Huifei Liu

TL;DR: It is shown that specific ablation of YY1 in mouse B cells caused a defect in somatic rearrangement in the immunoglobulin heavy-chain (IgH) locus and a block in the progenitor-B-to-precursor- B-cell transition, which was partially rescued by a prerearranged IgH transgene.

TL;DR: Functional assays revealed that both YY1 and INO80 are essential in homologous recombination–based DNA repair (HRR), which was further supported by the finding that YY 1 preferentially bound a recombination-intermediate structure in vitro.

TL;DR: Genome-wide expression profiling identified a plethora of Yy1 target genes that have been implicated in cell growth, proliferation, cytokinesis, apoptosis, development, and differentiation, suggesting that YY1 coordinates multiple essential biological processes through a complex transcriptional network.

TL;DR: It is shown that chronic rapamycin treatment in mice led to insulin resistance with suppression of insulin/IGF signaling and genes associated within this pathway, such as Igf1-2, Irs1-1, and Akt1-3, and that skeletal muscle-specific YY1 knockout mice were protected fromRapamycin-induced diabetic-like symptoms.

TL;DR: It is reported that skeletal-muscle-specific YY1 knockout mice have severely defective mitochondrial morphology and oxidative function associated with exercise intolerance, signs of mitochondrial myopathy, and short stature and how its inactivation might contribute to exercise intolerance and mitochondrial myopathies is explained.