Hun‐Taeg Chung

ORCID: 0000-0003-4802-7467
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About
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Research Areas
  • Heme Oxygenase-1 and Carbon Monoxide
  • Nitric Oxide and Endothelin Effects
  • Alcohol Consumption and Health Effects
  • Autophagy in Disease and Therapy
  • Neonatal Health and Biochemistry
  • Endoplasmic Reticulum Stress and Disease
  • Eicosanoids and Hypertension Pharmacology
  • Cannabis and Cannabinoid Research
  • Thermal Regulation in Medicine
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Adipose Tissue and Metabolism
  • Immune Response and Inflammation
  • Asthma and respiratory diseases
  • Phytochemistry and Biological Activities
  • Biofield Effects and Biophysics
  • Curcumin's Biomedical Applications
  • Traditional Chinese Medicine Analysis
  • Genomics, phytochemicals, and oxidative stress
  • Sirtuins and Resveratrol in Medicine
  • NF-κB Signaling Pathways
  • Natural product bioactivities and synthesis
  • Galectins and Cancer Biology
  • Bioactive Compounds and Antitumor Agents
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Calcium signaling and nucleotide metabolism

Daegu Haany University
2024-2025

University of Ulsan
2014-2023

Jeonbuk National University
1995-2019

Ulsan College
2009-2016

Ulsan University Hospital
2010-2012

Wonkwang University
2001-2010

National Research Foundation of Korea
2010

Gwangju Institute of Science and Technology
2007

Kangwon National University
2007

Bipar
1994-2004

Mitogen-activated protein kinases (MAPKs) are serine-threonine that play the major role in signal transduction from cell surface to nucleus. MAPKs, which consist of growth factor-regulated extracellular signal-related (ERKs), and stress-activated c-jun NH 2 -terminal (JNKs) p38 part a three-kinase signaling module composed MAPK, an MAPK kinase (MAP2K) (MAP3K). MAP3Ks phosphorylate MAP2Ks, turn activate MAPKs. phosphatases (MKPs), recognize TXY amino acid motif present dephosphorylate...

10.1155/2011/792639 article EN cc-by Journal of Signal Transduction 2011-02-06

Abstract Heme oxygenase-1 (HO-1) catabolizes heme into CO, biliverdin, and free iron serves as a protective enzyme by virtue of its anti-inflammatory, antiapoptotic, antiproliferative actions. Previously, we have demonstrated that human CD4+ T cells express HO-1 HO-1-overexpressing Jurkat tend to display lower proliferative response. The aim this study is elucidate the mechanism(s) which can mediate effect on cells. Among three byproducts, only CO showed suppressive cell proliferation in...

10.4049/jimmunol.172.8.4744 article EN The Journal of Immunology 2004-04-15

In this report, we tested the hypothesis that cellular content of non-heme iron determined whether cytotoxic levels nitric oxide (NO) resulted in apoptosis <i>versus</i> necrosis. The consequences NO exposure on cell viability were RAW264.7 cells (a type with low levels) and hepatocytes (cells high content). Whereas micromolar concentrations donor<i>S</i>-nitroso-<i>N</i>-acetyl-dl-penicillamine induced cells, millimolar required to induce necrosis hepatocytes. Caspase-3 activation...

10.1074/jbc.275.15.10954 article EN cc-by Journal of Biological Chemistry 2000-04-01

Mitochondrial cytochrome c release plays a critical role in apoptotic signal cascade after the activation of cell surface death receptors. We investigated played by nitric oxide (NO) mitochondrial signaling tumor necrosis factor α (TNF-α) plus actinomycin D (TNF-α/ActD)-induced apoptosis. NO produced either S-nitroso-N-acetyl-DL-penicillamine (SNAP) or inducible synthase (iNOS) prevented TNF-α/ActD-induced apoptosis hepatocytes and also inhibited both caspase-8-like (IETDase) caspase-3-like...

10.1053/jhep.2000.18291 article EN Hepatology 2000-10-01

Although nitric oxide (NO) induces neuronal cell death under some conditions, it also can prevent apoptosis resulting from growth factor withdrawal. We investigated the molecular mechanism by which NO protects undifferentiated and differentiated PC12 cells trophic deprivation-induced apoptosis. underwent apoptotic in association with increased caspase-3-like activity, DNA fragmentation, poly(ADP-ribose) polymerase (PARP) cleavage, cytochrome c release after 24 hr of serum The was inhibited...

10.1523/jneurosci.19-16-06740.1999 article EN Journal of Neuroscience 1999-08-15

Fractalkine (FKN) has been implicated in modulation of angiogenesis and vascular inflammation, but the underlying mechanism not elucidated. We have investigated molecular by which FKN regulates angiogenesis. found that recombinant increases vitro proliferation, migration, tube formation human umbilical vein endothelial cells stimulates vivo FKN-induced was accompanied phosphorylation ERK, Akt, nitric oxide (NO) synthase (eNOS), as well an increase NO production. These biochemical events were...

10.1152/ajpheart.00113.2006 article EN AJP Heart and Circulatory Physiology 2006-07-29

Carbon monoxide (CO), a reaction product of the cytoprotective heme oxygenase (HO)-1, is antiapoptotic in variety models cellular injury, but precise mechanisms remain to be established. In human umbilical vein endothelial cells, exogenous CO activated Nrf2 through phosphorylation protein kinase R-like endoplasmic reticulum (PERK), resulting HO-1 expression. CO-induced activation PERK was followed by eukaryotic translation initiation factor 2alpha and expression activating transcription 4....

10.1161/circresaha.107.154781 article EN Circulation Research 2007-09-07

IL-1β and TNF-α are important proinflammatory cytokines that respond to mutated self-antigens of tissue damage exogenous pathogens. The endoplasmic reticulum (ER) stress unfolded protein responses related the induction cytokines. However, detailed molecular pathways by which ER mediates cytokine gene expression have not been investigated. In this study, we found stress-induced inositol-requiring enzyme (IRE)1α activation differentially regulates via glycogen synthase kinase (GSK)-3β X-box...

10.4049/jimmunol.1401399 article EN The Journal of Immunology 2015-03-28

The mechanisms underlying pathophysiological states such as metabolic syndrome and obesity include endoplasmic reticulum (ER) stress aberrant inflammatory responses. ER results from the accumulation of misfolded proteins during conditions. However, precise by which modulates inflammation remain incompletely understood. In this study, we hypothesized that alone could represent a sufficient signal for modulation inflammasome-dependent cytokine We found several stress-inducing chemicals free...

10.1177/1753425913508593 article EN Innate Immunity 2013-11-11

Obesity-induced hepatic lipid accumulation causes lipotoxicity, mitochondrial dysfunction, oxidative stress, and insulin resistance, is implicated in non-alcoholic pathologies such as steatohepatitis fibrosis. Heme oxygenase-1 (HO-1), an important antioxidant enzyme catalyzing the rate-limiting step heme degradation, protects against inflammation, metabolic dysregulation. Here, we demonstrate that phytochemical, quercetin, a natural polyphenol flavonoid, steatosis obese mice fed high-fat...

10.1186/s12986-015-0030-5 article EN cc-by Nutrition & Metabolism 2015-10-05

The immunoresponsive gene 1 (IRG1) protein has crucial functions in embryonic implantation and neurodegeneration. IRG1 promotes endotoxin tolerance by increasing A20 expression macrophages through reactive oxygen species (ROS). cytoprotective heme oxygenase-1 (HO-1), which generates endogenous carbon monoxide (CO), is expressed the lung during Lipopolysaccharide (LPS) cross tolerance. However, detailed molecular mechanisms functional links between HO-1 innate immune system remain unknown. In...

10.1038/cmi.2015.02 article EN cc-by-nc-nd Cellular and Molecular Immunology 2015-02-02

Nonalcoholic fatty liver disease (NAFLD), the hepatic manifestation of metabolic syndrome, has emerged as one most common causes chronic in developed countries over last decade. NAFLD comprises a spectrum pathological changes, including steatosis, steatohepatitis, advanced fibrosis, and cirrhosis. Autophagy, homeostatic process for protein organelle turnover, is decreased during development NAFLD. Previously, we have shown that carbon monoxide (CO), reaction product heme oxygenase (HO)...

10.1016/j.freeradbiomed.2017.05.026 article EN cc-by-nc-nd Free Radical Biology and Medicine 2017-06-01

Nitric oxide (NO) functions not only as an important signaling molecule in the brain by producing cGMP, but also regulates neuronal cell apoptosis. The mechanism which NO apoptosis is unclear. In this study, we demonstrated that NO, produced either from donor S-nitroso-N-acetyl-d,l-penicillamine (SNAP) or transfection of synthase, suppressed 6-hydroxydopamine (6-OHDA)-induced PC12 cells inhibiting mitochondrial cytochrome c release, caspase-3 and -9 activation, DNA fragmentation. This...

10.1096/fj.02-0738com article EN The FASEB Journal 2003-05-28

10.1016/s1360-1385(99)01462-4 article EN Trends in Plant Science 1999-09-01

Prostaglandin E2(PGE2), a major product of cyclooxygenase, has been implicated in modulating angiogenesis, vascular function, and inflammatory processes, but the underlying mechanism is not clearly elucidated. We here investigated molecular by which PGE 2 regulates angiogenesis. Treatment human umbilical vein endothelial cells (HUVEC) with increased phosphorylation Akt nitric oxide synthase (eNOS), eNOS activity, (NO) production activation cAMP-dependent protein kinase (PKA)...

10.1038/emm.2005.72 article EN cc-by Experimental & Molecular Medicine 2005-12-01
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