• Proceedings of the Korea Contents Association Conference
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• 2015.05a
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• pp.337-338
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• 2015

알츠하이머병은 뇌에 비이상적으로 베타아밀로이드 단백질의 축적으로 인해 신경세포가 손상되는 질병으로 아직까지 명확한 질병의 메커니즘이 밝혀지지 않고 있다. 새로운 알츠하이머병의 생물학적 모델을 제시하기 위해, KEGG의 알츠하이머병의 신호전달패스웨이와 문헌정보를 기반으로 구축된 신호전달 네트워크를 병합함으로써 새로운 질병의 모델을 생성하였다. 분석결과 로바스타틴하부경로를 포함하는 새로운 알츠하이머 생물학적 경로 모델을 제시하고자 한다. 향후 메디컬 페스웨이의 병합기술을 통해 보다 다양한 질병의 원인 기작을 연구하는데 활용하고자 한다.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.1
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• pp.1-8
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• 2013

Understanding the cellular and molecular mechanisms involved in the development and progression of pulmonary hypertension (PH) remains imperative if we are to successfully improve the quality of life and life span of patients with the disease. A whole plethora of mechanisms are associated with the development and progression of PH. Such complexity makes it difficult to isolate one particular pathway to target clinically. Changes in intracellular free calcium concentration, the most common intracellular second messenger, can have significant impact in defining the pathogenic mechanisms leading to its development and persistence. Signaling pathways leading to the elevation of $[Ca^{2+}]_{cyt}$ contribute to pulmonary vasoconstriction, excessive proliferation of smooth muscle cells and ultimately pulmonary vascular remodeling. This current review serves to summarize the some of the most recent advances in the regulation of calcium during pulmonary hypertension.

• International Journal of Oral Biology
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• v.44 no.4
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• pp.130-143
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• 2019

Rheumatoid arthritis, osteoarthritis, and periodontal disease are bone destructive diseases mainly caused by inflammation. Various studies are being conducted to develop treatments for inflammatory bone destructive diseases. Many of these studies involve plant-derived natural compounds. In these studies, cell differentiation, signal transduction pathways, and bone resorption were measured at the cellular level. In disease-induced animal models, the amount of inflammatory mediators or matrix destructive enzymes and serum metabolic markers were measured. This study examined the effects of plant-derived natural compounds, such as flavonoids, on inflammatory bone destructive diseases. In addition, we structurally classified various substances used to maintain bone health and summarized the biological effects and related mechanisms of the components.

• Animal cells and systems
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• v.12 no.1
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• pp.1-9
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• 2008

In the developing limb, chondrogenesis is an important prerequisite for the formation of cartilage whose template is required for bone formation. Chondrogenesis is a tightly regulated multi-step process, including mesenchymal cell recruitment/migration, prechondrogenic condensation of the mesenchymal cells, commitment to the chondrogenic lineage, and differentiation into chondrocytes. This process is controlled exquisitely by cellular interactions with the surrounding matrix and regulating factors that initiate or suppress cellular signaling pathways and transcription of specific genes in a temporal-spatial manner. Understanding the cellular and molecular mechanisms of chondrogenesis is important not only in the context of establishing basic principle of developmental biology but also in providing research direction toward preventive and/or regenerative medicine. Here, I will overview the current understanding of cellular and molecular mechanisms contributing to prechondrogenic condensation processes, the crucial steps for chondrogenesis, focusing on cell-cell and cell-matrix interactions.

• Genomics & Informatics
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• v.10 no.4
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• pp.234-238
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• 2012

Genetic epidemiology studies have established that the natural variation of gene expression profiles is heritable and has genetic bases. A number of proximal and remote DNA variations, known as expression quantitative trait loci (eQTLs), that are associated with the expression phenotypes have been identified, first in Epstein-Barr virus-transformed lymphoblastoid cell lines and later expanded to other cell and tissue types. Integration of the eQTL information and the network analysis of transcription modules may lead to a better understanding of gene expression regulation. As these network modules have relevance to biological or disease pathways, these findings may be useful in predicting disease susceptibility.

• BMB Reports
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• v.35 no.1
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• pp.94-105
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• 2002

Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to actively participate in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents that target this cell death process. This review will focus on molecular cell death pathways that are responsible for generating the apoptotic phenotype. It will also summarize what is currently known about the apoptotic signals that are activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.

• BMB Reports
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• v.45 no.4
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• pp.213-220
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• 2012

Viruses have evolved to manipulate the host cell machinery for virus propagation, in part by interfering with the host cellular signaling network. Molecular studies of individual pathways have uncovered many viral host-protein targets; however, it is difficult to predict how viral perturbations will affect the signaling network as a whole. Systems biology approaches rely on multivariate, context-dependent measurements and computational analysis to elucidate how viral infection alters host cell signaling at a network level. Here we describe recent advances in systems analyses of signaling networks in both viral and non-viral biological contexts. These approaches have the potential to uncover virus- mediated changes to host signaling networks, suggest new therapeutic strategies, and assess how cell-to-cell variability affects host responses to infection. We argue that systems approaches will both improve understanding of how individual virus-host protein interactions fit into the progression of viral pathogenesis and help to identify novel therapeutic targets.

• BMB Reports
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• v.35 no.6
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• pp.537-546
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• 2002

NF-${\kappa}B$/Rel transcription factor family participates in diverse biological processes including embryo development, hematopoiesis, immune regulation, as well as neuronal functions. In this review, the NF-${\kappa}B$/Rel signal transduction pathways and their important roles in the regulation of immune system will be discussed. NF-${\kappa}B$/Rel members execute distinct functions in multiple immune cell types via the regulation of target genes essential for cell proliferation, survival, effector functions, cell trafficking and communication, as well as the formation of lymphoid architecture. Consequently, proper activation of NF-${\kappa}B$/Rel during immune responses to allergens, auto-antigens, allo-antigens, and pathogenic infection is crucial for the integrity of host innate and adaptive immunity.

• BMB Reports
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• v.41 no.1
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• pp.11-22
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• 2008

Apoptosis (programmed cell death) is a cellular self-destruction mechanism that is essential for a variety of biological events, such as developmental sculpturing, tissue homeostasis, and the removal of unwanted cells. Mitochondria play a crucial role in regulating cell death. $Ca^{2+}$ has long been recognized as a participant in apoptotic pathways. Mitochondria are known to modulate and synchronize $Ca^{2+}$ signaling. Massive accumulation of $Ca^{2+}$ in the mitochondria leads to apoptosis. The $Ca^{2+}$ dynamics of ER and mitochondria appear to be modulated by the Bcl-2 family proteins, key factors involved in apoptosis. The number and morphology of mitochondria are precisely controlled through mitochondrial fusion and fission process by numerous mitochondria-shaping proteins. Mitochondrial fission accompanies apoptotic cell death and appears to be important for progression of the apoptotic pathway. Here, we highlight and discuss the role of mitochondrial calcium handling and mitochondrial fusion and fission machinery in apoptosis.

• BMB Reports
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• v.51 no.2
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• pp.65-72
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• 2018

The endothelial to mesenchymal transition (EndMT) is a newly recognized, fundamental biological process involved in development and tissue regeneration, as well as pathological processes such as the complications of diabetes, fibrosis and pulmonary arterial hypertension. The EndMT process is tightly controlled by diverse signaling networks, similar to the epithelial to mesenchymal transition. Accumulating evidence suggests that microRNAs (miRNAs) are key regulators of this network, with the capacity to target multiple messenger RNAs involved in the EndMT process as well as in the regulation of disease progression. Thus, it is highly important to understand the molecular basis of miRNA control of EndMT. This review highlights the current fund of knowledge regarding the known links between miRNAs and the EndMT process, with a focus on the mechanism that regulates associated signaling pathways and discusses the potential for the EndMT as a therapeutic target to treat many diseases.