Showing papers by "Jae Hong Seol published in 2015"
TL;DR: It is demonstrated that NEDD4 ubiquitylates and destabilizes WW45 and LATS kinase, both of which are required for active Hippo signalling, and promotes intestinal stem cell renewal in Drosophila by suppressing HippO signalling.
Abstract: The Hippo pathway plays a role in regulating organ size and stem cell renewal but the regulatory mechanisms that fine-tune this pathway are not well understood. Here the authors report on the role of NEDD4 as a negative regulator of the Hippo signalling components, WW45 and LATS kinase, and in controlling cell proliferation and intestinal stem cell homeostasis.
52 citations
TL;DR: Investigation of the role of SENP2 in fatty acid metabolism in C2C12 myotubes and in vivo indicates that muscle SENP1 could be a novel therapeutic target for the treatment of obesity-linked metabolic disorders and identifies SENP 2 as an important regulator of fatty acids metabolism in skeletal muscle.
Abstract: Small ubiquitin-like modifier (SUMO)-specific proteases (SENPs) that reverse protein modification by SUMO are involved in the control of numerous cellular processes, including transcription, cell division, and cancer development However, the physiological function of SENPs in energy metabolism remains unclear Here, we investigated the role of SENP2 in fatty acid metabolism in C2C12 myotubes and in vivo In C2C12 myotubes, treatment with saturated fatty acids, like palmitate, led to nuclear factor-κB–mediated increase in the expression of SENP2 This increase promoted the recruitment of peroxisome proliferator–activated receptor (PPAR)δ and PPARγ, through desumoylation of PPARs, to the promoters of the genes involved in fatty acid oxidation (FAO), such as carnitine-palmitoyl transferase-1 (CPT1b) and long-chain acyl-CoA synthetase 1 (ACSL1) In addition, SENP2 overexpression substantially increased FAO in C2C12 myotubes Consistent with the cell culture system, muscle-specific SENP2 overexpression led to a marked increase in the mRNA levels of CPT1b and ACSL1 and thereby in FAO in the skeletal muscle, which ultimately alleviated high-fat diet–induced obesity and insulin resistance Collectively, these data identify SENP2 as an important regulator of fatty acid metabolism in skeletal muscle and further implicate that muscle SENP2 could be a novel therapeutic target for the treatment of obesity-linked metabolic disorders
49 citations
TL;DR: Results suggest that unknown alternations of splicing machinery in C6 and A172 cells and the glioblastoma brain tissues are responsible for the deleterious exon skipping, and indicate that the c-CblExon skipping contributes to human glioma and its malignant behavior.
10 citations