S
Suhn Hee Kim
Researcher at Chonbuk National University
Publications - 200
Citations - 4185
Suhn Hee Kim is an academic researcher from Chonbuk National University. The author has contributed to research in topics: Atrial natriuretic peptide & Apoptosis. The author has an hindex of 35, co-authored 198 publications receiving 3870 citations. Previous affiliations of Suhn Hee Kim include UPRRP College of Natural Sciences.
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Journal ArticleDOI
Sulforaphane protects ischemic injury of hearts through antioxidant pathway and mitochondrial KATP channels
Cheng Shi Piao,Shan Gao,Geum-Hwa Lee,Do-Sung Kim,Byung-Hyun Park,Soo Wan Chae,Han-Jung Chae,Suhn Hee Kim +7 more
TL;DR: The results suggest that the protective effects of sulforaphane against I/R injury may be partly mediated through mitochondrial K(ATP) channels and antioxidant pathway.
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Presence and biological activity of c-type natriuretic peptide-dependent guanylate cyclase-coupled receptor in the penile corpus cavernosum
TL;DR: It is suggested for the first time that CNP modulates the erectile smooth muscle tone of penis by predominant activation of B-subtype of NPR with augmentation of cGMP production via particulate GC.
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An ROS generator, antimycin A, inhibits the growth of HeLa cells via apoptosis.
TL;DR: It is demonstrated that AMA potently generates ROS, induces the depletion of GSH content in He La cells, and strongly inhibits the growth of HeLa cells throughout apoptosis.
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Arsenic trioxide inhibits growth of As4.1 juxtaglomerular cells via cell cycle arrest and caspase-independent apoptosis
TL;DR: It is demonstrated that arsenic trioxide as a ROS generator potently inhibited the growth of As4.1 JG cells through S phase arrest of the cell cycle and caspase-independent apoptosis and was significantly decreased and O(2)(*-) was increased.
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Arsenic trioxide inhibits the growth of Calu-6 cells via inducing a G2 arrest of the cell cycle and apoptosis accompanied with the depletion of GSH.
TL;DR: It is demonstrated that ATO inhibits the growth of Calu-6 cells by inducing a G2 arrest of the cell cycle and by triggering apoptosis accompanied with the depletion of GSH.