Lin28 mediates the terminal uridylation of let-7 precursor MicroRNA.

By Inha Heo, Chirlmin Joo, Jun Cho, Minju Ha, Jinju Han, V. Narry Kim. Molecules and Cells, 2008

1,055 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/04a3de4e114d3fde50fe96e061a3423b47e94230

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. David P. Bartel
2. Scott M. Hammond
3. John S. Mattick
4. V. Narry Kim
5. Marcel E. Dinger
6. J. Ruby
7. Young‐Kook Kim
8. Tim R. Mercer

In Molecular Biology

1. David P. Bartel
2. John S. Mattick
3. Scott M. Hammond
4. V. Narry Kim
5. Marcel E. Dinger
6. Tim R. Mercer
7. Phillip D. Zamore
8. Richard I. Gregory

Citations in the corpus

• An epigenetic switch involving NF-κB, Lin28, let-7 microRNA, and IL6 links inflammation to cell transformation (2009, positive): “Lin28B plays a critical role in processing let-7RNA (Heo et al., 2008; Viswanathan et al., 2008), and our results indicate that NF-kB inhibits let-7 RNA levels primarily by activating transcription of lin-28B via direct binding to a highly conserved NF-kB site in the first intron.”
• 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].”
• Mammalian microRNAs: experimental evaluation of novel and previously annotated genes. (2010, background): “TUT4-catalyzed poly(U) addition to the let-7 premiRNA , which is specified by Lin28, plays an important role in post-transcriptional repression of let-7 expression (Heo et al. 2008, 2009; Hagan et al. 2009).”
• 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).”
• Genetic variation in microRNA networks: the implications for cancer research (2010, positive): “, suggesting the possibility of a negative feedback loop, similar to that between Let-7 and Lin28 (Ref”
• An overview of microRNAs (2015, background): “enzyme Tut4 to add an oligouridine tail to let-7 precursors, marking them for degradation[131-134].”
• Metazoan MicroRNAs (2018, background): “Lin28 binds to the terminal loop of let-7 pre-RNAs, which promotes oligo(U)-tailing at the 3′ end of these pre-miRNAs, through the recruitment of terminal uridylyl transferases, TUT4 and TUT7 (Heo et al., 2008; Hagan et al., 2009; Heo et al., 2009; Nam et al., 2011).”
• Oncogenic Lin28A and Lin28B inhibit let-7 microRNA biogenesis by distinct mechanisms (2011, neutral): “The developmentally regulated RNA-binding protein Lin28 was found to selectively repress expression of let-7 miRNAs (Heo et al., 2008; Newman et al., 2008; Rybak et al., 2008; Viswanathan et al., 2008).”
• 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).”
• The role of let-7 in cell differentiation and cancer. (2010, background): “It was found that in cells with blocked let-7 processing, pre-let-7 was posttranscriptionally modified and carried a 14-nt long extension mostly comprising uridine (Heo et al. 2008).”
• Overview of MicroRNA Biology (2015, background): “46 However, when pre-let-7 was monouridylated, there was an increase in Dicer activity resulting in higher levels of mature let-7.”