Laboratory of Stem Cell Differentiation(줄기세포분화연구실)

Kang, Jong-Sun

Stem cell function control mechanism, muscle/cardiovascular disease mechanism and treatment development Laboratory
The goal of the research in my laboratory is to understand the molecular regulatory pathways that control proliferation and differentiation of stem cells during regeneration and underlying molecular mechanisms in stem cell dysfunction related to aging or degenerative diseases. Our current research is focused on the elucidation of regulatory mechanisms and in vivo function of key stem niche signals (Sonic hedgehog and Wnt), cell adhesion molecules and protein arginine methyltransferases by utilizing knockout mice, disease animal models and stem cells as model systems. The long-term goal of this research is to identify molecular targets for the development of therapeutic tools to intervene the aging-related muscle atrophy, cardiovascular diseases or degenerative diseases.
&8729 Kim et al., 2020. Indoprofen prevents muscle wasting in aged mice through activation of PDK1/AKT pathway. Journal of Cachexia, Sarcopenia and Muscle. In press.

&8729 Bae et al., 2020. Satellite cell-specific ablation of Cdon impairs integrin activation, FGF signaling, and muscle regeneration. Journal of Cachexia, Sarcopenia and Muscle. In press.

&8729 Voung et al., 2019. Prmt7 methylates and suppresses Gli2 binding to SUFU thereby promoting its activation. Cell Death & Differentiation, 27(1), 15-28.

&8729 Jeong et al., 2019. Prmt7 promotes myoblast differentiation via methylation of p38MAPK. Cell Death & Differentiation, 27,573-586.

&8729 Choi et al., 2018. Skeletal muscle-specific PRMT1 deletion causes muscle atrophy via deregulation of PRMT6/FOXO3 axis. Autophagy, 15(6), 1069.

&8729 Pyun et al., 2018. Cardiac specific PRMT1 ablation causes heart failure through CaMKII dysregulation. Nature Communications, 9(1), 5107.

&8729 Jeong et al., 2017. Cdon deficiency causes cardiac remodeling through hyperactivation of Wnt/&61538-catenin signaling, PNAS, 114(8).
(Tel) 031-299-6135,  (Email)