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MicroRNA profiling by array of miRNAs regulated by Ars2 and DGCR8

ABSTRACT: siRNAs were used to deplete either Ars2 or DGCR8 proteins from cells and were compared to control siRNA treated cells.

ORGANISM(S): Homo sapiens

SUBMITTER: Joshua Gruber

PROVIDER: E-MTAB-898 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcription profiling by array of mRNAs regulated by Ars2 and DGCR8

Project description:siRNAs were used to deplete either Ars2 or DGCR8 proteins from cells and were compared to control siRNA treated cells.

2012-02-01 | E-MTAB-899 | biostudies-arrayexpress

Effects of Ars2 or DGCR8 siRNA on gene expression

Project description:Ars2 is a component of the nuclear cap-binding complex that is required for cellular proliferation and contributes to microRNA biogenesis. Arrays were performed to determine the repertoire of genes that change following knock-down of Ars2. Knock-down of DGCR8 was also performed to determine which changes in Ars2 knock-down cells resulted from defects in microRNA expression. 9 samples were analyzed including: three biological replicates of control siRNA-transfected HeLa cells, HeLa cells transfected with three independent siRNAs targeting Ars2, or HeLa cells transfected with three independent siRNAs targeting DGCR8.

2012-02-01 | E-GEOD-34679 | biostudies-arrayexpress

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Project description:Ars2 is a component of the nuclear cap-binding complex that is required for cellular proliferation and contributes to microRNA biogenesis. Arrays were performed to determine the repertoire of microRNAs that change following knock-down of Ars2. Knock-down of DGCR8 was also performed to determine which microRNAs were expressed and had half-lives short enough to significantly decrease over the duration of the experiment. 9 samples were analyzed including: three biological replicates of control siRNA-transfected HeLa cells, HeLa cells transfected with three independent siRNAs targeting Ars2, or HeLa cells transfected with three independent siRNAs targeting DGCR8.

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Effects of Ars2 or DGCR8 siRNA on gene and microRNA expression

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Project description:We have analyzed gene expression in cone photoreceptors isolated from wild type and C-DGCR8 (DiGeorge Syndrome Critical Region Gene 8) KO mice at five different time points to get a mechanistic inside into the altered molecular pathways after microRNAs depletion. Cones were isolated by FACS from wild type and C-DGCR8 KO mice expressing Cre recombinase postnatally specifically in cones (D4-Cre) and bearing conditional null Dgcr8 allele. Experiments were performed in duplicates from different time points (P30, P40, P50, P60, and P90). Total RNA was extracted and next-generation RNA sequencing was performed.

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Stabilizing Heterochromatin by DGCR8 Alleviates Senescence and Osteoarthritis

Project description:DiGeorge syndrome critical region 8 (DGCR8) is a critical component of the canonical microprocessor complex for microRNA biogenesis. However, the non-canonical functions of DGCR8 have not been studied. Here, we demonstrate that DGCR8 plays an important role in maintaining heterochromatin organization and attenuating aging. An N-terminal-truncated version of DGCR8 (DR8dex2) accelerated senescence in human mesenchymal stem cells (hMSCs) independent of its miRNA-processing activity, which is mediated by its C-terminal domains. Further studies revealed that DGCR8 maintained heterochromatin organization by interacting with the nuclear envelope protein Lamin B1, and heterochromatin-associated proteins, KAP1 and HP1 Overexpression of any of these proteins, including DGCR8, reversed premature senescent phenotypes in DR8dex2 hMSCs. Finally, DGCR8 was downregulated in pathologically and naturally aged hMSCs, whereas DGCR8 overexpression alleviated hMSC aging and osteoarthritis in mice. Taken together, these analyses uncovered a novel, miRNA processing-independent role for DGCR8 in maintaining heterochromatin organization and attenuating senescence. DGCR8 may therefore represent a new therapeutic target for alleviating human aging-related disorders.

2019-05-28 | PXD013856 | Pride

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