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Dong Hoon Shin

Researcher at New Generation University College

Publications -  382
Citations -  4877

Dong Hoon Shin is an academic researcher from New Generation University College. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 34, co-authored 343 publications receiving 4412 citations. Previous affiliations of Dong Hoon Shin include Dankook University & Seoul National University.

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Bortezomib inhibits tumor adaptation to hypoxia by stimulating the FIH-mediated repression of hypoxia-inducible factor-1

TL;DR: It is proposed that the mechanism underlying the inhibitory effects of bortezomib on tumor angiogenesis and hypoxic adaptation involves the repression of HIF-1alpha transcriptional activity by reinforcing the FIH-mediated inhibition of p300 recruitment.
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A novel mode of action of YC-1 in HIF inhibition: stimulation of FIH-dependent p300 dissociation from HIF-1{alpha}.

TL;DR: YC-1 inhibits HIF-1α via the FIH-dependent CAD inactivation as well as via the protein down-regulation, and it is suggested that the functional inactivation of Hif-α contributes to the YC- 1-induced deregulation of hypoxia-induced genes.
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RAGE regulates BACE1 and Aβ generation via NFAT1 activation in Alzheimer’s disease animal model

TL;DR: The receptor for advanced glycation end products (RAGE) is a multiligand cell surface receptor, and amyloid P peptide (Aβ) is one of the ligands for RAGE, which regulates BACE1 and Aβ generation via NFAT1 activation in Alzheimer's disease animal model.
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Tracing hepatitis B virus to the 16th century in a Korean mummy.

TL;DR: This study describes the complete sequence of the oldest HBV isolate and the most ancient full viral genome known so far, which probably represents the earliest human HBV sequence that colonized Southeast Asia by human migration.
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SIRT1 and AMPK Mediate Hypoxia-Induced Resistance of Non–Small Cell Lung Cancers to Cisplatin and Doxorubicin

TL;DR: It is demonstrated that a SIRT1 activator SRT1720 augmented the antitumor effects of cisplatin, and these effects could be blocked by administration of an AMPK inhibitor compound C.