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It has been reported that the gene encoding human DROSHA also encodes a potential miRNA and that this miRNA may act upon, at least, one of DROSHA transcripts.
Depletion of drosha ribonuclease III (Drosha) significantly reduces DNA repair by both homologous recombination (HR) and non-homologous end joining (NHEJ).
Increased Drosha expression was found in chronic lymphocytic leukemia patients without chromosomal deletions.
point mutations in the RNaseIIIb domain of Drosha implicated in Wilms tumors differentially affected cleavage of the 5' and 3' strands of pri-miRNAs in vitro.
the DICER (show DICER1 Proteins) rs1057035 TT genotype and DROSHA rs644236 CC genotype were associated with the development of GD and the differentiation between GD and HD, respectively. The expression levels of DICER (show DICER1 Proteins) and DROSHA genes were low in AITD and differed depending on the intractability of GD and the severity of HD, respectively.
Overexpression of LAMC2 (show LAMC2 Proteins) and knockdown of CD82 (show CD82 Proteins) markedly promoted GC cell invasion and activated EGFR (show EGFR Proteins)/ERK1/2-MMP7 (show MMP7 Proteins) signaling via upregulation of the expression of phosphorylated (p)-EGFR (show EGFR Proteins), p-ERK1/2 and MMP7 (show MMP7 Proteins).
A significant association was observed between 2 candidate genes and AD, TARBP2 (show TARBP2 Proteins) rs784567 genotype and AD (chi=6.292, P=0.043), and a trend for RNASEN rs10719 genotype (chi=4.528, P=0.104) and allele (P=0.035). On controlling for Age, we found that for the TARBP2 (show TARBP2 Proteins)-RNASEN association with AD the age variation was a risk factor for AD risk (P<0.001; OR=1.104; 95% CI, 1.059-1.151)
BRG1 (show SMARCA4 Proteins) and SMARCAL1 (show SMARCAL1 Proteins), members of the ATP-dependent chromatin remodelling family, are shown to co-regulate the transcription of DROSHA, DGCR8 (show DGCR8 Proteins), and DICER (show DICER1 Proteins) in response to double-strand DNA breaks
Mechanistic dissection reveals that NEAT1 broadly interacts with the NONO (show NONO Proteins)-PSF (show IGFBP7 Proteins) heterodimer as well as many other RNA-binding proteins and that multiple RNA segments in NEAT1, including a 'pseudo pri-miRNA' near its 3' end, help attract the Drosha-DGCR8 (show DGCR8 Proteins) Microprocessor.
Results show that Mammalian DROSHA genes have evolved a conserved hairpin structure spanning a specific exon-intron junction serving as a substrate for the microprocessor in human but not in murine cells. This hairpin element decides whether the overlapping exon is alternatively or constitutively spliced. Also, DROSHA promotes skipping of the overlapping exon in human cells independently of its cleavage function.
Drosha knockout indicated a role for let-7 miRNAs in developmental hematopoiesis.
Identification of Microprocessor component DROSHA as a novel DNMT1 (show DNMT1 Proteins)-interactor.
Results show that Mammalian DROSHA genes have evolved a conserved hairpin structure spanning a specific exon-intron junction serving as a substrate for the microprocessor in human but not in murine cells.
Knockdown of NFIB (show NFIB Proteins) in Drosha-deficient hippocampal neural stem cells restores neurogenesis, suggesting that the Drosha/NFIB (show NFIB Proteins) mechanism robustly prevents oligodendrocyte fate acquisition in vivo.
FMRP (show FMR1 Proteins) is involved in pri-miRNA processing via enhancing DROSHA expression that may play an important role in fragile X (show FMR1 Proteins) syndrome.
our findings suggest that DROSHA is involved in stromal decidualization and may play an important role in embryo implantation in mice.
These data indicate that oocyte DICER (show DICER1 Proteins) expression in the fetal ovary is required, and oocyte DROSHA is dispensable, for postnatal follicular development and female fertility in adulthood.
Drosha repressed the expression of two mRNAs encoding inhibitors of myelopoiesis in early hematopoietic progenitors.
Early postnatal ablation of the microRNA-processing enzyme, Drosha, causes chondrocyte death and impairs the structural integrity of the articular cartilage.
Data indicate that Arf-deficient cells transformed by oncogenic Ras were dependent on increased Drosha expression as Drosha knockdown was sufficient to inhibit Ras-dependent cellular transformation.
Members of the ribonuclease III superfamily of double-stranded (ds) RNA-specific endoribonucleases participate in diverse RNA maturation and decay pathways in eukaryotic and prokaryotic cells (Fortin et al., 2002
, ribonuclease 3
, Ribonuclease 3
, RNase III
, drosha, double-stranded RNA-specific endoribonuclease
, nuclear RNase III Drosha
, protein Drosha
, putative protein p241 which interacts with transcription factor Sp1
, putative ribonuclease III
, ribonuclease III, nuclear
, ribonuclease type III, nuclear
, ethanol induced 2