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La protein is an important microprocessor component regulating miRNA processing efficiency by association with DGCR8 to regulate formation of the DGCR8-Drosha (show DROSHA Proteins) complex for miRNA processing.
this study shows an unexpected function of DGCR8 in the repair of UV-induced DNA lesions that is independent of miRNA processing.
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 (show DROSHA Proteins), DGCR8, 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 (show DROSHA Proteins)-DGCR8 Microprocessor.
data suggest a model in which the bis-cysteine thiolate ligand environment of Fe(III) DGCR8 is necessary for establishing proper pri-miRNA binding and enabling processing activity.
The rs417309 and rs1640299 polymorphisms of the DGCR8 gene as well as rs6877842 of the DROSHA (show DROSHA Proteins) gene might be associated with a risk of laryngeal cancer occurrence in the Polish population.
studies support retention of DGCR8 cysteine coordination upon reduction, a conclusion distinct from those of previous studies of a different ferrous DGCR8 isoform
Drosha (show DROSHA Proteins) and DGRC8 were significantly downregulated in healthy-appearing perilesional skin from hidradenitis suppurativa patients compared to healthy controls.
Authors found that DENV4 infection exhibited the highest viral load 3 days post-infection. Dicer (show DICER1 Proteins), Drosha (show DROSHA Proteins), and DGCR8 showed reduced expression following DENV4 infection as compared with negative controls.
Results demonstrated that DGCR8 is significantly upregulated in invasive ductal breast carcinoma, suggesting that increased expression of DGCR8 may play a fundamental role during the process of breast carcinogenesis.
We show that Dgcr8 mutations induce an earlier and stronger phenotype in the developing nervous system compared to Dicer (show DICER1 Proteins) mutants and that miRNA-independent functions of DGCR8 are critical for corticogenesis.
this study shows that B-cell specific cre-mediated DGCR8 deletion blocks B-cell development at the transition from the pro-B to the pre-B cell stage
DGCR8 in the modulates of the alternative splicing of Tcf7l1 (show TCF7L1 Proteins) mRNA in addition to its established function in microRNA biogenesis, controlling embryonic stem cell exit from pluripotency.
we suggest that DGCR8-dependent canonical microRNAs are essential for uterine development and physiological processes such as proper immune modulation, reproductive cycle, and steroid hormone responsiveness in mice.
DGCR8 is required for the progression, but not initiation, of Akt (show AKT1 Proteins) induced prostate cancer in vivo.
DGCR8 is required for microRNA biogenesis and normal mouse embryonic stem cell proliferation and differentiation.
These results reveal a new pathway in the DNA damage response wherein ABL (show ABL1 Proteins)-dependent tyrosine phosphorylation of DGCR8 stimulates the processing of selective primary miRNAs.
Conditional gene deletion of the essential miRNA-processing enzyme Dgcr8 in the developing renal tubular system results in severe developmental defects and kidney failure.
Dgcr8 is responsible for modulation of gene expression programs underlying myelin formation and maintenance as well as suppression of an injury-related gene expression program
Dgcr8 mutant mice, which have a defective miRNA pathway while retaining an intact endo-siRNA pathway, were infertile and displayed cumulative defects in meiotic and haploid phases of spermatogenesis, resulting in oligo-, terato-, and azoospermia.
DiGeorge syndrome critical region gene 8 (dgcr8) in zebrafish germ line was deleted and demonstrated that the maternal-zygotic dgcr8 (MZdgcr8) embryos exhibit MZdicer-like phenotypes with morphological defects which could be rescued by miR (show MYLIP Proteins)-430.
This gene encodes a subunit of the microprocessor complex which mediates the biogenesis of microRNAs from the primary microRNA transcript. The encoded protein is a double-stranded RNA binding protein that functions as the non-catalytic subunit of the microprocessor complex. This protein is required for binding the double-stranded RNA substrate and facilitates cleavage of the RNA by the ribonuclease III protein, Drosha. Alternate splicing results in multiple transcript variants.
hypothetical protein LOC432110
, DiGeorge syndrome critical region gene 8
, DiGeorge syndrome critical region 8
, microprocessor complex subunit DGCR8
, diGeorge syndrome critical region 8 homolog
, DiGeorge syndrome critical region 8 homolog