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Methylation of three CpGs (DROSHA: cg23230564, TNRC6B: cg06751583, and TNRC6B: cg21034183) was prospectively associated with time to cancer development (positively for cg06751583, inversely for cg23230564 and cg21034183), whereas methylation of one CpG site (DROSHA: cg16131300) was positively associated with cancer prevalence.
DROSHA mutations contribute to the development of vascular abnormalities in hereditary hemorrhagic telangiectasia.
The DROSHA rs10719, rs6877842 SNPs, and DGCR8 rs417309 SNP play pivotal roles in carcinogenesis. (Review, Meta-analysis)
analysis of the recurrent homozygous deletion of DROSHA and microduplication of PDE4DIP in pineoblastoma
Our study provides mechanistic insights into the function of miR-128-3p as a key regulator of the malignant phenotype of lung cancer cells...and in particular it highlights a role for Drosha in non-small-cell lung cancer cells migration
Different genotypes frequency of DROSHA (rs10719, rs642321 and rs2291102) were determined by sequencing method in 385 infertile men and 120 fertile controls. No significant differences were seen between cases and controls for DROSHA expression.
The Drosha rs10719TC and CC genotypes were associated with PE risk. The CC-GG combined genotype and C-G haplotype of Drosha rs10719 and rs6877842 polymorphisms may increase PE susceptibility.
Primary microRNA transcripts (pri-miRs) are cleaved by Microprocessor, a complex containing the RNase Drosha and its partner protein, DGCR8. Although DGCR8 is known to bind heme, the molecular role of heme in pri-miR processing is unknown. Here we show that heme is critical for Microprocessor to process pri-miRs with high fidelity.
Taken together, our results provided the potential evidence that rs10719 and rs493760 might contribute to the risk of CL/P and suggested potential genetic basis and mechanisms of CL/P.
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 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 and DROSHA genes were low in AITD and differed depending on the intractability of GD and the severity of HD, respectively.
Overexpression of LAMC2 and knockdown of CD82 markedly promoted GC cell invasion and activated EGFR/ERK1/2-MMP7 signaling via upregulation of the expression of phosphorylated (p)-EGFR, p-ERK1/2 and MMP7.
A significant association was observed between 2 candidate genes and AD, TARBP2 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-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 and SMARCAL1, members of the ATP-dependent chromatin remodelling family, are shown to co-regulate the transcription of DROSHA, DGCR8, and DICER in response to double-strand DNA breaks
Mechanistic dissection reveals that NEAT1 broadly interacts with the NONO-PSF 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 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.
Report DROSHAnumerous processing sites on primary microRNAs and noncanonical substrates which may serve as cis-elements for DROSHA-mediated gene regulation.
Mice lacking Drosha in the vascular endothelium developed a vascular phenotype resembling hereditary hemorrhagic telangiectasia that included dilated and disorganized vasculature, arteriovenous fistulae, and hemorrhages.
Drosha knockout indicated a role for let-7 miRNAs in developmental hematopoiesis.
Identification of Microprocessor component DROSHA as a novel DNMT1-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 in Drosha-deficient hippocampal neural stem cells restores neurogenesis, suggesting that the Drosha/NFIB mechanism robustly prevents oligodendrocyte fate acquisition in vivo.
FMRP is involved in pri-miRNA processing via enhancing DROSHA expression that may play an important role in fragile X 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 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.
Drosha is required for VSMC survival by targeting multiple signaling pathways.
the podocyte-specific deletion of Drosha results in a similar phenotype to Dicer mutants, confirming that the Dicer mutant phenotype is due to the loss of miRNAs
DROSHA is essential mainly for the canonical miRNA production, and DROSHA-mediated miRNA production is essential for normal spermatogenesis and male fertility.
Drosha is required for maintenance of neural stem cell self-renewal.
epidermal Dicer and Drosha have multiple functions in postnatal skin
The expression profiles of Hoxd4 and miR-10b transcripts during neural differentiation of mouse embryonal carcinoma (EC) P19 cells are co-ordinately regulated and generated by Drosha cleavage.
Drosha recognizes and directly cleaves many protein-coding messenger RNAs (mRNAs) with secondary stem-loop structures
alternative Drosha processing might be a novel mechanism for diversification of the miRNA target gene pool
a Microprocessor, containing the RNA binding protein Dgcr8 and RNase III enzyme Drosha, is responsible for processing primary microRNAs to precursor microRNAs
Maternal diabetes led to a marked downregulation of Dicer protein in embryoblast cells and Drosha protein in trophoblast cells.
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