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anti-Human DGCR8 Antibodies:
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Cow (Bovine) Polyclonal DGCR8 Primary Antibody for IHC, WB - ABIN2776557
Shiohama, Sasaki, Noda, Minoshima, Shimizu: Nucleolar localization of DGCR8 and identification of eleven DGCR8-associated proteins. in Experimental cell research 2007
Show all 4 Pubmed References
Human Polyclonal DGCR8 Primary Antibody for ICC, IF - ABIN440648
Havens, Reich, Duelli, Hastings: Biogenesis of mammalian microRNAs by a non-canonical processing pathway. in Nucleic acids research 2012
Human Polyclonal DGCR8 Primary Antibody for ELISA, WB - ABIN565740
Luers, Loudig, Berman: MicroRNAs are expressed and processed by human primary macrophages. in Cellular immunology 2010
Human Polyclonal DGCR8 Primary Antibody for IF, WB - ABIN527085
Márquez, Kohli, Arteta, Chang, Li, Goldblatt, Vidal-Vanaclocha: Identification of hepatic microvascular adhesion-related genes of human colon cancer cells using random homozygous gene perturbation. in International journal of cancer. Journal international du cancer 2013
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.
Genotype AG in rs3757 DGCR8 exhibits protective effect, decreasing the risk of primary open angle glaucoma, while the homozygote GG is probably associated with increased risk of glaucoma.
La protein is an important microprocessor component regulating miRNA processing efficiency by association with DGCR8 to regulate formation of the DGCR8-Drosha 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 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.
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 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 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, Drosha, 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.
DGCR8 and Drosha assemble into a heterotrimeric complex on RNA, comprising two DGCR8 molecules and one Drosha molecule.
Results show that DGCR8 forms an alternative complex with the RRP6-containing form of the exosome, acts as an adaptor to recruit the exosome to target structured RNAs, and the DGCR8/hRRP6 complex controls the stability of human telomerase RNA.
We aimed to evaluate the expression of the major components of microRNA biogenesis machinery including Drosha, Dicer and DiGeorge syndrome critical region gene 8 (DGCR8) in multiple sclerosis patients
These results reveal a new pathway in the DNA damage response wherein ABL-dependent tyrosine phosphorylation of DGCR8 stimulates the processing of selective primary miRNAs.
DGCR8 functions as an oncogene in ovarian cancer, which is in part mediated by miR-27b.
Together with a 23-amino acid peptide from DGCR8, DROSHA constitutes a minimal functional core. DROSHA serves as a "ruler" by measuring 11 bp from the basal ssRNA-dsRNA junction. DGCR8 interacts with the stem and apical elements through its dsRNA-binding domains and RNA-binding heme domain, respectively, allowing efficient and accurate processing.
Data show decreased DGCR8 expression and miRNA dysregulation in individuals with 22q11.2 deletion syndrome
These data show that hepatitis B virus proteins repress DGCR8 promoter activity by upregulating the expression of transcription factor YY1.
The Ddx6 knockout cells were phenotypically and molecularly similar to cells lacking all microRNAs (Dgcr8 knockout ESCs). These data show that the loss of DDX6 can separate the two canonical functions of microRNAs: translational repression and transcript destabilization
Deletion of DGCR8 results in loss of vascular reactivity, reduced blood pressure and neointima formation.
these results strongly indicate that DGCR8-dependent generation of miR-22 is essential for bone formation
We show that Dgcr8 mutations induce an earlier and stronger phenotype in the developing nervous system compared to Dicer 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 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 induced prostate cancer in vivo.
DGCR8 is required for microRNA biogenesis and normal mouse embryonic stem cell proliferation and differentiation.
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.
Adipose tissue-specific Dgcr8 knockout mice displayed enlarged but pale interscapular brown fat with decreased expression of genes characteristic of brown fat and were intolerant to cold exposure.
Data indicate that DiGeorge syndrome critical region gene 8 (DGCR8)-dependent miRs are indispensable for osteoclastic control of bone metabolism.
This suggests that Dgcr8-microRNA-Drd2-dependent thalamocortical disruption is a pathogenic event underlying schizophrenia-associated psychosis.
These data reveal a role for DeltaNp63 in the transcriptional regulation of DGCR8 to reprogram adult somatic cells into multipotent stem cells.
Data suggest that Dgcr8-mediated regulation of microRNA is likely to underlie Cxcr4/Cxcl12 signaling and associated neurodevelopmental defects.
The results of this study suggested that robust alterations in synaptic properties within the prefrontal cortex, which to a large extent but not entirely can be accounted for by Dgcr8 deficiency.
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-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