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Insulin-like growth factor-1 protects H9c2 cardiac myoblasts from oxidative stress-induced apoptosis via phosphatidylinositol 3-kinase and extracellular signal-regulated kinase pathways.

Hong, F, S J Kwon, B S Jhun, S S Kim, J Ha, S J Kim, N W Sohn, C Kang, and I Kang. 2001. “Insulin-Like Growth Factor-1 Protects H9c2 Cardiac Myoblasts from Oxidative Stress-Induced Apoptosis via Phosphatidylinositol 3-Kinase and Extracellular Signal-Regulated Kinase Pathways.”. Life Sciences 68 (10): 1095-105.

PKA phosphorylates histone deacetylase 5 and prevents its nuclear export, leading to the inhibition of gene transcription and cardiomyocyte hypertrophy.

Ha, Chang Hoon, Ji Young Kim, Jinjing Zhao, Weiye Wang, Bong Sook Jhun, Chelsea Wong, and Zheng Gen Jin. 2010. “PKA Phosphorylates Histone Deacetylase 5 and Prevents Its Nuclear Export, Leading to the Inhibition of Gene Transcription and Cardiomyocyte Hypertrophy.”. Proceedings of the National Academy of Sciences of the United States of America 107 (35): 15467-72.

Overexpression of ryanodine receptor type 1 enhances mitochondrial fragmentation and Ca2+-induced ATP production in cardiac H9c2 myoblasts.

O-Uchi, Jin, Bong Sook Jhun, Stephen Hurst, Sara Bisetto, Polina Gross, Ming Chen, Sarah Kettlewell, et al. 2013. “Overexpression of Ryanodine Receptor Type 1 Enhances Mitochondrial Fragmentation and Ca2+-Induced ATP Production in Cardiac H9c2 Myoblasts.”. American Journal of Physiology. Heart and Circulatory Physiology 305 (12): H1736-51.