Yun-Sil Lee

TL;DR: In this paper, the c-Myc (hereafter referred to as Myc) oncogenic transcription factor, which is known to regulate microRNAs and stimulate cell proliferation, transcriptionally represses miR-23a and miR23b, resulting in greater expression of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 prostate cancer cells.

TL;DR: In this paper, the c-Myc oncogenic transcription factor (Myc) is pathologically activated in many human malignancies and the predominant consequence of activation of Myc is widespread repression of miRNA expression.

TL;DR: It is shown here that Myc regulates a much broader set of miRNAs than previously anticipated, and extensive reprogramming of the miRNA transcriptome by Myc contributes to tumorigenesis.

TL;DR: It is shown that Fst mutant mice exhibit haploinsufficiency, with muscles of Fst heterozygotes having significantly reduced size, a shift toward more oxidative fiber types, an impairment of muscle remodeling in response to cardiotoxin-induced injury, and a reduction in tetanic force production yet a maintenance of specific force.

TL;DR: It is shown that myostatin/activin A inhibition can cause muscle hypertrophy in mice lacking either syndecan4 or Pax7, both of which are important for satellite cell function and development and support that inhibition of this signaling pathway can be an effective therapeutic approach for increasing muscle growth even in disease settings characterized by satellite cell dysfunction.