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Antitumor Effects of Camptothecin Combined with Conventional Anticancer Drugs on the Cervical and Uterine Squamous Cell Carcinoma Cell Line SiHa
SangWonHa, YunJeongKim, WonyongKim, ChungSooLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.2 7 115-122 (8 pages)
in mitochondria are involved in the induction of cell death in cancer cells. We assessed the toxic effect of camptothecin against the human cervical and uterine tumor cell line SiHa with respect to the mitochondria-mediated cell death process, and examined the combined effect of camptothecin and anticancer drugs. Camptothecin caused apoptosis in SiHa cells by inducing mitochondrial membrane permeability changes that lead to the loss of mitochondrial membrane potential, decreased Bcl-2 levels,... -
Cilostazol Attenuates 4-hydroxynonenal-enhanced CD36 Expression on Murine Macrophages via Inhibition of NADPH Oxidase-derived Reactive Oxygen Species Production
MiRanYun, HyeMiPark, KyoWonSeo, ChaeEunKim, JungWookYoon, ChiDaeKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.2 5 99-106 (8 pages)
in macrophages are unclear. This study investigated the role of cilostazol on CD36 expression of murine macrophages enhanced by HNE, a byproduct of lipid peroxidation. The stimulation of macrophages with HNE led to an increased expression of CD36, which was significantly attenuated by NAC, an antioxidant. Moreover, the increased production of ROS by HNE was completely abolished by NADPH oxidase inhibitors, DPI and apocynin, as well as by the 5-LO inhibitor, MK886, but not by inhibitors for other... -
P2 Receptor-mediated Inhibition of Vasopressin-stimulated Fluid Transport and cAMP Responses in AQP2-transfected MDCK Cells
YangHooKim, YoungJinChoi, HaeRahnBae, JaeSukWoo 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.1 2 9-14 (6 pages)
of cell monolayers to basolateral AVP resulted in stimulation of apical to basolateral net fluid transport driven by osmotic gradient which was formed by addition of 500 mM mannitol to basolateral bathing solution. Pre-exposure of the basolateral surface of cell monolayers to ATP (100 µM) for 30 min significantly inhibited the AVP-stimulated net fluid transport. In these cells, AVP-stimulated cAMP production was suppressed as well. Profile of the effects of different nucleotides suggested... -
Heat Acclimatization in Hot Summer for Ten Weeks Suppress the Sensitivity of Sweating in Response to Iontophoretically-administered Acetylcholine
Jeong-BeomLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.6 10 349-356 (8 pages)
by the axon reflex was 2.06±0.24 mg/cm2 and 1.39±0.32 mg/cm2 before and after acclimatization in July and September, respectively (p<0.001). The sweat volume of the DIR was 5.88±1.33 mg/cm2 and 4.98±0.94 mg/cm2 before and after acclimatization in July and September, respectively (p<0.01). These findings suggest that lower peripheral sudomotor responses of the ACh receptors are indicative of a blunted sympathetic nerve response to ACh during exposure to hot summer weather conditions. -
Functional Connectivity Map of Retinal Ganglion Cells for Retinal Prosthesis
JangHeeYe, SangBaekRyu, KyungHwanKim, YongSookGoo 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.6 4 307-314 (8 pages)
Retinal prostheses are being developed to restore vision for the blind with retinal diseases such as retinitis pigmentosa (RP) or age-related macular degeneration (AMD). Among the many issues for prosthesis development, stimulation encoding strategy is one of the most essential electrophysiological issues. The more we understand the retinal circuitry how it encodes and processes visual information, the greater it could help decide stimulation encoding strategy for retinal prosthesis. Therefore,... -
Forskolin Enhances Synaptic Transmission in Rat Dorsal Striatum through NMDA Receptors and PKA in Different Phases
HyeongSeokCho, HyunHoLee, SeJoonChoi, KiJungKim, SeungHyunJeun, Qing-ZhongLi, Ki-WugSung 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.6 2 293-298 (6 pages)
The effect of forskolin on corticostriatal synaptic transmission was examined by recording excitatory postsynaptic currents (EPSCs) in rat brain slices using the whole-cell voltage-clamp technique. Forskolin produced a dose-dependent increase of corticostriatal EPSCs (1, 3, 10, and 30ՌM) immediately after its treatment, and the increase at 10 and 30ՌM was maintained even after its washout. When the brain slices were pre-treated with <FONT SIZE=2>(DL)-2-amino-5-phosphonovaleric... -
PKC-Independent Stimulation of Cardiac Na+/Ca2+ Exchanger by Staurosporine
TongMookKang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.5 7 259-266 (8 pages)
was observed during the Ca2+ transients, neither a selective PKC inhibitor (calphostin C) nor a PKC activator (PMA) changed the degrees of rundown. By comparison, a non-specific PKC inhibitor, staurosporine (STS), reversed rundown in a dose-dependent and reversible manner. The action of STS was unaffected by pretreatment of the cells with calphostin C, PMA, or forskolin. Taken together, the results suggest that the stimulation of reverse NCX1 by STS is independent of PKC and/or PKA inhibition. -
Netrin-1 Specifically Enhances Cell Spreading on Fibronectin in Human Glioblastoma Cells
HyunKyoungLee, InAeSeo, YoonKyungShin, SangHwaLee, Su-YoungSeo, DukJoonSuh, HwanTaePark 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.5 2 225-230 (6 pages)
Netrins are secreted molecules and involved in axon guidance, cell migration and tumor development. Recent studies revealed that netrins perform novel functions in such processes as epithelial development and angiogenesis without operating through the classical netrin receptors, DCC (Deleted in Colorectal Cancer) and Unc5h. In the present study, we investigated the roles of netrin-1 and its receptors in cell spreading of human glioblastoma cells, and found that netrin-1 haptotactically enhanced... -
Sorting Nexin 17 Interacts Directly with Kinesin Superfamily KIF1Bβ Protein
Dae-HyunSeog, JinHan 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.4 11 199-204 (6 pages)
a member of the Kinesin superfamily proteins (KIFs), which are microtubule-dependent molecular motors that are involved in various intracellular organellar transport processes. KIF1BՂ is not restricted to neuronal systems, however, is widely expressed in other tissues, even though the function of KIF1BՂ is still unclear. To elucidate the KIF1BՂ-binding proteins in non-neuronal cells, we used the yeast two-hybrid system, and found a specific interaction of KIF1BՂ and the... -
Long-term Activation of c-Jun N-terminal Kinase through Receptor Interacting Protein is Associated with DNA Damage-induced Cell Death
JeongHoSeok, KyeongAhPark, HeeSunByun, MinhoWon, SangheeShin, Byung-LyulChoi, HyunjiLee, Young-RaeKim, JangHeeHong, JongsunPark, GangMinHu 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.4 9 185-192 (8 pages)
Activation of c-Jun N-terminal kinase (JNK), a member of the mitogen-activated protein kinase family, is an important cellular response that modulates the outcome of the cells which are exposed to the tumor necrosis factor (TNF) or the genotoxic stress including DNA damaging agents. Although it is known that JNK is activated in response to genotoxic stress, neither the pathways to transduce signals to activate JNK nor the primary sensors of the cells that trigger the stress response have been...


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