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Nitric Oxide Prevents the Bovine Cerebral Endothelial Cell Death Induced by Serum-Deprivation
ChulHoonKimYoungSooAhn 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 1997, Vol.1 No.5 6 515-521 (7 pages)
Endothelial cells play a central role in the inflammatory processes, and activation of nuclear factor kappa B (NF-κB) is a key component in that inflammatory processes. Previously, we reported that tumor necrosis factor alpha(TNFα) had protective effect of cell death induced by serum deprivation and this protection was related to NF-κB activation. Inducible nitric oxide synthase (iNOS) is a member of the molecules which transcription is regulated mainly by NF-κB. And the role of nitric oxide... -
Rpi-blb2-Mediated Hypersensitive Cell Death Caused by Phytophthora infestans AVRblb2 Requires SGT1, but not EDS1, NDR1, Salicylic Acid-, Jasmonic Acid-, or Ethylene-Mediated Signaling
한국식물병리학회 The Plant Pathology Journal 7 Pages
한국식물병리학회 The Plant Pathology Journal 2014, 30권 3호 3 254-260 (7 pages)
coiled-coil-nucleotide binding site and leucine-rich repeat (CC-NBS-LRR) motif that recognizes the Phytophthora infestans AVRblb2 effector and triggers hypersensitive cell death (HCD). To better understand the components required for Rpi-blb2-mediated HCD in plants, we used virus-induced gene silencing to repress candidate genes in Rpi-blb2-transgenic Nicotiana benthamiana plants and assayed the plants for AVRblb2 effector. Rpi-blb2 triggers HCD through NbSGT1-mediated pathways, but not NbEDS1-... -
Influence of defective sites in Pt/C catalysts on the anode of direct methanol fuel cell and their role in CO poisoning: a first-principles study
Soonchul Kwon, Seung Geol Lee 한국탄소학회 Carbon Letters 5 Pages
한국탄소학회 Carbon Letters 2015, Vol.16 No.3 6 198-202 (5 pages)
Carbon-supported Pt catalyst systems containing defect adsorption sites on the anode of direct methanol fuel cells were investigated, to elucidate the mechanisms of H2 dissociation and carbon monoxide (CO) poisoning. Density functional theory calculations were carried out to determine the effect of defect sites located neighboring to or distant from the Pt catalyst on H2 and CO adsorption properties, based on electronic properties such as adsorption energy and electronic band gap. Interestingly,... -
Cilostazol attenuates kainic acid-induced hippocampal cell death
Young-SeopPark, ZhenJin, EunAeJeong, Chin-okYi, JongYoulLee, InSungPark, GuSeobRoh 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2018, Vol.22 No.1 7 63-70 (8 pages)
neuroprotective agent. However, little is known about cilostazol’s effect on excitotoxicity induced neuronal cell death. Therefore, this study evaluated the neuroprotective effect of cilostazol treatment against hippocampal neuronal damage in a mouse model of kainic acid (KA)-induced neuronal loss. Cilostazol pretreatment reduced KA-induced seizure scores and hippocampal neuron death. In addition, cilostazol pretreatment increased cAMP response element-binding protein (CREB) phosphorylation and... -
Quercetin induces apoptosis and cell cycle arrest in triple-negative breast cancer cells through modulation of Foxo3a activity
LichThiNguyen, Yeon-HeeLee, AshishRanjanSharma, Jong-BongPark, SupriyaJagga, GarimaSharma, Sang-SooLee, Ju-SukNam 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2017, Vol.21 No.2 8 205-213 (9 pages)
and GADD45 signaling activities. We also observed that quercetin induced protein level, transcriptional activity and nuclear translocation of Foxo3a. Knockdown of Foxo3a caused significant reduction in the effect of quercetin on cell apoptosis and cell cycle arrest. In addition, treatment of JNK inhibitor (SP 600125) abolished quercetin-stimulated Foxo3a activity, suggesting JNK as a possible upstream signaling in regulation of Foxo3a activity. Knockdown of Foxo3a and inhibition of JNK activity... -
Activation of K+ channel by 1-EBIO rescues the head and neck squamous cell carcinoma cells from Ca2+ ionophore-induced cell death
MingZheYin, Seok-WooPark, , TaeWookKang, KyungSooKim, , , HaeYoungYoo6, JunhoLee, J.HunHah, , MyungHunSung, , SungJoonKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2016, Vol.20 No.1 4 25-33 (9 pages)
investigate the role of Ca2+-activated K+ channel (SK4) in head and neck squamous cell carcinoma cells (HNSCCs) of dif-ferent cell lines; SNU-1076, OSC-19 and HN5. Treatment with 1 μM ionomycin induced cell death in all the three cell lines. Whole-cell patch clamp study suggested common expressions of Ca2+-activated Cl− channels (Ano-1) and Ca2+-activated nonselective cation channels (CAN). 1-EBIO, an activator of SK4, induced outward K+ current (ISK4) in SNU-1076 and OSC-19. In HN5, ISK4... -
Involvement of ROS in Curcumin-induced Autophagic Cell Death
YounJuLee, Nam-YiKim, Young-AhSuh, ChuHeeLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2011, Vol.15 No.1 1 1-8 (8 pages)
of autophagosome- lysosome fusion, and cell viability assay was further confirmed that cucurmin-induced cell death was partially blocked by bafilomycin A as well as NAC. We also observed that NAC abolished curcumin- induced activation of extracelluar signal-regulated kinases (ERK) 1/2 and p38 mitogen-activated protein kinases (MAPK), but not Jun N-terminal kinase (JNK). However, the activation of ERK1/2 and p38 MAPK seemed to have no effect on the curcumin-induced autophagy, since both the... -
Functional Expression of TRPV4 Cation Channels in Human Mast Cell Line (HMC-1)
KyungSooKim, DongHoonShin, JooHyunNam, KyungSunPark, YinHuaZhang, WooKyungKim, SungJoonKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.6 11 419-425 (7 pages)
allergens and also by various nonspecific stimuli, which might induce physical urticaria. This study investigated the functional expression of temperature sensitive transient receptor potential vanilloid (TRPV) subfamily in the human mast cell line (HMC-1) using whole-cell patch clamp techniques. The temperature of perfusate was raised from room temperature (RT, 23∼25oC) to a moderately high temperature (MHT, 37∼39oC) to activate TRPV3/4, a high temperature (HT, 44∼46oC) to activate TRPV1, or... -
Bark Constituents from Mushroom-detoxified Rhus verniciflua Suppress Kainic Acid-induced Neuronal Cell Death in Mouse Hippocampus
Jong-SeonByun, YoonHeeHan, Sung-JunHong, Sung-MiHwang, Yong-SooKwon, HeeJaeLee, Sung-SooKim, Myong-JoKim, WanjooChun 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 5 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.5 5 279-283 (5 pages)
in significant apoptotic neuronal cell death in the CA3 region of mouse hippocampus. However, seven daily administrations of RVH-1 or RVH-2 prior to KA injection significantly attenuated KA-induced pyramidal neuronal cell death in the CA3 region. Furthermore, pretreatment with RVH-1 and RVH-2 also suppressed KA-induced microglial activation in the mouse hippocampus. The present study demonstrates that RVH-1 and RVH-2 isolated from Rhus verniciflua and detoxified using mushroom species possess... -
Neuroprotective Effect of Visnagin on Kainic Acid-induced Neuronal Cell Death in the Mice Hippocampus
Min-SooKwon, Jin-KooLee, Soo-HyunPark, Yun-BeomSim, Jun-SubJung, Moo-HoWon, Seon-MiKim, Hong-WonSuh 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.5 2 257-263 (7 pages)
neuroprotective effect against kainic acid (KA)-induced neuronal cell death. In the cresyl violet staining, pre-treatment or post-treatment visnagin (100 mg/kg, p.o. or i.p.) showed a neuroprotective effect on KA (0.1Ռg) toxicity. KA-induced gliosis and proinflammatory marker (IL-1Ղ, TNF-Ձ, IL-6, and COX-2) inductions were also suppressed by visnagin administration. These results suggest that visnagin has a neuroprotective effect in terms of suppressing KA-induced pathogenesis...


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