• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2002년도 제9회 학술 발표회 프로그램과 논문초록
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• pp.35-35
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• 2002

The large conductance $Ca^{2＋}$ -activated $K^{＋}$ channels ($BK_{Ca}$) in vascular smooth muscle have been considered to function as a negative feedback in pressure-induced vasoconstriction. In the present study, the function of cytoskeletons in the regulation of $BK_{Ca}$ and its stretch sensitivity was investigated. Using the inside-out patch clamp technique, we recorded single channel activities of $BK_{Ca}$ with 150 mM KCl in the bath solution (pCa=6.5).(omitted)itted)

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.188.2-188.2
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• 2003

Large-conductance $Ca^{2+}$ activated potassium channels $(BK_{ca})$ are widely distributed and play key roles in various cell functions. In nerve cells, B $K_{ca}$ channels shorten the duration of action potentials and block $Ca^{2+}$ entry thereby repolarizing excitable cells after excitation. $(BK_{ca})$ channel opening has been postulated to confer neuroprotection during stroke and has attracted attention as a means for therapeutic intervention in asthma, hypertension, convulsion, and traumatic brain injury. (omitted)

• 대한약리학회지
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• 제22권2호
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• pp.151-156
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• 1986

최근 심근세포 또는 신경세포에서 발표된 여러 종류의 calcium channel중 calcium antagonist로 차단되는 channel 또는 차단되지 않는 channel 등이 있는지 알아보기 위해 실험을 시행하였다. 돼지 소장 평활근으로부터 고농도의 KCl(150mM)로 부하된 세포 포막낭을 만들어 고농도의$K^+$ 또는 전기자극으로 $^{45}Ca$의 이동을 유발시켜 다음과 같은 성적을 얻었다. 저농도의 $K^+$용액에서의 $^{45}Ca$이동보다 고농도의 $K^+$-용액에서의 $^{45}Ca$이동이 유의하게 증가되었으며(p<0. 05) 이때 유입되는 $^{45}Ca$의 양은 시간에 따라 서서히 감소되었다. 전기자극(3V, 15Hz, 25msec)을 하였을때 유입되는 $^{45}Ca$의 양은 전기자극을 하지 않은 대조군에 비하여 현저하게 증가되었고, 자극시간에 따른 $^{45}Ca$의 유입량은 2분 동안 계속 증가되었다. Diltiazem 또는 nifedipine을 처치하였을때, 고농도의 $K^+$-용액에 의한 $^{45}Ca$의 유입은 억제되지 않았으나 전기자극에 의해 유도되는 $^{45}Ca$의 유입은 유의하게 억제되었다(p<0.005). 상기의 실험성적으로 돼지 소장 평활근으로부터 분리한 세포막에서의 calcium이동 중 전기자극에 의해 이루어지는 것은 calcium antagonist로 차단되는 calcium channel을 통하여 이루어지는 것으로 사료된다.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2003년도 정기총회 및 학술발표회
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• pp.43-43
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• 2003

Large-conductance $Ca^{2+}$-actived $K^{+}$ channels ($BK_{Ca}$ channels) play a key role in setting the pace of contractile activity in muscle and are involved in the regulation of neurotransmitter release in neuron. $BK_{Ca}$ channels are activated by depolarizing membrane potential and the elevated level of intracellular calcium. Using yeast-two hybrid assay, we have identified a novel protein interacting with the cytosolic carboxyl terminus of rSlo, the brain isoform of rat large-conductance $Ca^{2+}$-activated $K^{+}$ channel $\alpha$-subunit. The novel gene encodes 51 kDa protein and is named as SIRK(rSlo-interacting RGS-like protein). SIRK is expressed in various tissues and localized in the cytosolic and the membrane fraction. Biochemical and immunological studies indicated that SIRK physically interacted with the cytosolic region of rSlo. To investigate whether SIRK can modulate the activity of rSlo, GFP-fused SIRK and rSlo were transiently transfected into COS-7 cells and the effects of SIRK was studied using electrophysiological means. We concluded that the overexpression of SIRK alters the surface expression of rSlo channel with only a limited effect on the biophysical characteristics of the channel.the channel.

• 한국통신학회논문지
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• 제32권7B호
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• pp.463-471
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• 2007

Ad hoc 무선망의 동적인 특성으로 인하여 히든노드 문제가 나타날 수 있기 때문에 ad hoc 무선망에서는 분산방식으로 네트워크가 동작되어야 한다. Ad hoc 무선망에서 CSMA/CA는 비동기적 데이터 트래픽을 위해 가장 많이 사용되는 MAC Protocol 중의 하나이다. 그러나 CSMA/CA는 멀티미디어 데이터의 특성을 보장하지 못한다. 또한 경쟁형(Contention)이므로 채널을 먼저 잡은 하나의 스테이션이 채널을 독점해서 사용하여 채널 기아(starvation)로 인한 공평성문제(fairness problem)가 발생한다. 본 논문에서는 무선 ad hoc망에서 멀티미디어 데이터의 특성을 고려하여, QoS 보장을 위한 MAC protocol을 제안한다.

• The Plant Pathology Journal
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• 제35권6호
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• pp.684-691
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• 2019

Evolution of adaptive mechanisms to abiotic stress is essential for plant growth and development. Plants adapt to stress conditions by activating the abscisic acid (ABA) signaling pathway. It has been suggested that the ABA receptor, clade A protein phosphatase, SnRK2 type kinase, and SLAC1 anion channel are important components of the ABA signaling pathway. In this study, we report that the shaker type potassium (K⁺) channel, GORK, modulates plant responses to ABA and abiotic stresses. Our results indicate that the full length of PP2CA is needed to interact with the GORK C-terminal region. We identified a loss of function allele in gork that displayed ABA-hyposensitive phenotype. gork and pp2ca mutants showed opposite responses to ABA in seed germination and seedling growth. Additionally, gork mutant was tolerant to the NaCl and mannitol treatments, whereas pp2ca mutant was sensitive to the NaCl and mannitol treatments. Thus, our results indicate that GORK enhances the sensitivity to ABA and negatively regulates the mechanisms involved in high salinity and osmotic stresses via PP2CA-mediated signals.

• BMB Reports
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• 제50권6호
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• pp.323-328
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• 2017

Lysophosphatidylcholine (LPC) is a major phospholipid component of oxidized low-density lipoprotein (ox-LDL) and is implicated in its atherogenic activity. This study investigated the effects of LPC on cell viability, intracellular calcium homeostasis, and the protective mechanisms of chlorogenic acid (CGA) in human umbilical vein endothelial cells (HUVECs). LPC increased intracellular calcium ($[Ca^{2+}]_i$) by releasing $Ca^{2+}$ from intracellular stores and via $Ca^{2+}$ influx through store-operated channels (SOCs). LPC also increased the generation of reactive oxygen species (ROS) and decreased cell viability. The mRNA expression of Transient receptor potential canonical (TRPC) channel 1 was increased significantly by LPC treatment and suppressed by CGA. CGA inhibited LPC-induced $Ca^{2+}$ influx and ROS generation, and restored cell viability. These results suggested that CGA inhibits SOC-mediated $Ca^{2+}$ influx and ROS generation by attenuating TRPC1 expression in LPC-treated HUVECs. Therefore, CGA might protect endothelial cells against LPC injury, thereby inhibiting atherosclerosis.

• The Korean Journal of Physiology and Pharmacology
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• 제4권6호
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• pp.463-469
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• 2000

It has been well known that 4-aminopyridine (4-AP) has an excitatory effect on vascular smooth muscle due to causing membrane depolarization by blocking $K^+-channel$. However, we observed that 4-AP had an inhibitory effect on the mesenteric artery of rat. Therefore, we investigated the mechanism of 4-AP-induced vasorelaxation. The mesenteric arcuate artery and its branches were isolated and cut into ring. The ring segment was immersed in HEPES-buffered solution and its isometric tension was measured. 4-AP $(0.1{\sim}10\;mM)$ induced a concentration-dependent relaxation, which was unaffected by NO synthase inhibitor, $N^G-nitro-L-arginine$ methylester $(100\;{\mu}M)$ or soluble guanylate cyclase inhibitor, methylene blue $(100\;{\mu}M).$ Glibenclamide $(100\;{\mu}M)$, ATP-sensitive $K^+$ channel blocker, did not exert any effect on the 4-AP-induced vasorelaxation. 4-AP relaxed the sustained contraction induced by 100 mM $K^+$ or $Ca^{2+}$ ionophore, A23187 $(100\;{\mu}M)$ in a dose-dependent manner. In addition, 4-AP significantly decreased the phasic contractile response to norepinephrine in the absence of extracellular $Ca^{2+}$. However, 4-AP did not block the $^{45}Ca$ influx of rat aorta. From the above results, we suggest that 4-AP may not block the $Ca^{2+}$ influx through $Ca^{2+}-channel,$ but act as a nonspecific vasorelaxant in arterial smooth muscle.

• The Korean Journal of Physiology
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• 제24권2호
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• pp.281-291
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• 1990

The $Ca^{2+}-substitutional$ roles of strontium for the contractile processes were investigated in the rabbit renal artery. The contractions induced by either norepinephrine or high $K^+$ in the condition which intra- and extracellular $Ca^{2+}$ were replaced by $Sr^{2+}$, i.e. $Sr^{2+}-mediated$ contractions, were dose-dependent. And then the maximal amplitude of contraction, as compared with $Ca^{2+}-mediated$ contraction, was about 50% in norepinephrine and about 70% in high $K^+$. The $Sr^{2+}-mediated$ contractions were independent in the contraction by norepinephrine $(10^{-5}M)$ but dependent in those by high $K^+(100\;mM)$ on the extracellular $Sr^{2+}$ concentration. Also $Sr^{2+}-mediated$ contractions induced by norepinephrine were observed in the $Sr^{2+}-free$ Tyrode's solution. The $Sr^{2+}-mediated$ contractions induced by either norepinephrine or high $K^+$ were suppressed by verapamil, a $Ca^{2+}-channel$ blocker. By extracellular addition of $Sr^{2+}$, the $Ca^{2+}-mediated$ contractions induced by norepinephrine $(10^{-5}M)$ or 40 mM $K^+$ were inhibited but those by high $K^+(100\;mM)$ were increased. And the $Sr^{2+}-mediated$ contractions were increased by extracellular addition of $Ca^{2+}$ but did not reach the level of $Ca^{2+}-mediated$ contraction. Therfore it is suggested that in the vascular smooth muscle of rabbit renal artery $Sr^{2+}$ could enter the smooth muscle cells easily through the potential-operated calcium channel (POC) but not easily through the receptor-operated calcium channel (ROG), and $Sr^{2+}$ might be stored in the intracellular $Ca^{2+}-binding$ site and released by NE and induced the contraction by a way of activating directly the contractile apparatus.

• The Korean Journal of Physiology and Pharmacology
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• 제22권6호
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• pp.697-703
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• 2018

Myoblast fusion depends on mitochondrial integrity and intracellular $Ca^{2+}$ signaling regulated by various ion channels. In this study, we investigated the ionic currents associated with $[Ca^{2+}]_i$ regulation in normal and mitochondrial DNA-depleted(${\rho}0$) L6 myoblasts. The ${\rho}0$ myoblasts showed impaired myotube formation. The inwardly rectifying $K^+$ current ($I_{Kir}$) was largely decreased with reduced expression of KIR2.1, whereas the voltage-operated $Ca^{2+}$ channel and $Ca^{2+}$-activated $K^+$ channel currents were intact. Sustained inhibition of mitochondrial electron transport by antimycin A treatment (24 h) also decreased the $I_{Kir}$. The ${\rho}0$ myoblasts showed depolarized resting membrane potential and higher basal $[Ca^{2+}]_i$. Our results demonstrated the specific downregulation of $I_{Kir}$ by dysfunctional mitochondria. The resultant depolarization and altered $Ca^{2+}$ signaling might be associated with impaired myoblast fusion in ${\rho}0$ myoblasts.