• Molecules and Cells
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• 제39권1호
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• pp.6-19
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• 2016

Redox signalling comprises the biology of molecular signal transduction mediated by reactive oxygen (or nitrogen) species. By specific and reversible oxidation of redoxsensitive cysteines, many biological processes sense and respond to signals from the intracellular redox environment. Redox signals are therefore important regulators of cellular homeostasis. Recently, it has become apparent that the cellular redox state oscillates in vivo and in vitro, with a period of about one day (circadian). Circadian timekeeping allows cells and organisms to adapt their biology to resonate with the 24-hour cycle of day/night. The importance of this innate biological timekeeping is illustrated by the association of clock disruption with the early onset of several diseases (e.g. type II diabetes, stroke and several forms of cancer). Circadian regulation of cellular redox balance suggests potentially two distinct roles for redox signalling in relation to the cellular clock: one where it is regulated by the clock, and one where it regulates the clock. Here, we introduce the concepts of redox signalling and cellular timekeeping, and then critically appraise the evidence for the reciprocal regulation between cellular redox state and the circadian clock. We conclude there is a substantial body of evidence supporting circadian regulation of cellular redox state, but that it would be premature to conclude that the converse is also true. We therefore propose some approaches that might yield more insight into redox control of cellular timekeeping.

• Molecules and Cells
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• 제39권1호
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• pp.40-45
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• 2016

Peroxiredoxins are highly conserved and abundant peroxidases. Although the thioredoxin peroxidase activity of peroxiredoxin (Prx) is important to maintain low levels of endogenous hydrogen peroxide, Prx have also been shown to promote hydrogen peroxide-mediated signalling. Mitogen activated protein kinase (MAPK) signalling pathways mediate cellular responses to a variety of stimuli, including reactive oxygen species (ROS). Here we review the evidence that Prx can act as both sensors and barriers to the activation of MAPK and discuss the underlying mechanisms involved, focusing in particular on the relationship with thioredoxin.

• The Korean Journal of Physiology and Pharmacology
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• 제5권2호
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• pp.139-146
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• 2001

L-type $Ca^{2+}$ channels play an important role in regulating cytosolic $Ca^{2+}$ and thereby regulating hormone secretions in neuroendocrine cells. Since hormone secretions are also regulated by various kinds of protein kinases, we investigated the role of some kinase activators and inhibitors in the regulation of the L-type $Ca^{2+}$ channel currents in rat pituitary $GH_3$ cells using the patch-clamp technique. Phorbol 12,13-dibutyrate (PDBu), a protein kinase C (PKC) activator, and vanadate, a protein tyrosine phosphatase (PTP) inhibitor, increased the $Ba^{2+}$ current through the L-type $Ca^{2+}$ channels. In contrast, bisindolylmaleimide I (BIM I), a PKC inhibitor, and genistein, a protein tyrosine kinase (PTK) inhibitor, suppressed the $Ba^{2+}$ currents. Forskolin, an adenylate cyclase activator, and isobutyl methylxanthine (IBMX), a non-specific phosphodiesterase inhibitor, reduced $Ba^{2+}$ currents. The above results show that the L-type $Ca^{2+}$ channels are activated by PKC and PTK, and inhibited by elevation of cyclic nucleotides such as cAMP. From these results, it is suggested that the regulation of hormone secretion by various kinase activity in $GH_3$ cells may be attributable, at least in part, to their effect on L-type $Ca^{2+}$ channels.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2001년도 학술 발표회 진행표 및 논문초록
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• pp.54-54
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• 2001

The effects of protein kinase C inhibitors, chelerythrine and bisindolylmaleimide I, on acetylcholine activated $K^{＋}$ currents ( $I_{KACh}$) were examined in atrial myocytes of mice using patch clamp technique. Chelerythrine and bisindolylmaleimide I inhibited $I_{KACh}$ in reversible and dose-dependent manners. Half maximal effective concentrations were 0.49 $\pm$ 0.01 $\mu$M for chelerythrine and 98.69 $\pm$ 12.68 nM for bisindolylmaleimide I.(omitted)

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2001년도 학술 발표회 진행표 및 논문초록
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• pp.17-17
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• 2001

It is well known that myocardial stretch causes changes in electrical signalling and contractility of the heart. For example, mechanical stretch depolarises the membrane potential of cardiac cells and alters the shape of action potentials. As a result, these effects either accelerate the frequency of heart rate or induce arrhythmias of the heart.(omitted)

• 한국통신학회논문지
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• 제28권9B호
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• pp.774-782
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• 2003

일반적으로 Mobile IP 기술에 있어 이동 노드에게 실시간 서비스를 제공하기 위한 방안으로 RSVP 사용이 제시되고 있다. 그러나 Mobile IP와 RSVP(Resource Reservation Protocol) 연동시 이동 노드의 핸드오프는 등록 지연, RSVP 예약 지연 및 시그널링 오버헤드를 증가시킨다. 특히 이동 노드와 대응 노드 사이의 경로에 대한 자원 예약은 핸드오프 이전과 이후 경로가 대부분 같기 때문에 중복 예약이며, 불필요한 시그널링의 생성과 자원 낭비를 초래한다. 만약 무선 인터페이스를 제공하는 셀의 반경이 작다면 이동 노드의 핸드오프는 증가할 것이며 따라서 시그널링 오버헤드와 자원 중복 예약이 크게 증가할 것이다. 본 논문은 RSVP proxy 방안의 Cellular IP와 RSVP 통합 모델을 제안한다. Cellular IP 프로토콜은 마이크로 셀 네트워크에서 핸드오프에 의한 등록 지연, 전송 지연 및 손실을 최소화하며, RSVP proxy는 자원 중복 예약을 최소화하는 방안으로 이동 노드의 예약 주소를 사용하여 Cellular IP 외부 네트워크에서의 RSVP 세션 경로 변경이 일어나지 않도록 한다. 제안 방안은 셀 반경과 핸드오프율에 대해 자원 예약 실패 확률을 이용 기존 Mobile IP와 RSVP 연동 방안과 비교 평가하였다.

• 통합자연과학논문집
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• 제6권3호
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• pp.125-137
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• 2013

Promising evidence suggests that amyloid beta peptide ($A{\beta}$), a key mediator in age-dependent neuronal and cerebrovascular degeneration, activates death signalling processes leading to neuronal as well as non-neuronal cell death in the central nervous system. A major cellular event in $A{\beta}$-induced apoptosis of non-neuronal cells, including cerebral endothelial cells, astrocytes and oligodendrocytes, is mitochondrial dysfunction. The apoptosis signalling cascade upstream of mitochondria entails $A{\beta}$ activation of neutral sphingomyelinase, resulting in the release of ceramide from membrane sphingomyelin. Ceramide then activates protein phosphatase 2A (PP2A), a member in the ceramide-activated protein phosphatase (CAPP) family. PP2A dephosphorylation of Akt and FKHRL1 plays a pivotal role in $A{\beta}$-induced Bad translocation to mitochondria and transactivation of Bim. Bad and Bim are pro-apoptotic proteins that cause mitochondrial dysfunction characterized by excessive ROS formation, mitochondrial DNA (mtDNA) damage, and release of mitochondrial apoptotic proteins including cytochrome c, apoptosis inducing factor (AIF), endonuclease G and Smac. The cellular events activated by $A{\beta}$ to induce death of non-neuronal cells are complex. Understanding these apoptosis signalling processes will aid in the development of more effective strategies to slow down age-dependent cerebrovascular degeneration caused by progressive cerebrovascular $A{\beta}$ deposition.

• Asian Pacific Journal of Cancer Prevention
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• 제15권16호
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• pp.6463-6475
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• 2014

The mammalian target of rapamycin (mTOR) kinase plays an important role in regulating cell growth and cell cycle progression in response to cellular signals. It is a key regulator of cell proliferation and many upstream activators and downstream effectors of mTOR are known to be deregulated in various types of cancers. Since the mTOR signalling pathway is commonly activated in human cancers, many researchers are actively developing inhibitors that target key components in the pathway and some of these drugs are already on the market. Numerous preclinical investigations have also suggested that some herbs and natural phytochemicals, such as curcumin, resveratrol, timosaponin III, gallic acid, diosgenin, pomegranate, epigallocatechin gallate (EGCC), genistein and 3,3'-diindolylmethane inhibit the mTOR pathway either directly or indirectly. Some of these natural compounds are also in the clinical trial stage. In this review, the potential anti-cancer and chemopreventive activities and the current status of clinical trials of these phytochemicals are discussed.

• Molecules and Cells
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• 제43권2호
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• pp.188-197
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• 2020

Cells are designed to be sensitive to a myriad of external cues so they can fulfil their individual destiny as part of the greater whole. A number of well-characterised signalling pathways dictate the cell's response to the external environment and incoming messages. In healthy, well-ordered homeostatic systems these signals are tightly controlled and kept in balance. However, given their powerful control over cell fate, these pathways, and the transcriptional machinery they orchestrate, are frequently hijacked during the development of neoplastic disease. A prime example is the Wnt signalling pathway that can be modulated by a variety of ligands and inhibitors, ultimately exerting its effects through the β-catenin transcription factor and its downstream target genes. Here we focus on the interplay between the three-member family of RUNX transcription factors with the Wnt pathway and how together they can influence cell behaviour and contribute to cancer development. In a recurring theme with other signalling systems, the RUNX genes and the Wnt pathway appear to operate within a series of feedback loops. RUNX genes are capable of directly and indirectly regulating different elements of the Wnt pathway to either strengthen or inhibit the signal. Equally, β-catenin and its transcriptional co-factors can control RUNX gene expression and together they can collaborate to regulate a large number of third party co-target genes.

• 한국통신학회논문지
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• 제31권1B호
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• pp.1-8
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• 2006

현재 유${\cdot}$무선 통합망에서 인터넷 서비스를 제공하기 위한 많은 작업이 진행 중이며 IP 이동성 문제를 해결하기 위한 방식으로 Mobile IP를 사용하고 있다. 그러나 Mobile IP는 셀룰러 기반의 무선 접속망에서 잦은 핸드오프를 처리하는데 있어서 여러 가지 제한점을 갖는다. 이러한 문제점을 해결하기 위해서 마이크로 이동성 프로토콜이 제안되고 있으며, 마이크로 이동성 프로토콜 방식으로 Cellular IP, HAWAII, Hierarchical Mobile IP 등이 있다. Cellular IP는 일정 지역 내에서 seamless 한 이동성을 제공하기 때문에 특별한 관심을 받고 있다. 그러나 Cellular IP 인다이렉트 핸드오프 방식은 핸드오프가 발생할 경우 새로운 영역의 BS이 핸드오프를 인식하는 과정이 필요하기 때문에 핸드오프 인식과정에서 패킷 유실 및 중복이 발생하여 UDP 및 TCP 성능저하가 발생한다. 본 논문에서는 Cellular IP 인다이렉트 핸드오프 방식을 개선한 핸드오프 방식을 제안하였으며, 문제점을 해결하기 위하여 크로스오버 노드를 통한 시그널링 과정과 버퍼링 과정을 사용하였다. 새로운 영역의 BS에게 핸드오프 사실을 알리기 위해서 게이트웨이까지 전송되는 핸드오프 요청 패킷을 크로스오버 노드에서 처리함으로서 불필요한 시그널링 트래픽을 감소 시켰다.