Targeted deletion reveals essential and overlapping functions of the miR-17 through 92 family of miRNA clusters.

By A. Ventura, Amanda G. Young, M. Winslow, L. Lintault, Alexander Meissner, S. Erkeland, J. Newman, R. Bronson, D. Crowley, James R. Stone and 3 more. Cell, 2008

1,699 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/6a58496ae31af9ec50f2fcfed5d23762cbeb7ee2

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Citations in the corpus

MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice. (2009, neutral): “miR-208a and miR-208b are of similar sequence with identical seed regions (Figure 1A), which suggests they might be functionally redundant (21).”
Metazoan MicroRNAs (2018, neutral): “3) miR-17 18 19a 20a 19b-1 92a-1, miR-106b 93 25 Embryonic lethality at midgestation, complete penetrance (Ventura et al., 2008)”
MicroRNAs in stress signaling and human disease (2012, background): “…mice has been documented only for the miR-17-92 and miR-106b-25 clusters, which act together to regulate multiple aspects of embryonic development (Ventura et al., 2008), miR133a-1 and miR-133a-2, which together are required for appropriate cardiac and skeletal muscle development (Liu et al.,…”
Preparing for the First Breath: Genetic and Cellular Mechanisms in Lung Development (2010, neutral): “Deletion of Dicer from the epithelium inhibits lung development (Harris et al., 2006) and the miR17–92 cluster promotes early distal progenitor proliferation, possibly by controlling factors that regulate cell division (Lu et al., 2007; Ventura et al., 2008).”
MicroRNAs in development and disease. (2011, positive): “Knockout of miR-17 92 confirmed that this phenotype is indeed predominantly attributed to this miRNA cluster versus any of the others that were depleted by the loss of Dicer (633).”
Repair and regeneration of the respiratory system: complexity, plasticity, and mechanisms of lung stem cell function (2014, neutral): “Two miRNA clusters play important roles in lung epithelial endoderm proliferation and differentiation. miR17-92 and miR302-367 are both highly expressed during early lung endoderm development but are significantly down-regulated or extinguished by birth (Tian et al., 2011; Ventura et al., 2008).”