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PMID |
Sentence |
1 |
14576312
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The fragile X syndrome repeats form RNA hairpins that do not activate the interferon-inducible protein kinase, PKR, but are cut by Dicer.
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2 |
18725525
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Dicer-deficient T reg lineage cells failed to remain stable, as a subset of cells down-regulated the T reg cell-specific transcription factor FoxP3, whereas the majority expressed altered levels of multiple genes and proteins (including Neuropilin 1, glucocorticoid-induced tumor necrosis factor receptor, and cytotoxic T lymphocyte antigen 4) associated with the T reg cell fingerprint.
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3 |
18725525
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In fact, a significant percentage of the T reg lineage cells took on a T helper cell memory phenotype including increased levels of CD127, interleukin 4, and interferon gamma.
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4 |
20010811
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The 16 kilobase (kb) heterochromatin domain between the chicken beta-globin locus and the folate receptor gene is used here to study the roles of RNA-dependent mechanisms and histone modifications in the maintenance of a constitutive heterochromatic structure.
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5 |
20010811
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We also show that the chicken Argonaute 2 homologue binds the 16 kb region in a Dicer-dependent manner and is necessary for a condensed chromatin structure.
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6 |
22216196
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Beta-cell specific deletion of Dicer1 leads to defective insulin secretion and diabetes mellitus.
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7 |
22216196
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To investigate the importance of miRNAs in mouse insulin secreting β-cells, we have generated mice with a β-cells specific disruption of the Dicer1 gene using the Cre-lox system controlled by the rat insulin promoter (RIP).
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8 |
22216196
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Immunohistochemical, flow cytometric and ultrastructural analyses revealed altered islet morphology, marked decreased β-cell mass, reduced numbers of granules within the β-cells and reduced granule docking in adult RIP-Cre Dicer1(Δ/Δ) mice. β-cell specific Dicer1 deletion did not appear to disrupt fetal and neonatal β-cell development as 2-week old RIP-Cre Dicer1(Δ/Δ) mice showed ultrastructurally normal β-cells and intact insulin secretion.
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9 |
22216196
|
Beta-cell specific deletion of Dicer1 leads to defective insulin secretion and diabetes mellitus.
|
10 |
22216196
|
To investigate the importance of miRNAs in mouse insulin secreting β-cells, we have generated mice with a β-cells specific disruption of the Dicer1 gene using the Cre-lox system controlled by the rat insulin promoter (RIP).
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11 |
22216196
|
Immunohistochemical, flow cytometric and ultrastructural analyses revealed altered islet morphology, marked decreased β-cell mass, reduced numbers of granules within the β-cells and reduced granule docking in adult RIP-Cre Dicer1(Δ/Δ) mice. β-cell specific Dicer1 deletion did not appear to disrupt fetal and neonatal β-cell development as 2-week old RIP-Cre Dicer1(Δ/Δ) mice showed ultrastructurally normal β-cells and intact insulin secretion.
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12 |
22216196
|
Beta-cell specific deletion of Dicer1 leads to defective insulin secretion and diabetes mellitus.
|
13 |
22216196
|
To investigate the importance of miRNAs in mouse insulin secreting β-cells, we have generated mice with a β-cells specific disruption of the Dicer1 gene using the Cre-lox system controlled by the rat insulin promoter (RIP).
|
14 |
22216196
|
Immunohistochemical, flow cytometric and ultrastructural analyses revealed altered islet morphology, marked decreased β-cell mass, reduced numbers of granules within the β-cells and reduced granule docking in adult RIP-Cre Dicer1(Δ/Δ) mice. β-cell specific Dicer1 deletion did not appear to disrupt fetal and neonatal β-cell development as 2-week old RIP-Cre Dicer1(Δ/Δ) mice showed ultrastructurally normal β-cells and intact insulin secretion.
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15 |
22910415
|
EWS interacts with the microprocessor complex involving Drosha and DGCR8, which play roles as the cofactors of primary microRNA processing.
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16 |
22910415
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Here, we show that endogenous EWS interacts with endogenous Drosha by IP-western blotting.
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17 |
22910415
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In addition, EWS knockout mouse decreased the expression of Drosha.
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18 |
22910415
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Also, expression levels of Dicer and CCND1 (Cyclin D1), which are known target genes of the let-7 family were upregulated.
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19 |
23382448
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Dicer1-deficient β-cells lost insulin expression while maintaining the expression of β-cell transcription factors such as Pdx1 and Nkx6.1 early in the postnatal period.
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20 |
23518926
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Further study of Dicer-KO adrenals demonstrated a significant loss of steroidogenic factor 1-expressing cortical cells that was histologically evident as early as E16.5 coincident with an increase in p21 and cleaved-caspase 3 staining in the cortex.
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21 |
23518926
|
Consistent with the absence of Dicer and the associated loss of miRNA-mediated mRNA degradation, we observed an up-regulation of a small subset of adrenal transcripts in Dicer-KO mice, most notably the transcripts coded by the genes Nr6a1 and Acvr1c.
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22 |
23518926
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Indeed, several miRNAs, including let-7, miR-34c, and miR-21, that are predicted to target these genes for degradation, were also markedly down-regulated in Dicer-KO adrenals.
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