Recombinant Mouse Microprocessor complex subunit DGCR8 (Dgcr8)

1. 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 PMID: 30044225
2. Deletion of DGCR8 results in loss of vascular reactivity, reduced blood pressure and neointima formation. PMID: 29362439
3. these results strongly indicate that DGCR8-dependent generation of miR-22 is essential for bone formation PMID: 28739418
4. 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. PMID: 28232627
5. 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 PMID: 27641147
6. 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. PMID: 28100686
7. 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. PMID: 26833131
8. Deletion of the Dgcr8 gene inhibits tumor progression in a Pten-knockout mouse model of prostate cancer PMID: 26206718
9. DGCR8 is required for the progression, but not initiation, of Akt induced prostate cancer in vivo. PMID: 26206718
10. DGCR8 is required for microRNA biogenesis and normal mouse embryonic stem cell proliferation and differentiation. PMID: 17259983
11. 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. PMID: 26126715
12. Conditional gene deletion of the essential miRNA-processing enzyme Dgcr8 in the developing renal tubular system results in severe developmental defects and kidney failure. PMID: 25881298
13. 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 PMID: 26272614
14. 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. PMID: 25244517
15. 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. PMID: 25008181
16. Data indicate that DiGeorge syndrome critical region gene 8 (DGCR8)-dependent miRs are indispensable for osteoclastic control of bone metabolism. PMID: 24420069
17. This suggests that Dgcr8-microRNA-Drd2-dependent thalamocortical disruption is a pathogenic event underlying schizophrenia-associated psychosis. PMID: 24904170
18. These data reveal a role for DeltaNp63 in the transcriptional regulation of DGCR8 to reprogram adult somatic cells into multipotent stem cells. PMID: 24449888
19. Data suggest that Dgcr8-mediated regulation of microRNA is likely to underlie Cxcr4/Cxcl12 signaling and associated neurodevelopmental defects. PMID: 24101523
20. 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. PMID: 24027283
21. Several schizophrenia-associated genes were downregulated in the hippocampus of Dgcr8(+/-) mice, and one of them, insulin-like growth factor 2 PMID: 23719809
22. a novel candidate for Dgcr8-independent microRNA genesis PMID: 22912678
23. Deletion of Dgcr8 results in a severe deficit in inhibitory synaptic transmission and reduction of inhibitory synapses in pyramidal neurons . PMID: 22728723
24. DGCR8 gene is required for vascular development through the regulation of VSMC proliferation, apoptosis, and differentiation. PMID: 22511778
25. Dgcr8 controls neural crest cells survival in cardiovascular development. PMID: 22138056
26. loss of Dicer1 resulted in an earlier lethality, more severe structural abnormalities, and increased apoptosis relative to that from Dgcr8 loss PMID: 21712401
27. In this study, we show that Dgcr8+/- mice display reduced expression of a subset of microRNAs in the prefrontal cortex PMID: 21466685
28. The effect of Dgcr8 deficiency was determined on the structure and function of cortical circuits by assessing their laminar organization. PMID: 21368174
29. ING1 binds to the DGCR8 promoter and controls its transcription through chromatin regulation. ING1 and DGCR8 can cooperate in restraining proliferation. PMID: 20179197
30. a Microprocessor, containing the RNA binding protein Dgcr8 and RNase III enzyme Drosha, is responsible for processing primary microRNAs to precursor microRNAs PMID: 19759829
31. Analysis of mouse knockout ES cells shows that DGCR8 is essential for biogenesis of miRNAs PMID: 17259983
32. Haploinsufficiency of the Dgcr8 gene is associated with behavioral and neuronal deficits PMID: 18469815
33. most abundantly expressed skin microRNAs are dependent on both Dicer and DGCR8 PMID: 19114655
34. Cardiomyocyte-specific deletion of dgcr8, a gene required for microRNA biogenesis, revealed a fully penetrant phenotype that begins with left ventricular malfunction progressing to a dilated cardiomyopathy and premature lethality PMID: 19679836

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KEGG: mmu:94223

STRING: 10090.ENSMUSP00000009321

UniGene: Mm.447352