Affinage

DROSHA

Ribonuclease 3 · UniProt Q9NRR4

Length
1374 aa
Mass
159.3 kDa
Annotated
2026-06-09
100 papers in source corpus 41 papers cited in narrative 41 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

DROSHA is the catalytic nuclease that initiates microRNA biogenesis, executing the nuclear cleavage of primary miRNA transcripts (pri-miRNAs) into pre-miRNA hairpins (PMID:14508493, PMID:26976605). Its two RNase III domains form an intramolecular dimer that cleaves the 3' and 5' strands of the pri-miRNA stem, and it operates within a ~650 kDa complex that depends on the dsRNA-binding cofactor DGCR8 (PMID:15574589). Substrate selection is governed by a molecular-ruler mechanism: cryo-EM structures of the Microprocessor show that Belt and Wedge regions clamp the basal ssRNA-dsRNA junction while dsRBDs measure stem length between the basal and apical junctions, positioning the catalytic centers ~11 nt from the basal junction and ~22 nt from the apical loop (PMID:32220646, PMID:32220645, PMID:24297910, PMID:15565168), with DGCR8-bound heme enhancing processing fidelity (PMID:29170488). Cofactors tune Microprocessor activity toward specific pri-miRNA subsets, including the DEAD-box helicases p68/DDX5 and p72/DDX17 (PMID:17435748), TGF-β/BMP SMAD transducers acting through DDX5 (PMID:18548003), BRCA1 (PMID:22492723), and SRSF3, which recruits DROSHA via a CNNC motif positioned at a defined distance from the cleavage site (PMID:29615481). Beyond canonical miRNA production, DROSHA directly cleaves miRNA-like hairpins embedded in mRNAs—including DGCR8, Neurogenin2, and myelopoiesis inhibitors—to destabilize them in a miRNA-independent manner, controlling neural stem cell fate and dendritic cell development (PMID:19135890, PMID:22706270, PMID:26437240), and it participates in the DNA damage response by generating site-specific DDRNAs and DNA:RNA hybrids at double-strand breaks required for secondary recruitment of DDR mediators and efficient repair (PMID:22722852, PMID:29416038, PMID:26906421). DROSHA protein abundance and activity are extensively regulated post-translationally: phosphorylation at S300/S302 controls nuclear localization and is potentiated by GSK3β but disrupted by stress-activated p38 MAPK (PMID:20554852, PMID:27907888, PMID:25699712), while Mdm2-mediated ubiquitination downstream of mTORC1 drives degradation and is opposed by p300/CBP/GCN5 acetylation (PMID:25639470, PMID:24009686). DROSHA RNase IIIb domain mutations cause Wilms tumor through a dominant-negative block of global miRNA biogenesis (PMID:25190313, PMID:24909261).

Mechanistic history

Synthesis pass · year-by-year structured walk · 26 steps
  1. 2003 High

    Established that miRNA maturation requires a dedicated nuclear nuclease, identifying Drosha as the enzyme that performs the initiation cleavage of pri-miRNA.

    Evidence In vitro cleavage with immunopurified Drosha plus RNAi knockdown with Northern/RT-PCR readout

    PMID:14508493

    Open questions at the time
    • Did not define cofactor requirements
    • Did not establish substrate recognition rules
  2. 2004 High

    Resolved the catalytic architecture and identified DGCR8 as the essential partner, defining the Microprocessor and explaining how two RNase III domains cut the two stem strands.

    Evidence RNase III domain mutagenesis, size fractionation, Co-IP, DGCR8 RNAi, biochemical reconstitution

    PMID:15574589

    Open questions at the time
    • No atomic structure of substrate engagement
    • Roles of additional complex subunits unknown
  3. 2004 High

    Defined the first substrate recognition rules—loop size and helical-turn measurements—showing how Drosha positions its cuts relative to RNA structural landmarks.

    Evidence In vitro cleavage with systematic mutant pri-miRNA substrates

    PMID:15565168

    Open questions at the time
    • Did not resolve the basal junction contribution clarified later
    • Structural basis of measurement unknown
  4. 2007 High

    Showed that DEAD-box helicases p68/p72 are Microprocessor subunits needed for processing a subset of pri-miRNAs and for rRNA processing, establishing cofactor-selective regulation.

    Evidence Mouse knockouts, miRNA microarray, in vitro processing with purified complex, ATPase-dead rescue

    PMID:17435748

    Open questions at the time
    • Which pri-miRNAs depend on helicases not fully mapped
    • Mechanism of helicase-assisted processing unresolved
  5. 2008 High

    Linked extracellular signaling to miRNA biogenesis by showing SMADs recruit to pri-miR-21 via DDX5 to accelerate its processing, revealing signal-responsive Microprocessor activity.

    Evidence RIP, Western/Northern, siRNA, SMAD4-null cells

    PMID:18548003

    Open questions at the time
    • Generality across other pri-miRNAs limited
    • Direct contact of SMAD with RNA vs DROSHA not fully separated
  6. 2009 High

    Discovered the DROSHA-DGCR8 homeostatic feedback loop and a class of miRNA-independent mRNA targets, broadening DROSHA function beyond miRNA biogenesis.

    Evidence Reporter assays, Co-IP, reciprocal knockdown Westerns, microarray; tiling array in Drosophila

    PMID:19135890 PMID:19223442

    Open questions at the time
    • Physiological scope of non-miRNA cleavage targets unclear
    • How specificity for mRNA hairpins is achieved unknown
  7. 2010 High

    Identified S300/S302 phosphorylation as the determinant of Drosha nuclear localization, introducing post-translational control of Microprocessor compartmentalization.

    Evidence Truncation mapping, mass spectrometry, alanine/phosphomimetic mutagenesis, fractionation/IF

    PMID:20554852

    Open questions at the time
    • Kinase identity not established here
    • Conditions regulating phosphorylation unknown
  8. 2012 High

    Extended DROSHA into the DNA damage response, showing DROSHA/DICER-generated DDRNAs are required for DDR focus formation and checkpoint activation.

    Evidence siRNA knockdown, DDR foci IF, RNase A treatment, single-break deep sequencing, DDRNA rescue

    PMID:22722852

    Open questions at the time
    • Mechanism of DDRNA biogenesis at breaks not fully defined
    • Direct vs indirect role of DROSHA catalysis unclear
  9. 2012 High

    Demonstrated miRNA-independent mRNA cleavage controls cell fate, showing DROSHA destabilizes Neurog2 mRNA to maintain neural stem cell identity distinct from Dicer.

    Evidence Conditional Drosha/DGCR8 (not Dicer) knockout in mouse forebrain, RIP, forced Ngn2 rescue, conservation analysis

    PMID:22706270

    Open questions at the time
    • Full target repertoire in neural progenitors unknown
    • Regulation of this cleavage activity unclear
  10. 2012 Medium

    Identified BRCA1 as a Microprocessor-associated factor enhancing processing of specific pri-miRNAs, adding a tumor-suppressor input to miRNA biogenesis.

    Evidence Co-IP, in vitro processing, Northern blot, direct RNA-binding assay

    PMID:22492723

    Open questions at the time
    • Single-lab finding
    • Mechanism of pri-miRNA selectivity by BRCA1 unclear
  11. 2013 High

    Refined the cleavage-site rules into a dual-junction ruler model, explaining isomiR generation when junction distances are non-optimal.

    Evidence moRNA cleavage-site mapping, lower/upper junction mutations, in-cell processing assays

    PMID:24297910

    Open questions at the time
    • Structural basis awaited cryo-EM
    • Quantitative contribution of each junction not fully partitioned
  12. 2013 Medium

    Showed acetylation/ubiquitination antagonism controls DROSHA protein stability, and that pathogen infection can lower DROSHA via ubiquitination.

    Evidence Deacetylase and proteasome inhibitor treatment, Co-IP for acetylation, Western, miR-143 readout

    PMID:24009686

    Open questions at the time
    • E3 ligase not identified here
    • Acetylation sites not precisely mapped
  13. 2013 Medium

    Identified transcriptional and translational inputs to DROSHA levels, with c-Myc transactivating the promoter and FMRP enhancing DROSHA translation.

    Evidence ChIP and reporter assays (c-Myc); polysome analysis and Fmr1-KO mice (FMRP)

    PMID:23735886 PMID:26993298

    Open questions at the time
    • Single-lab findings
    • Interplay with post-translational regulation not integrated
  14. 2014 High

    Established DROSHA as a cancer driver, showing RNase IIIb mutations (including E1147K) act dominant-negatively to globally suppress miRNA biogenesis in Wilms tumor.

    Evidence Exome sequencing, in vitro processing with mutants, CRISPR editing, miRNA profiling

    PMID:24909261 PMID:25190313

    Open questions at the time
    • Tumor-specific miRNA targets driving phenotype not fully defined
    • Therapeutic vulnerability unexplored
  15. 2014 Medium

    Revealed cleavage-independent DROSHA functions in splicing and uncovered MeCP2 as an inhibitor of Microprocessor assembly, expanding regulatory inputs.

    Evidence Splicing reporters with catalytic-dead Drosha (eIF4H); Co-IP and neuronal morphology (MeCP2-DGCR8)

    PMID:24636259 PMID:24786770

    Open questions at the time
    • Single-lab findings
    • Generality of cleavage-independent splicing role unknown
  16. 2015 High

    Connected nutrient/stress signaling to DROSHA turnover, identifying Mdm2 as its mTORC1-driven E3 ligase and p38 MAPK as a stress kinase driving export and degradation.

    Evidence Tsc1/Raptor genetics, Mdm2 knockdown/overexpression and ubiquitination assays; p38 kinase assay, fractionation, calpain inhibition, cell death assays

    PMID:25639470 PMID:25699712

    Open questions at the time
    • Crosstalk between phosphorylation and ubiquitination not fully integrated
    • Physiological triggers in vivo partially defined
  17. 2015 High

    Generalized miRNA-independent mRNA cleavage to hematopoiesis, showing DROSHA degrades myelopoiesis-inhibitor mRNAs to enable dendritic cell development.

    Evidence Conditional Drosha/Dicer knockout in progenitors, in vitro cleavage of target stem-loops, mRNA expression

    PMID:26437240

    Open questions at the time
    • Full set of hematopoietic mRNA substrates unknown
    • Regulation of target selection unclear
  18. 2016 High

    Defined DROSHA as essential for essentially all canonical miRNAs using clean genetic knockouts, distinguishing its role from XPO5-mediated export.

    Evidence CRISPR knockout of DROSHA/XPO5/DICER in one human line, small RNA-seq, Northern

    PMID:26976605

    Open questions at the time
    • Mechanism of DROSHA-independent non-canonical miRNAs not fully resolved
  19. 2016 Medium

    Showed DROSHA can act outside the nucleus, with RS-domain-deficient alternative isoforms processing pri-miRNAs in the cytoplasm in a DGCR8-dependent manner.

    Evidence RT-PCR isoform identification, fractionation/IF, processing assays, KO-cell reporter, cytoplasmic cleavage assays

    PMID:27185895 PMID:27471035

    Open questions at the time
    • Physiological significance of cytoplasmic processing unclear
    • Single-lab findings
  20. 2016 High

    Identified GSK3β as the kinase phosphorylating Drosha at S300/S302 to promote cofactor binding and pri-miRNA processing activity, linking the localization sites to catalytic regulation.

    Evidence Co-IP with Microprocessor components, kinase assay, phosphomimetic mutants, pri-miRNA accumulation, GSK3β inhibition

    PMID:27907888

    Open questions at the time
    • Signaling upstream of GSK3β toward Drosha unclear
    • Interplay with p38-mediated phosphorylation not resolved
  21. 2017 High

    Mapped DROSHA cleavage genome-wide at single-nucleotide resolution and identified DGCR8-bound heme as a fidelity determinant, refining mechanistic understanding of substrate processing.

    Evidence fCLIP-seq cleavage mapping; in vitro processing with heme-depleted/reconstituted and heme-mutant DGCR8 plus conformational assays

    PMID:28431232 PMID:29170488

    Open questions at the time
    • Functional roles of many non-miRNA cleavage sites unknown
    • How heme sensing is physiologically regulated unclear
  22. 2017 Medium

    Demonstrated DROSHA autoregulates its own pre-mRNA splicing via a conserved hairpin independent of catalysis, adding a feedback layer to its expression.

    Evidence Minigene splicing reporters, catalytic-dead mutant, endogenous mRNA analysis, knockdown, conservation analysis

    PMID:28400409

    Open questions at the time
    • Species specificity (human not mouse) mechanism unclear
    • Single-lab finding
  23. 2018 High

    Resolved the structural basis of substrate recognition by cryo-EM, defining the Belt/Wedge basal-junction clamp and dsRBD molecular ruler, with autoinhibitory and partially docked states.

    Evidence Two independent cryo-EM structures of Drosha-DGCR8 with/without pri-miRNA plus structure-guided mutagenesis

    PMID:32220645 PMID:32220646

    Open questions at the time
    • Dynamics of conformational transitions during catalysis not fully captured
    • Structural basis of cofactor modulation not resolved
  24. 2018 High

    Strengthened the DDR role by showing DROSHA controls R-loop formation at breaks and is required for both HR and NHEJ and for secondary mediator recruitment.

    Evidence Drosha depletion, HR/NHEJ assays, DRIP-seq at DSBs, RNase H treatment, kinetics; NBS1 vs MDC1/53BP1 IF with DDRNA rescue

    PMID:26906421 PMID:29416038

    Open questions at the time
    • How DROSHA is recruited to breaks unknown
    • Relationship between DDRNA and R-loop functions not fully integrated
  25. 2018 Medium

    Extended DROSHA function to antiviral defense, showing CRM1-dependent nuclear-to-cytoplasmic translocation upon RNA virus infection coincides with viral RNA cleavage.

    Evidence Drosha-deletion cells with diverse RNA viruses, leptomycin B export block, cycloheximide, viral RNA quantification, IF

    PMID:24778219

    Open questions at the time
    • Trigger for export not defined
    • Single-lab finding without structural mechanism
  26. 2020 Medium

    Identified a cleavage-independent transcriptional role for DROSHA via β-Catenin to transactivate STC1 and an m6A-based mechanism stabilizing DROSHA mRNA in cancer stem cells.

    Evidence Co-IP with β-Catenin, m6A-deficient mutant, AURKA modulation, ChIP, IGF2BP2 pulldown

    PMID:32859993

    Open questions at the time
    • Single-lab finding
    • Generality of transcriptional coactivator role unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How DROSHA's distinct activities—canonical miRNA processing, miRNA-independent mRNA cleavage, DDR/R-loop functions, and cleavage-independent roles—are coordinated and selectively deployed across cellular contexts remains unresolved.
  • No unified model linking distinct functional modes
  • Recruitment determinants for non-miRNA substrates undefined
  • Integration of multilayered PTM regulation in vivo incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140098 catalytic activity, acting on RNA 5 GO:0003723 RNA binding 4 GO:0016787 hydrolase activity 3 GO:0140097 catalytic activity, acting on DNA 2
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 3 GO:0005654 nucleoplasm 2
Pathway
R-HSA-73894 DNA Repair 3 R-HSA-8953854 Metabolism of RNA 3 R-HSA-1643685 Disease 2 R-HSA-74160 Gene expression (Transcription) 2
Partners
BRCA1DDX17DDX5DGCR8GSK3BMDM2SRSF3
Complex memberships
Microprocessor complex

Evidence

Reading pass · 41 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 Human Drosha, a nuclear RNase III enzyme, is the core nuclease that executes the initiation step of miRNA processing: immunopurified Drosha cleaved pri-miRNA to release pre-miRNA in vitro, and RNAi-mediated depletion of Drosha caused accumulation of pri-miRNA and reduction of pre-miRNA and mature miRNA in vivo. In vitro cleavage assay with immunopurified Drosha; RNA interference knockdown with Northern blot/RT-PCR readout Nature High 14508493
2004 Drosha's two RNase III domains (A and B) form an intramolecular dimer and cleave the 3' and 5' strands of the pri-miRNA stem respectively, mirroring the mechanism of Dicer. Drosha functions in a ~650 kDa complex and requires DGCR8 (which contains two dsRNA-binding domains) as an essential partner for pri-miRNA processing, demonstrated by RNAi depletion of DGCR8 and biochemical reconstitution. Mutational analysis of RNase III domains; size-exclusion fractionation; co-immunoprecipitation; RNAi knockdown of DGCR8; biochemical reconstitution of processing complex Genes & development High 15574589
2004 Drosha selectively cleaves RNA hairpins bearing a large (≥10 nt) terminal loop, measuring ~two helical RNA turns (~22 nt) from the loop-stem junction into the stem to produce pre-miRNA; approximately one helical turn of stem extension beyond the cleavage site is also essential for efficient processing. In vitro cleavage assays with systematic mutant pri-miRNA substrates; measurement of cleavage site positions relative to structural features The EMBO journal High 15565168
2007 The DEAD-box RNA helicases p68 (DDX5) and p72 (DDX17) are subunits of the mouse Drosha complex; both are required for processing of a subset of pri-miRNAs and for 5.8S rRNA processing. The purified mouse Drosha large complex generates pre-miRNA and 5.8S rRNA in vitro, and the ATPase activity of p72 is required for its function. Genetic knockout of p68 and p72 in mice; microarray miRNA profiling; in vitro processing assay with purified Drosha complex; ATPase-dead mutant rescue experiment Nature cell biology High 17435748
2008 TGF-β/BMP-specific SMAD signal transducers are recruited to pri-miR-21 RNA in a complex with the RNA helicase p68 (DDX5), a component of the DROSHA microprocessor complex, promoting rapid post-transcriptional processing of pri-miR-21 into pre-miR-21 without requiring the shared cofactor SMAD4. RNA immunoprecipitation showing SMAD association with pri-miR-21 and DROSHA complex; Western blot and Northern blot for miR-21 processing; siRNA knockdown; SMAD4-null cell line experiments Nature High 18548003
2009 Drosha and DGCR8 post-transcriptionally regulate each other: the Drosha-DGCR8 complex cleaves hairpin structures embedded in DGCR8 mRNA to destabilize it, while DGCR8 stabilizes the Drosha protein via direct protein-protein interaction, forming a homeostatic feedback loop. Additionally, the Microprocessor can downregulate a subset of cellular mRNAs in a miRNA-independent manner. Reporter assays with DGCR8 mRNA hairpins; co-immunoprecipitation; Western blot for Drosha and DGCR8 protein levels under reciprocal knockdown; microarray analysis of mRNA targets Cell High 19135890
2009 Drosha/Pasha (DGCR8) complex cleaves hairpin structures in pasha/DGCR8 mRNA 5' UTR in a negative feedback loop; genome-wide tiling array identifies >100 additional non-miRNA Drosha-regulated transcripts containing evolutionarily conserved hairpins, distinct from dicer-1-regulated targets. Tiling microarray after Drosha RNAi in Drosophila S2 cells; comparison with Dicer-1 knockdown; bioinformatic evofold analysis for conserved hairpins RNA (New York, N.Y.) Medium 19223442
2010 Drosha nuclear localization requires phosphorylation at Serine300 or Serine302 in its N-terminal domain (aa 270–390). Double S300A/S302A mutations completely abolish nuclear localization, while phosphomimetic S300E/S302D mutations restore it; phosphorylation at either site alone is sufficient. Truncation constructs to map nuclear localization domain; mass spectrometry identification of phosphorylation sites; site-directed mutagenesis (alanine and phosphomimetic substitutions); subcellular fractionation and immunofluorescence Nucleic acids research High 20554852
2010 NMR solution structure of the Drosha C-terminal double-stranded RNA-binding domain (dsRBD) reveals an αβββα fold with a unique extended loop; the domain retains structural features consistent with RNA binding and may contribute to substrate recognition within the Microprocessor complex. NMR spectroscopy; structural comparison with other dsRBDs Silence Medium 20226070
2012 DROSHA and DICER generate site-specific small RNAs (DDRNAs) at DNA double-strand break sites that are required for activation of the DNA damage response (DDR); depletion of DROSHA impairs DDR foci formation and checkpoint activation, and in vitro-generated DROSHA/DICER cleavage products restore DDR in RNase A-treated cells. siRNA knockdown of DROSHA/DICER; DDR foci immunofluorescence; RNase A treatment; RNA deep sequencing at single inducible DSB; chemically synthesized and in vitro generated DDRNAs used for rescue Nature High 22722852
2012 BRCA1 directly associates with DROSHA, DDX5 (p68), Smad3, p53, and DHX9 within the DROSHA microprocessor complex, and directly binds primary miRNA transcripts via its DNA-binding domain; BRCA1 enhances processing of let-7a-1, miR-16-1, miR-145, and miR-34a pri-miRNAs. Co-immunoprecipitation; in vitro processing assay; Northern blot for pre-miRNA and mature miRNA levels; direct RNA-binding assay The Journal of cell biology Medium 22492723
2012 Drosha directly cleaves stem-loop structures within Neurogenin 2 (Ngn2) mRNA in neural progenitors in a miRNA-independent manner, destabilizing the transcript and thereby maintaining neural stem cell character; this is distinct from Dicer function, as Dicer deficiency does not phenocopy Drosha loss in this context. Conditional knockout of Drosha and DGCR8 (but not Dicer) in mouse forebrain neural progenitors; RNA immunoprecipitation showing Neurog2 mRNA association with Microprocessor; forced Ngn2 expression phenocopy; evolutionary conservation analysis of hairpins in Neurog2 mRNA Nature neuroscience High 22706270
2013 DGCR8 protein sequestration by expanded CGG RNA repeats (FXTAS) co-sequesters its partner DROSHA within nuclear CGG RNA aggregates, reducing miRNA processing and mature miRNA levels in neuronal cells; overexpression of DGCR8 rescues neuronal cell death induced by expanded CGG repeats. Immunofluorescence co-localization; DGCR8 overexpression rescue assay; miRNA profiling by qRT-PCR; analysis of FXTAS patient brain tissue Cell reports Medium 23478018
2013 Drosha cleavage site selection is determined by measuring distances from both the lower stem–ssRNA (basal) junction (~11 nt) and upper stem–ssRNA (apical loop) junction (~22 nt); non-optimal distances cause Drosha to cleave at multiple sites, generating multiple 5' isomiR variants. miRNA-offset RNA assay to define cleavage sites; systematic mutation of lower and upper junctions; in-cell processing assays in human cells Proceedings of the National Academy of Sciences of the United States of America High 24297910
2013 Ubiquitination and acetylation oppositely regulate Drosha protein stability: acetylation at the N-terminus by p300, CBP, or GCN5 competes with ubiquitination and inhibits proteasomal degradation of Drosha; H. pylori infection promotes ubiquitination and reduction of Drosha protein without affecting mRNA levels. Deacetylase inhibitor treatment (TSA, NIA); proteasome inhibitor treatment (MG132); co-immunoprecipitation for acetylation; Western blot; miRNA sensor assay and qPCR for miR-143 PloS one Medium 24009686
2014 DROSHA RNase IIIB domain missense mutations in Wilms tumors act via a dominant-negative mechanism to globally inhibit miRNA biogenesis, distinct from DICER1 mutations which preferentially impair 5'-arm miRNA processing; demonstrated by in vitro processing assays and genomic editing in human cell lines. Whole-exome sequencing; in vitro pri-miRNA processing assays with mutant DROSHA; CRISPR/genomic editing to introduce mutations; miRNA expression profiling Nature communications High 25190313
2014 The recurrent DROSHA E1147K mutation (affecting a metal-binding residue in the RNase IIIb domain) predominantly downregulates a subset of mature miRNAs without affecting pri-miRNA levels, confirming that this mutation specifically impairs pri-miRNA processing activity. Whole-exome sequencing; targeted sequencing; miRNA expression profiling; cell lines expressing mutant DROSHA; confirmation that pri-miRNA levels are unchanged Nature communications High 24909261
2014 MeCP2 directly binds DGCR8 and interferes with assembly of the Drosha-DGCR8 complex, suppressing nuclear miRNA processing; gain-of-function MeCP2 inhibits dendritic and spine growth through this DGCR8-interaction-dependent mechanism. Co-immunoprecipitation of MeCP2 with DGCR8; in vitro binding assay; miRNA processing assay; neuronal morphology analysis with MeCP2-DGCR8 interaction mutants Developmental cell Medium 24636259
2014 Drosha has a cleavage-independent role in promoting splicing of the alternatively spliced exon 5 of eIF4H, which contains a hairpin resembling a Drosha substrate; Drosha binds this exon and enhances its splicing in a structure-dependent but cleavage-independent manner. In vitro cleavage assay; splicing reporter assays in cells; Drosha knockdown; catalytic mutant Drosha constructs to separate cleavage from binding function PLoS genetics Medium 24786770
2015 mTORC1 activation increases expression of Mdm2, which functions as the ubiquitin E3 ligase for Drosha, promoting its ubiquitination and degradation; conversely, nutrient/energy deprivation (which suppresses mTORC1) stabilizes Drosha. TSC1 mutation (activating mTORC1) reduces miRNA levels via Drosha degradation, while Raptor mutation increases miRNA biogenesis. Genetic mutation of Tsc1 and Raptor; Mdm2 identified as necessary and sufficient E3 ligase by knockdown/overexpression; ubiquitination assays; high-throughput miRNA library screen Molecular cell High 25639470
2015 Under stress, p38 MAPK directly phosphorylates Drosha at its N-terminus, reducing its interaction with DGCR8, promoting nuclear export of Drosha, and leading to its degradation by calpain, thereby inhibiting Drosha-mediated miRNA biogenesis and sensitizing cells to stress-induced death. Kinase assay showing direct p38 phosphorylation of Drosha; co-immunoprecipitation for Drosha-DGCR8 interaction; subcellular fractionation; calpain inhibitor experiments; cell death assays with Drosha overexpression/depletion Molecular cell High 25699712
2015 Drosha directly cleaves stem-loop structures within mRNAs encoding two inhibitors of myelopoiesis in early hematopoietic progenitors in a miRNA-independent manner, and this mRNA degradation is necessary for dendritic cell development and myelopoiesis; Drosha deficiency completely halted DC development, a more severe phenotype than Dicer deficiency. Conditional knockout of Drosha and Dicer in hematopoietic progenitors; in vitro cleavage assays showing direct Drosha cleavage of target mRNA stem-loops; mRNA expression analysis Nature immunology High 26437240
2016 DROSHA is essential for canonical miRNA production: DROSHA knockout in human cells completely abolishes canonical miRNA biogenesis, while only a few DROSHA-independent non-canonical miRNAs persist. In contrast, XPO5 knockout has only modest effects on most miRNAs, indicating complementary nuclear export mechanisms exist. CRISPR knockout of DROSHA, XPO5, and DICER in the same human cell line; small RNA sequencing; northern blotting Proceedings of the National Academy of Sciences of the United States of America High 26976605
2016 SRSF3 (SRp20) recruits DROSHA to the basal junction of pri-miRNAs by binding the CNNC motif located ~17 nt from the Microprocessor cleavage site; this stimulation of processing efficiency only occurs when CNNC is at this precise position, establishing a distance-dependent mechanism for cofactor-assisted DROSHA recruitment. In vitro processing assays with CNNC-mutant pri-miRNA substrates; co-immunoprecipitation of SRSF3 with DROSHA; CNNC position-scanning substrates; SRSF3 knockdown RNA (New York, N.Y.) High 29615481
2016 Alternative splicing of Drosha produces isoforms lacking part of the arginine/serine-rich (RS) domain that localize to both nucleus and cytoplasm, in contrast to full-length isoforms which are exclusively nuclear; cytoplasmic isoforms retain pri-miRNA processing activity and cofactor binding. Endogenous mRNA isoform expression correlates with subcellular distribution of Drosha protein. RT-PCR identification of splice isoforms; subcellular fractionation; immunofluorescence; processing activity assays with isoform-specific constructs; correlation of endogenous isoform mRNA with protein localization Nucleic acids research Medium 27185895
2016 A cytoplasmic Drosha isoform generated by alternative splicing (lacking the nuclear localization signal) can process pri-miRNAs in the cytoplasm in a DGCR8-dependent manner; in vitro-transcribed pri-miRNAs transfected into cells are processed to mature miRNAs in the cytoplasm. Identification of cytoplasmic Drosha isoforms; Drosha/DGCR8 knockout cell reporter assay; cytoplasmic cleavage assay with truncated Drosha mutant; transfection of in vitro-generated pri-miRNA into cells Nucleic acids research Medium 27471035
2017 fCLIP-seq (formaldehyde crosslinking, immunoprecipitation, and sequencing) maps DROSHA cleavage sites at single-nucleotide resolution genome-wide, revealing widespread end modifications during miRNA maturation, alternative processing yielding multiple miRNA isoforms, and dozens of DROSHA cleavage substrates on non-miRNA loci that may serve as cis-regulatory elements. fCLIP-seq (formaldehyde crosslinking + IP + sequencing); single-nucleotide resolution cleavage site mapping; comparison with canonical and non-canonical substrates Molecular cell High 28431232
2017 Heme bound to DGCR8 is critical for Microprocessor to process pri-miRNAs with high fidelity; heme induces a conformational change in DGCR8 (rather than altering its oligomerization state) that enables it to correct erroneous Drosha binding events on pri-miRNAs, specifically by recognizing the terminal loop near the 3' single-stranded segment. In vitro processing assays with heme-depleted/reconstituted DGCR8; heme-binding mutant DGCR8; FRET/structural assays for DGCR8 conformational change; processing fidelity assays with multiple pri-miRNA substrates Nature communications High 29170488
2017 DROSHA targets a conserved hairpin structure spanning an exon-intron junction in its own pre-mRNA to promote skipping of the overlapping exon, regulating its own alternative splicing independently of its cleavage activity; this autoregulation is present in human but not murine cells. Minigene splicing reporter assays; catalytic-dead DROSHA mutant; endogenous DROSHA mRNA analysis; DROSHA knockdown; evolutionary conservation analysis RNA (New York, N.Y.) Medium 28400409
2017 GSK3β associates with DGCR8 and p72 within the Microprocessor complex in an RNA-dependent manner, phosphorylates Drosha at S300 and/or S302, and thereby promotes Drosha activity, cofactor interactions, and pri-miRNA binding. Inhibition of GSK3β reduces Drosha activity toward pri-miRNAs, accumulating unprocessed pri-miRNAs without altering Drosha protein levels or localization. Co-immunoprecipitation of GSK3β with Microprocessor components; kinase assay; phosphomimetic Drosha mutants (S300E/S302D); pri-miRNA accumulation by RT-PCR; pharmacological GSK3β inhibition Nucleic acids research High 27907888
2018 Drosha controls formation of DNA:RNA hybrids (R-loops) around DNA double-strand break sites; depletion of Drosha reduces DNA repair by both homologous recombination and non-homologous end joining, and is required within minutes of break induction. Removal of the RNA component of these DNA:RNA hybrid structures impairs repair. siRNA/shRNA depletion of Drosha; HR and NHEJ repair assays; DNA:RNA hybrid sequencing (DRIP-seq) around DSB sites; RNase H treatment to remove R-loops; kinetics of Drosha requirement after break induction Nature communications High 29416038
2018 In response to RNA virus infection, Drosha undergoes exportin 1 (XPO1/CRM1)-dependent translocation from the nucleus to the cytoplasm independently of de novo protein synthesis or type I IFN signaling; cytoplasmic Drosha correlates with cleavage of viral genomic RNA and modulation of the host transcriptome, contributing to antiviral defense. Drosha deletion cells infected with diverse RNA viruses; CRM1 inhibitor (leptomycin B) blocking nuclear export; cycloheximide to exclude new protein synthesis; viral RNA quantification; Drosha localization by immunofluorescence Proceedings of the National Academy of Sciences of the United States of America Medium 24778219
2018 TDP-43 and FUS proteins interact with Drosha and stabilize it; phosphomimetic TDP-43 (S409/410E) disrupts FUS-Drosha protein-protein interaction, reducing Drosha stability and inducing cytotoxicity in neuronal cells. Co-immunoprecipitation of TDP-43/FUS with Drosha; cycloheximide chase for protein stability; gain- and loss-of-function of TDP-43/FUS; site-directed phosphomimetic mutagenesis; cell viability assay Biochemical and biophysical research communications Low 26102026
2020 Cryo-EM structure of human Drosha-DGCR8 Microprocessor with pri-miRNA docked in the active site reveals that the basal junction is recognized by a four-way intramolecular junction in Drosha via Belt and Wedge regions that clamp over ssRNA; two dsRBDs act as a molecular ruler measuring stem length between the two dsRNA-ssRNA junctions. A second structure (partially docked state) shows the apical junction dsRBD organization is independent of Drosha core domains. Cryo-electron microscopy structure determination; mutagenesis of Belt and Wedge regions; pri-miRNA processing fidelity assays Molecular cell High 32220646
2020 Cryo-EM structure of Drosha-DGCR8 without and with pri-miRNA shows that a helix hairpin in the extended PAZ domain and the mobile basic (MB) helix in the RNase IIIa domain coordinate to recognize the ssRNA-dsRNA basal junction; the dsRBD makes extensive contacts with the RNA stem. An autoinhibitory conformation of the PAZ helix hairpin is revealed in the apo structure. Cryo-electron microscopy structure determination of RNA-bound and apo Drosha-DGCR8 complex; structure-guided mutagenesis Molecular cell High 32220645
2020 DROSHA interacts with β-Catenin to transactivate STC1 in an RNA cleavage-independent manner, contributing to breast cancer stem-like cell properties. DROSHA mRNA is stabilized by AURKA-promoted m6A methylation (via METTL14 stabilization) and IGF2BP2-mediated recognition of m6A-modified DROSHA transcript. Co-immunoprecipitation of DROSHA with β-Catenin; DROSHA m6A methylation-deficient mutant; AURKA overexpression/knockdown; ChIP for β-Catenin at STC1 promoter; IGF2BP2 pulldown Cell research Medium 32859993
2013 c-Myc directly binds the E-box of the Drosha promoter (confirmed by ChIP) and transactivates Drosha mRNA expression, thereby upregulating Drosha protein levels and promoting miRNA processing both in vitro and in vivo. Chromatin immunoprecipitation (ChIP) at Drosha promoter; reporter assay; Western blot for Drosha protein; in vitro and in vivo miRNA processing assays Scientific reports Medium 23735886
2013 FMRP (Fragile X mental retardation protein) binds Drosha mRNA and enhances its translation without affecting mRNA stability, thereby promoting pri-miRNA processing; loss of FMRP in Fmr1-knockout mice reduces Drosha protein (not mRNA) and causes accumulation of pri-miRNAs with reduced pre-miRNA and mature miRNA. Co-immunoprecipitation and polysome analysis showing FMRP binding to Drosha mRNA; Western blot for Drosha protein vs mRNA in FMRP-KO mice; FMRP overexpression/knockdown; miRNA Northern blot Molecular neurobiology Medium 26993298
2011 Drosha knockdown in human mesenchymal stem cells causes G1 phase cell cycle arrest via a miRNA-independent mechanism, with increased p15 and p16 CDK inhibitors, reduced pRB, and significantly reduced 28S and 18S rRNA levels; Dicer knockdown does not phenocopy these effects, implicating Drosha in rRNA processing. Lentiviral inducible shRNA knockdown of Drosha and Dicer; cell cycle analysis by flow cytometry; ELISA for pRB; RT-PCR for rRNA transcripts; comparison of Drosha vs Dicer knockdown The international journal of biochemistry & cell biology Medium 21794839
2016 DICER and DROSHA are required for secondary recruitment of DDR mediators MDC1 and 53BP1 to DNA damage sites but are dispensable for primary recruitment of the DDR sensor NBS1; DDRNAs are specifically required for this secondary amplification step. DICER/DROSHA inactivation; immunofluorescence for NBS1 (primary sensor) vs MDC1 and 53BP1 (secondary mediators); RNase A treatment; rescue with purified DDRNAs Journal of cell science High 26906421
2018 Drosha mislocalization to neuronal cytoplasmic inclusions occurs specifically in C9orf72 mutation FTLD-TDP and ALS cases (not cases without C9orf72 mutation), where it co-localizes with dipeptide-repeat protein aggregates (p62+, ubiquilin-2+) but rarely with TDP-43 pathology, suggesting a sequestration mechanism. Immunohistochemistry and immunofluorescence co-localization in patient brain tissues (hippocampus, frontal cortex, cerebellum) with multiple antibodies Journal of neuropathology and experimental neurology Low 25756586

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 The nuclear RNase III Drosha initiates microRNA processing. Nature 3851 14508493
2004 The Drosha-DGCR8 complex in primary microRNA processing. Genes & development 1654 15574589
2008 SMAD proteins control DROSHA-mediated microRNA maturation. Nature 1107 18548003
2007 Role of Dicer and Drosha for endothelial microRNA expression and angiogenesis. Circulation research 652 17540974
2008 Dicer, Drosha, and outcomes in patients with ovarian cancer. The New England journal of medicine 562 19092150
2004 Recognition and cleavage of primary microRNA precursors by the nuclear processing enzyme Drosha. The EMBO journal 441 15565168
2012 Site-specific DICER and DROSHA RNA products control the DNA-damage response. Nature 440 22722852
2016 Re-evaluation of the roles of DROSHA, Export in 5, and DICER in microRNA biogenesis. Proceedings of the National Academy of Sciences of the United States of America 359 26976605
2009 Posttranscriptional crossregulation between Drosha and DGCR8. Cell 352 19135890
2007 DEAD-box RNA helicase subunits of the Drosha complex are required for processing of rRNA and a subset of microRNAs. Nature cell biology 334 17435748
2008 The RNAseIII enzyme Drosha is critical in T cells for preventing lethal inflammatory disease. The Journal of experimental medicine 323 18725527
2015 Mutations in the SIX1/2 pathway and the DROSHA/DGCR8 miRNA microprocessor complex underlie high-risk blastemal type Wilms tumors. Cancer cell 245 25670083
2015 Recurrent DGCR8, DROSHA, and SIX homeodomain mutations in favorable histology Wilms tumors. Cancer cell 228 25670082
2014 MeCP2 suppresses nuclear microRNA processing and dendritic growth by regulating the DGCR8/Drosha complex. Developmental cell 208 24636259
2013 Sequestration of DROSHA and DGCR8 by expanded CGG RNA repeats alters microRNA processing in fragile X-associated tremor/ataxia syndrome. Cell reports 202 23478018
2014 Somatic mutations in DROSHA and DICER1 impair microRNA biogenesis through distinct mechanisms in Wilms tumours. Nature communications 196 25190313
2018 Drosha drives the formation of DNA:RNA hybrids around DNA break sites to facilitate DNA repair. Nature communications 177 29416038
2012 The RNase III enzyme DROSHA is essential for microRNA production and spermatogenesis. The Journal of biological chemistry 152 22665486
2014 Recurrent somatic mutation in DROSHA induces microRNA profile changes in Wilms tumour. Nature communications 144 24909261
2006 RNASEN regulates cell proliferation and affects survival in esophageal cancer patients. Clinical cancer research : an official journal of the American Association for Cancer Research 142 17121874
2012 BRCA1 regulates microRNA biogenesis via the DROSHA microprocessor complex. The Journal of cell biology 140 22492723
2006 Genome-wide analysis of mRNAs regulated by Drosha and Argonaute proteins in Drosophila melanogaster. Molecular and cellular biology 117 16581772
2016 DICER, DROSHA and DNA damage response RNAs are necessary for the secondary recruitment of DNA damage response factors. Journal of cell science 112 26906421
2020 Oncogenic AURKA-enhanced N6-methyladenosine modification increases DROSHA mRNA stability to transactivate STC1 in breast cancer stem-like cells. Cell research 109 32859993
2020 Cryo-EM Structures of Human Drosha and DGCR8 in Complex with Primary MicroRNA. Molecular cell 104 32220646
2012 Drosha regulates neurogenesis by controlling neurogenin 2 expression independent of microRNAs. Nature neuroscience 103 22706270
2008 Integrative genomics analysis of chromosome 5p gain in cervical cancer reveals target over-expressed genes, including Drosha. Molecular cancer 103 18559093
2017 Genome-wide Mapping of DROSHA Cleavage Sites on Primary MicroRNAs and Noncanonical Substrates. Molecular cell 100 28431232
2009 Genome-wide identification of targets of the drosha-pasha/DGCR8 complex. RNA (New York, N.Y.) 96 19223442
2018 Noncanonical functions of microRNA pathway enzymes - Drosha, DGCR8, Dicer and Ago proteins. FEBS letters 94 30025156
2012 Impaired expression of DICER, DROSHA, SBDS and some microRNAs in mesenchymal stromal cells from myelodysplastic syndrome patients. Haematologica 91 22371183
2020 Structural Basis for pri-miRNA Recognition by Drosha. Molecular cell 87 32220645
2006 Drosha in primary microRNA processing. Cold Spring Harbor symposia on quantitative biology 87 17381280
2013 Lower and upper stem-single-stranded RNA junctions together determine the Drosha cleavage site. Proceedings of the National Academy of Sciences of the United States of America 82 24297910
2016 Dysregulation of microRNA biogenesis in cancer: the impact of mutant p53 on Drosha complex activity. Journal of experimental & clinical cancer research : CR 81 26971015
2012 Inducible deletion of epidermal Dicer and Drosha reveals multiple functions for miRNAs in postnatal skin. Development (Cambridge, England) 79 22434867
2015 Swiss army knives: non-canonical functions of nuclear Drosha and Dicer. Nature reviews. Molecular cell biology 77 26016561
2015 An mTORC1-Mdm2-Drosha axis for miRNA biogenesis in response to glucose- and amino acid-deprivation. Molecular cell 73 25639470
2010 Phosphorylation of the RNase III enzyme Drosha at Serine300 or Serine302 is required for its nuclear localization. Nucleic acids research 72 20554852
2018 SRSF3 recruits DROSHA to the basal junction of primary microRNAs. RNA (New York, N.Y.) 69 29615481
2013 MicroRNA-independent roles of the RNase III enzymes Drosha and Dicer. Open biology 68 24153005
2011 Expression of the ribonucleases Drosha, Dicer, and Ago2 in colorectal carcinomas. Virchows Archiv : an international journal of pathology 68 21769619
2012 Argonaute, Dicer, and Drosha are up-regulated along tumor progression in serous ovarian carcinoma. Human pathology 67 22647351
2017 Nuclear Drosha enhances cell invasion via an EGFR-ERK1/2-MMP7 signaling pathway induced by dysregulated miRNA-622/197 and their targets LAMC2 and CD82 in gastric cancer. Cell death & disease 65 28252644
2015 Stress induces p38 MAPK-mediated phosphorylation and inhibition of Drosha-dependent cell survival. Molecular cell 65 25699712
2011 Functional evidence that Drosha overexpression in cervical squamous cell carcinoma affects cell phenotype and microRNA profiles. The Journal of pathology 65 21590768
2014 Drosha as an interferon-independent antiviral factor. Proceedings of the National Academy of Sciences of the United States of America 62 24778219
2013 c-Myc modulates microRNA processing via the transcriptional regulation of Drosha. Scientific reports 61 23735886
2018 Recurrent homozygous deletion of DROSHA and microduplication of PDE4DIP in pineoblastoma. Nature communications 60 30030436
2015 High copy number variation of cancer-related microRNA genes and frequent amplification of DICER1 and DROSHA in lung cancer. Oncotarget 59 26156018
2007 Oncogenic All1 fusion proteins target Drosha-mediated microRNA processing. Proceedings of the National Academy of Sciences of the United States of America 59 17581865
2017 Heme enables proper positioning of Drosha and DGCR8 on primary microRNAs. Nature communications 58 29170488
2011 Dysregulated expression of dicer and drosha in breast cancer. Pathology oncology research : POR 55 21898071
2016 Alternative splicing affects the subcellular localization of Drosha. Nucleic acids research 48 27185895
2013 Acetylation of drosha on the N-terminus inhibits its degradation by ubiquitination. PloS one 48 24009686
2017 Emerging roles of DROSHA beyond primary microRNA processing. RNA biology 46 29171328
2015 Mutant p53 induces EZH2 expression and promotes epithelial-mesenchymal transition by disrupting p68-Drosha complex assembly and attenuating miR-26a processing. Oncotarget 46 26587974
2014 Drosha promotes splicing of a pre-microRNA-like alternative exon. PLoS genetics 44 24786770
2018 fCLIP-seq for transcriptomic footprinting of dsRNA-binding proteins: Lessons from DROSHA. Methods (San Diego, Calif.) 43 29902563
2016 Cytoplasmic Drosha activity generated by alternative splicing. Nucleic acids research 43 27471035
2013 DICER1, DROSHA and miRNAs in patients with non-small cell lung cancer: implications for outcomes and histologic classification. Carcinogenesis 43 23349018
2011 Drosha processing controls the specificity and efficiency of global microRNA expression. Biochimica et biophysica acta 40 21683814
2012 Expression of Dicer and Drosha in triple-negative breast cancer. Journal of clinical pathology 39 22259182
2012 Inducing cell proliferation inhibition and apoptosis via silencing Dicer, Drosha, and Exportin 5 in urothelial carcinoma of the bladder. Journal of surgical oncology 38 22766726
2020 Drosha-independent miR-6778-5p strengthens gastric cancer stem cell stemness via regulation of cytosolic one-carbon folate metabolism. Cancer letters 36 32142918
2013 A multifunctional protein EWS regulates the expression of Drosha and microRNAs. Cell death and differentiation 36 24185621
2014 Drosha-independent DGCR8/Pasha pathway regulates neuronal morphogenesis. Proceedings of the National Academy of Sciences of the United States of America 35 24474768
2014 The expression of Dicer and Drosha in matched normal tissues, tumours and lymph node metastases in triple negative breast cancer. BMC cancer 33 24725360
2014 Murine follicular development requires oocyte DICER, but not DROSHA. Biology of reproduction 33 24990804
2018 MicroRNA-128-3p-mediated depletion of Drosha promotes lung cancer cell migration. Carcinogenesis 32 29236960
2016 MicroRNA-dependent roles of Drosha and Pasha in the Drosophila larval ovary morphogenesis. Developmental biology 32 27339292
2015 Drosha inclusions are new components of dipeptide-repeat protein aggregates in FTLD-TDP and ALS C9orf72 expansion cases. Journal of neuropathology and experimental neurology 31 25756586
2015 Drosha controls dendritic cell development by cleaving messenger RNAs encoding inhibitors of myelopoiesis. Nature immunology 31 26437240
2010 GAM/ZFp/ZNF512B is central to a gene sensor circuitry involving cell-cycle regulators, TGF{beta} effectors, Drosha and microRNAs with opposite oncogenic potentials. Nucleic acids research 31 20639536
2015 Expression of the microRNA regulators Drosha, Dicer and Ago2 in non-small cell lung carcinomas. Cellular oncology (Dordrecht, Netherlands) 29 26227789
2015 Early postnatal ablation of the microRNA-processing enzyme, Drosha, causes chondrocyte death and impairs the structural integrity of the articular cartilage. Osteoarthritis and cartilage 28 25707934
2013 miRNA biogenesis enzyme Drosha is required for vascular smooth muscle cell survival. PloS one 28 23637774
2014 Upregulation of microRNA processing enzymes Drosha and Dicer in gestational diabetes mellitus. Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology 27 25295740
2013 Expression of the RNase III enzyme DROSHA is reduced during progression of human cutaneous melanoma. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 27 23370771
2017 BRG1 and SMARCAL1 transcriptionally co-regulate DROSHA, DGCR8 and DICER in response to doxorubicin-induced DNA damage. Biochimica et biophysica acta. Gene regulatory mechanisms 26 28716689
2016 Chromosomal anomalies at 1q, 3, 16q, and mutations of SIX1 and DROSHA genes underlie Wilms tumor recurrences. Oncotarget 26 26802027
2010 Short interfering RNA-mediated knockdown of drosha and pasha in undifferentiated Meloidogyne incognita eggs leads to irregular growth and embryonic lethality. International journal for parasitology 26 20398669
2017 A novel role for GSK3β as a modulator of Drosha microprocessor activity and MicroRNA biogenesis. Nucleic acids research 25 27907888
2016 Drosha and Dicer: Slicers cut from the same cloth. Cell research 25 27125999
2019 DROSHA-Dependent AIM2 Inflammasome Activation Contributes to Lung Inflammation during Idiopathic Pulmonary Fibrosis. Cells 24 31434287
2012 Correlation between hepatitis B virus protein and microRNA processor Drosha in cells expressing HBV. Antiviral research 24 22554933
2018 Leucine-rich repeat kinase 2 aggravates secondary brain injury induced by intracerebral hemorrhage in rats by regulating the P38 MAPK/Drosha pathway. Neurobiology of disease 23 30048803
2017 Perturbation of DROSHA and DICER expression by human papillomavirus 16 oncoproteins. Virology 22 28448850
2020 Circular RNA circ_DROSHA alleviates the neural damage in a cell model of temporal lobe epilepsy through regulating miR-106b-5p/MEF2C axis. Cellular signalling 21 33370579
2018 Inactivating mutations in Drosha mediate vascular abnormalities similar to hereditary hemorrhagic telangiectasia. Science signaling 21 29339534
2018 Neuronal activity regulates DROSHA via autophagy in spinal muscular atrophy. Scientific reports 21 29784949
2016 Multiplex CRISPR/Cas9-based genome engineering enhanced by Drosha-mediated sgRNA-shRNA structure. Scientific reports 21 27941919
2014 miRNA sensitivity to Drosha levels correlates with pre-miRNA secondary structure. RNA (New York, N.Y.) 21 24677349
2016 Drosha, DGCR8, and Dicer mRNAs are down-regulated in human cells infected with dengue virus 4, and play a role in viral pathogenesis. Genetics and molecular research : GMR 20 27173348
2012 Dicer and Drosha expression and response to Bevacizumab-based therapy in advanced colorectal cancer patients. European journal of cancer (Oxford, England : 1990) 20 23266047
2010 Solution structure of the Drosha double-stranded RNA-binding domain. Silence 20 20226070
2017 DROSHA targets its own transcript to modulate alternative splicing. RNA (New York, N.Y.) 19 28400409
2016 Involvement of FMRP in Primary MicroRNA Processing via Enhancing Drosha Translation. Molecular neurobiology 19 26993298
2015 A phosphomimetic mutant TDP-43 (S409/410E) induces Drosha instability and cytotoxicity in Neuro 2A cells. Biochemical and biophysical research communications 19 26102026
2011 Drosha regulates hMSCs cell cycle progression through a miRNA independent mechanism. The international journal of biochemistry & cell biology 18 21794839

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