DGCR8 is essential for microRNA biogenesis and silencing of embryonic stem cell self-renewal
By Yangming Wang, R. Medvid, Collin Melton, R. Jaenisch, Robert Blelloch. Nature Genetics, 2007
1,077 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/d064cd7ab98d70a7b260069b53960074f7475ff0
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In Cancer Research
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Citations in the corpus
- Non-coding RNAs as regulators of embryogenesis (2011, background): “miRNA activity is also essential for normal progression through mouse embryogenesis, as evidenced by the malformation and resorption of maternal–zygotic Dgcr8 mutant”
- An overview of microRNAs (2015, background): “Loss of either step in miRNA biogenesis results in embryonic lethality[140, 141].”
- MicroRNA dysregulation in cancer: diagnostics, monitoring and therapeutics. A comprehensive review (2012, neutral): “…important biological implications: DGR8 knock out mice arrest early in development and have defects in ES cell proliferation and differentiation (Wang et al, 2007); Lin-28, originally discovered as a heterochronic gene regulating developmental timing in worms, is able to block let-7 biogenesis…”
- MicroRNAs: key regulators of stem cells (2009, result): “Similar to the Dicer-null embryonic stem cells, DGCR8-deficient ES cells exhibit either delayed or reduced expression of differentiation markers, as well as delayed kinetics of cell cycle progressio”
- MicroRNA sponges: progress and possibilities. (2010, background): “A sensitized background of DGCR8 and/or Dicer heterozygosity, which 2048 RNA, Vol. 16, No. 11 shows partially reduced levels for some miRNAs (Murchison et al. 2005; Wang et al. 2007), might enhance the loss of function.”
- MicroRNA-145 regulates OCT4, SOX2, and KLF4 and represses pluripotency in human embryonic stem cells. (2009, neutral): “On the other hand, mutant DGCR8 ESCs do not fully downregulate pluripotency markers such as Oct4, Rex1, Sox2, and Nanog in response to differentiation (Wang et al., 2007).”
- MicroRNA regulation of cell lineages in mouse and human embryonic stem cells. (2008, neutral): “Indeed, ES cells lacking Dicer or Drosha , and therefore most mature miRNAs, cannot differentiate into most lineages (Kanellopoulou et al., 2005; Murchison et al., 2005; Wang et al., 2007).”
- Control of Embryonic Stem Cell State (2011, background): “…in this family have been implicated in cell proliferation (He et al., 2005; O’Donnell et al., 2005; Wang et al., 2008) and have been shown to rescue the proliferation defects observed in miRNA-deficient ES cells (Kanellopoulou et al., 2005; Murchison et al., 2005; Wang et al., 2007, 2008).”
- The mirtron pathway generates microRNA-class regulatory RNAs in Drosophila. (2007, neutral): “More recently, it was suggested that DGCR8/Pasha mutant cells more purely reflect a ‘‘miRNA null’’ state (Wang et al., 2007).”
- Highly efficient miRNA-mediated reprogramming of mouse and human somatic cells to pluripotency (2011, neutral): “These miRNAs belong to families of miRNAs that are expressed preferentially in embryonic stem cells and are thought to help maintain the ESC phenotype (Babiarz et al., 2008; Wang et al., 2007, 2008; Wang and Blelloch, 2009;).”
- Small non-coding RNAs in animal development (2008, background): “Deletion of Dicer1 and Dgcr8 results in early developmental arrest in mice, accompanied by defects in the proliferation of pluripotent stem cell”
- Biogenesis of small RNAs in animals (2009, background): “Mouse ES cells that are deficient in the Dgcr8 gene fail to produce miRNAs and manifest defects in proliferation and differentiation, thereby confirming the essential role of DGCR8 in the miRNA pathway and the importance of miRNAs in ES-cell functio”
- Connecting microRNA genes to the core transcriptional regulatory circuitry of embryonic stem cells (2008, background): “…miRNAs in this family have been implicated in cell proliferation (O’Donnell et al., 2005; He et al., 2005; Voorhoeve et al., 2006), consistent with the impaired self-renewal phenotype observed in miRNA-deficient ES cells (Kanellopoulou et al., 2005; Murchison et al., 2005; Wang et al., 2007).”
- Mouse ES cells express endogenous shRNAs, siRNAs, and other Microprocessor-independent, Dicer-dependent small RNAs. (2008, methodology): “ditioned media as described previously (Wang et al. 2007).”