Selective Blockade of MicroRNA Processing by Lin28
By Srinivas R. Viswanathan, George Q. Daley, R. I. Gregory. Science, 2008
1,539 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/50794319d60230e771a9e5ad967367c838d9acab
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In Cancer Research
- David P. Bartel
- John S. Mattick
- Scott M. Hammond
- Phillip A. Sharp
- V. Narry Kim
- Thomas Tuschl
- Frank J. Slack
- Marcel E. Dinger
In Molecular Biology
- David P. Bartel
- John S. Mattick
- Richard A. Young
- Phillip A. Sharp
- Scott M. Hammond
- Thomas Tuschl
- V. Narry Kim
- Phillip D. Zamore
Citations in the corpus
- MicroRNAs in development and disease. (2011, background): “In agreement, it was found that lin-28 binds the loop structure of let-7 and inhibits its processing by both Drosha in the nucleus (448, 638) and Dicer in the cytoplasm (518).”
- Non‐coding RNAs: regulators of disease (2010, background): “Likewise, the pluripotency factor LIN28 can bind to the conserved loop of the primary let-7 transcript (pri-let-7) to directly inhibit the Drosha cleavage steps [75–77] and can inhibit Dicer cleavage directly or by facilitating premiRNA degradation [78,79].”
- Small RNAs and Their Roles in Plant Development (2009, background): “The accumulation of mouse let-7 miRNA is regulated by LIN-28 at a post-transcriptional step, either pri-let-7 processing or stability of pre-let-7, or both (Heo et al. 2008, Viswanathan et al. 2008).”
- miRNAs in human cancer (2010, background): “First, LIN28A blocks processing of tumour suppressor pri- and pre-let-7 [81–85], thus maintaining expression of genes that drive self-renewal and proliferation (reviewed in [86]); tumours that express LIN28A were indeed shown to be poorly differentiated and more aggressive than LIN28A-negative tumou”
- Origins and Mechanisms of miRNAs and siRNAs (2009, background): “Drosha-mediated cleavage is inhibited by Lin28 (Heo et al., 2008; Newman et al., 2008; Viswanathan et al., 2008), as is Dicer-medi-ated cleavage (Heo et al., 2008; Rybak et al., 2008).”
- Posttranscriptional regulation of microRNA biogenesis in animals. (2010, background): “…to block accumulation of mature let-7 by repression of both Drosha and Dicer activities (Heo et al., 2008; Newman et al., 2008; Rybak et al., 2008; Viswanathan et al., 2008), recent studies demonstrate that LIN-28 can induce 30 terminal uridylation of pre-let-7 miRNA in mouse embryonic stem (ES)…”
- Child health, developmental plasticity, and epigenetic programming. (2011, background): “(227) reported that the LIN28B protein product selectively blocks the processing of pri-let-7 miRNAs in embryonic cells by blocking microprocessor-mediated cleavage of pri-let-7 miRNAs.”
- Control of Embryonic Stem Cell State (2011, background): “Loss of the key ESC transcription factors leads to downregulation of the miRNA regulator Lin28, withconsequentmaturationof theLet-7miRNAs,whicharehighly expressed in somatic tissues where they inhibit self-renewal genes (Melton et al., 2010; Viswanathan et al., 2008).”
- MicroRNA control of signal transduction (2010, background): “The levels of mature let-7 increase during differentiation, but this is not caused by an increase in its transcription rat”
- The role of let-7 in cell differentiation and cancer. (2010, background): “Two groups set out to biochemically identify this factor from differentiating P19 embryonic stem cells by coupling pre-let-7 molecules to beads and pulling down proteins that bound to the loop region of let-7 (Newman et al. 2008, Viswanathan et al. 2008).”
- The Lin28/let-7 axis regulates glucose metabolism (2011, background): “Another mechanism for let-7 downregulation involves the RNA-binding proteins Lin28a and Lin28b (collectively referred to as Lin28a/b), which are highly expressed during normal embryogenesis and upregulated in some cancers to potently and selectively block the maturation of let-7 (Heo et al., 2008; N”
- Induced pluripotency: history, mechanisms, and applications. (2010, background): “Indeed, lin28 represses let-7 miRNAs (Viswanathan et al. 2008), which are negative regulators of c-Myc translation (Akao et al. 2006; HH Kim et al. 2009), thus establishing a link between the two reprogramming cocktails (Oct4, Klf4, Sox2, and c-Myc, and Oct4, Sox2, Nanog, and Lin28).”