

79 ated at DNA double-strand breaks (DSBs) in a DROSHA- and DICER-dependent manner has been shown to reg

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 obvious developmental delay was observed in Drosha cKO embryos.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 8 that was mutually exclusive with the DGCR8-Drosha complex that processes pri-miRNAs in the nucleus.

119 iRNA biogenesis through interacting with the DROSHA complex.

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

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

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

123 s near the apical junction is independent of Drosha core domains, as observed in a second structure i

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

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

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

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

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

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

130 1, caused a broad reduction in miRNAs due to Drosha degradation.

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

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

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

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

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

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

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

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

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

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

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

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

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

144 lved in the formation of miRNAs includes the Drosha/DGCR8 complex, which processes primary-miRNA to p

145 c RNAs (scaRNAs) is directly mediated by the Drosha/DGCR8 complex.

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

147 iency of pri-mir-19a and mir-15b~16-2 by the DROSHA/DGCR8 microprocessor.

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

149 enzyme complex known as the Microprocessor (Drosha/DGCR8).

150 Although mir-451 is fully dependent on Drosha/DGCR8, its short stem and small terminal loop ren

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

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

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

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

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

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

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

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

159 Enhanced Drosha expression did not alter global miRNA production

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

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

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

163 hanism mediates stress-induced inhibition of Drosha function.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

192 DROSHA is a nuclear RNase III enzyme responsible for cle

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

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

195 However, little is known whether Drosha is regulated.

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

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

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

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

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

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

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

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

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

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

206 Drosha-knockdown cells produced extracellular vesicles t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Inhibition of DROSHA or Argonaute 2, or disruption of microRNA recogni

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

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

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

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

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

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 other miRNA processing cofactors, including DROSHA, PASHA, or Argonaute.

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

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

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

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

253 in primary-miRNAs (pri-miRNAs) and promotes DROSHA processing to precursor-miRNAs (pre-miRNAs).

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

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

256 structures are critical to the precision of Drosha processing.

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

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

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

260 that ubiquitination and acetylation regulate Drosha protein levels oppositely.

261 Elevated Drosha protein levels were required to maintain the incr

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

263 some inhibitors MG132 or Omuralide increases Drosha protein levels.

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

265 DGCR8 and Drosha recognize and cleave primary transcripts of micro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

280 ly parallel functional assay termed Dro-seq (Drosha sequencing) that enables testing of hundreds of k

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

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

283 cleavage sites suggested higher fidelity of Drosha than Dicer.

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

285 Drosha, the catalytic core of the microprocessor complex

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

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

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

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

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

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

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

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

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

295 zed by a four-way intramolecular junction in Drosha, triggered by the Belt and Wedge regions that cla

296 Drosha was induced by nutrient and energy deprivation an

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

298 (12Z) in which the miRNA processing enzyme, DROSHA, was knocked down resulted in an enrichment in th

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.