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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 (zeige DICER1 Proteine) 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 (zeige DICER1 Proteine) and DROSHA genes were low in AITD and differed depending on the intractability of GD and the severity of HD, respectively.
Overexpression of LAMC2 (zeige LAMC2 Proteine) and knockdown of CD82 (zeige CD82 Proteine) markedly promoted GC cell invasion and activated EGFR (zeige EGFR Proteine)/ERK1/2-MMP7 (zeige MMP7 Proteine) signaling via upregulation of the expression of phosphorylated (p)-EGFR (zeige EGFR Proteine), p-ERK1/2 and MMP7 (zeige MMP7 Proteine).
A significant association was observed between 2 candidate genes and AD, TARBP2 (zeige TARBP2 Proteine) 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 (zeige TARBP2 Proteine)-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 (zeige SMARCA4 Proteine) and SMARCAL1 (zeige SMARCAL1 Proteine), members of the ATP-dependent chromatin remodelling family, are shown to co-regulate the transcription of DROSHA, DGCR8 (zeige DGCR8 Proteine), and DICER (zeige DICER1 Proteine) in response to double-strand DNA breaks
Mechanistic dissection reveals that NEAT1 broadly interacts with the NONO (zeige NONO Proteine)-PSF (zeige IGFBP7 Proteine) 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 (zeige DGCR8 Proteine) 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 (zeige DNMT1 Proteine)-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 (zeige NFIB Proteine) in Drosha-deficient hippocampal neural stem cells restores neurogenesis, suggesting that the Drosha/NFIB (zeige NFIB Proteine) mechanism robustly prevents oligodendrocyte fate acquisition in vivo.
FMRP (zeige FMR1 Proteine) is involved in pri-miRNA processing via enhancing DROSHA expression that may play an important role in fragile X (zeige FMR1 Proteine) 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 (zeige DICER1 Proteine) 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