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Intracellular ADP-ribose inhibits ATP-sensitive K^+ channels in rat ventricular myocytes
KWAK, YONG-GEUN,PARK, SEOK-KI,KIM, UH-HYUN,HAN, MYUNG-KWAN,EUN, JAE-SOON,CHO, KYU-PARK,CHAE, SOO-WAN 우석대학교 의약품개발연구소 1996 藥學硏究誌 Vol.1 No.-
Intracellular ADP-ribose inhibits ATP-sensitive K^+ channels in rat ventricular myocytes. Am. J. Physiol. 271 (Cell Physiol. 40): C464-c468,1996.-Cyclic ADP-ribose(cADPR), an NAD metabolite, has been shown to be a messenger for Ca^2+ mobilization from intracellular Ca^2+ stroes. However, the physiological role of ADP-ribose(ADPR), another metabolite of NAD, is not known. We examined the effects of cADPR and ADPR and the ATP-sensitive K^+ channel (K_ATP) activity in rat ventricular myocytes by use of the inside-out patch-clamp configuration. ADPR, but not cADPR, inhibited the channel activity at micromolar range with an inhibitor constant(K_i) of 38.4uM. The Hill coefficient was 0.9. ATP inhabited the K_2 channel with a K_i of 77.8 ??, and not Hill coefficient was 1.8. Single-channel conductance was not affected by ADPR. These findings strongly suggest that ADPR may act as a regulator of K_ATP channel activity.
Torilin from Torilis japonica (Houtt.) DC. Blocks hKv1.5 Channel Current
Yong Geun Kwak,김대근,Tian-Ze Ma,박선아,Hoon Park,정영훈,유동진,은재순 대한약학회 2006 Archives of Pharmacal Research Vol.29 No.10
Torilin was purified from Torilis japonica (Houtt.) DC., and its effects on a rapidly activating delayed rectifier K+ channel (hKv1.5), cloned from human heart and stably expressed in Ltk- cells, as well as the corresponding K+ current (the ultrarapid delayed rectifier, IKUR) were assessed in human atrial myocytes. Using the whole cell configuration of the patch-clamp technique, torilin was found to inhibit the hKv1.5 current in time and voltage-dependent manners, with an IC50 value of 2.51±0.34 μM at +60 mV. Torilin accelerated the inactivation kinetics of the hKv1.5 channel, and slowed the deactivation kinetics of the hKv1.5 current, resulting in a tail crossover phenomenon. Additionally, torilin inhibited the hKv1.5 current in a usedependent manner. These results strongly suggest that torilin is a type of open-channel blocker of the hKv1.5 channel.
Torilin from Torilis japonica (Houtt.) DC. Blocks hKv1.5 Channel Current
Kwak, Yong-Geun,Kim, Dae-Keun,Ma, Tian-Ze,Park, Sun-Ah,Park, Hoon,Jung, Young-Hoon,Yoo, Dong-Jin,Eun, Jae-Soon The Pharmaceutical Society of Korea 2006 Archives of Pharmacal Research Vol.29 No.10
Torilin was purified from Torilis japonica (Houtt.) DC., and its effects on a rapidly activating delayed rectifier $K^+$ channel (hKv1.5), cloned from human heart and stably expressed in Ltk cells, as well as the corresponding $K^+$ current (the ultrarapid delayed rectifier, $I_{KUR}$) were assessed in human atrial myocytes. Using the whole cell configuration of the patch-clamp technique, torilin was found to inhibit the hKv1.5 current in time and voltage-dependent manners, with an $IC_50$ value of $2.51{\pm}0.34\;{\mu}M$ at +60 mV. Torilin accelerated the inactivation kinetics of the hKv1.5 channel, and slowed the deactivation kinetics of the hKv1.5 current, resulting in a tail crossover phenomenon. Additionally, torilin inhibited the hKv1.5 current in a use dependent manner. These results strongly suggest that torilin is a type of open-channel blocker of the hKv1.5 channel.
Yong-Geun Kwak,Soo-Wan Chae 대한생리학회-대한약리학회 1999 The Korean Journal of Physiology & Pharmacology Vol.3 No.3
<P> <I> </I>The influences of specific protein phosphatase and protein kinase inhibitors on the ATP-sensitive K<SUP></SUP> (K<SUB>ATP</SUB>) channel-opening effect of pinacidil were investigated in single rat ventricular myocytes using patch clamp technique. In cell-attached patches, pinacidil (100 μM) induced the opening of the K<SUB>ATP</SUB> channel, which was blocked by the pretreatment with H-7 (100 μM) whereas enhanced by the pretreatment with genistein (30 μM) or tyrphostin A23 (10 μM). In inside-out patches, pinacidil (10 μM) activated the K<SUB>ATP</SUB> channels in the presence of ATP (0.3 mM) or AMP-PNP (0.3 mM) and in a partial rundown state. The effect of pinacidil (10 μM) was not affected by the pretreatment with protein tyrosine phosphatase 1B (PTP1B, 10 μg ml<SUP>1</SUP>), but blocked by the pretreatment of protein phosphatase 2A (PP2A, 1 U ml<SUP>1</SUP>). In addition, pinacidil (10 μM) could not induce the opening of the reactivated K<SUB>ATP</SUB> channels in the presence of H-7 (100 μM) but enhanced it in the presence of ATP (1 mM) and genistein (30 μM). These results indicate that the K<SUB>ATP</SUB> channel-opening effect of pinacidil is not mediated via phosphorylation of K<SUB>ATP</SUB> channel protein or associated protein, although it still requires the phosphorylation of serine/threonine residues as a prerequisite condition.
Effects of Cl<SUP></SUP> Channel Blockers on the Cardiac ATP-sensitive K<SUP></SUP> Channel
Yong-Geun Kwak 대한생리학회-대한약리학회 1999 The Korean Journal of Physiology & Pharmacology Vol.3 No.3
<P> To explore whether Cl<SUP></SUP> channel blockers interact with the ATP-sensitive K<SUP> </SUP>(K<SUB>ATP</SUB>) channel, I have examined the effect of two common Cl<SUP></SUP> channel blockers on the K<SUB>ATP</SUB> channel activity in isolated rat ventricular myocytes using patch clamp techniques. In inside-out patches, 4,4 -diisothio-cyanatostilbene- 2,2 -disulfonic acid (DIDS) and niflumic acid applied to bath solution inhibited the K<SUB>ATP</SUB> channel activity in a concentration-dependent manner with IC<SUB>50</SUB> of 0.24 and 927μM, respectively. The inhibitory action of DIDS was irreversible whereas that of niflumic acid was reversible. Furthermore, DIDS-induced block was not recovered despite exposure to ATP (1 mM). In cell-attached and inside-out patches, DIDS blocked the pinacidil- or 2,4-dinitrophenol (DNP)-induced K<SUB>ATP</SUB> channel openings. In contrast, niflumic acid did not block the pinacidil-induced K<SUB>ATP</SUB> channel openings in inside-out patches, but inhibited it in cell-attached patches. DIDS and niflumic acid produced additional block in the presence of ATP and did not affect current-voltage relationship and channel kinetics. All these results indicate that DIDS among Cl<SUP></SUP> channel blockers specifically blocks the cardiac K<SUB>ATP</SUB> channel.
Geun-Ho Kwak,Chan-Won Park,Ho-Yong Ahn,Sang-Il Na,Kyung-Do Lee,박노욱 대한원격탐사학회 2020 大韓遠隔探査學會誌 Vol.36 No.4
This study investigates the potential of bidirectional long short-term memory (Bi-LSTM) for efficient modeling of temporal information in crop classification using multitemporal remote sensing images. Unlike unidirectional LSTM models that consider only either forward or backward states, Bi-LSTM could account for temporal dependency of time-series images in both forward and backward directions. This property of Bi-LSTM can be effectively applied to crop classification when it is difficult to obtain full time-series images covering the entire growth cycle of crops. The classification performance of the Bi-LSTM is compared with that of two unidirectional LSTM architectures (forward and backward) with respect to different input image combinations via a case study of crop classification in Anbadegi, Korea. When full time-series images were used as inputs for classification, the Bi-LSTM outperformed the other unidirectional LSTM architectures; however, the difference in classification accuracy from unidirectional LSTM was not substantial. On the contrary, when using multitemporal images that did not include useful information for the discrimination of crops, the Bi-LSTM could compensate for the information deficiency by including temporal information from both forward and backward states, thereby achieving the best classification accuracy, compared with the unidirectional LSTM. These case study results indicate the efficiency of the Bi-LSTM for crop classification, particularly when limited input images are available.
곽용근,오남휴,김용기,채수완,조규박 의과학연구소 1990 全北醫大論文集 Vol.14 No.2
This study was purposed to evaluate the cardiovascular effect of RU24213 and the interaction between DA_1 and DA_2 activity in anesthetzed cat. The results obtained were as follows; 1. Intravenous or intraventricular RU24213 elicited dose-related hypotension and bradycardia. 2. The hypotensive effect of intravenous Ru24313 was blocked not by intravenous SCH23390 but by intravenous sulpiride, and the bradycardiac effect of intravenous RU24313 was blocked by intravenous SCH23390 or intravenous sulpiride. 3. The cardiovascular effect of intravenous RU24313 was blocked by intravenous phenoxybenzamine, propranolol, hexamethonium or atropine, and bilateral vagotomy did not ihhibit the htpotensive effect of intravenous RU2413 but inhibited bradycardiac effect of the drug. 4. The hypotensive and bradycardisc effects of intravenous RU24213 were inhibited by pretreatment with SKF38393. From the above results. it is suggested that hypotensive effect of RU24313 was developed via central and peripheral dopamine receptors, while bradycardiac effect of the drug was related to the peipheral of DA_1 receptor inhibits the action of DA_2 agonist in cardiovascular system of cat. (Key Wards: RU24213, dopamine D_1, dopamine D_2 receptor, cardiovascular ststem, cat)