• The Korean Journal of Physiology
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• v.27 no.2
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• pp.123-138
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• 1993

The mechanism of insulin action to increase glucose transport is attributed to glucose transporter translocation from intracellular storage pools to the plasma membrane in insulin-sensitive cells. The present study was designed to visualize the redistribution of the glucose transporter by means of an immunogold labelling method. Our data clearly show that glucose transporter molecules were visible by this method. According to the method this distribution of glucose transporters between cell surface and intracellular pool was different in adipocytes. The glucose transporter molecules were randomly distributed at the cell surface whereas the molecules at LDM were farmed as clusters. By insulin treatment the number of homogeneous random particles increased at the cell surface whereas the cluster forms decreased at the intracellular storage pools. It suggests that the active molecules needed to be evenly distributed far effective function and that the inactive molecules in storage pools gathered and termed clusters until being transferred to the plasma membrane.

• Molecules and Cells
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• v.27 no.1
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• pp.1-3
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• 2009

Mitotic spindle mediates the segregation of chromosomes in the cell cycle and the proper function of the spindle is crucial to the high fidelity of chromosome segregation and to the stability of the genome. Nucleation of microtubules (MTs) from centrosomes and chromatin represents two well-characterized pathways essential for the assembly of a dynamic spindle in mitosis. Recently, we identified a third MT nucleation pathway, in which existing MTs in the spindle act as a template to promote the nucleation and polymerization of MTs, thereby efficiently amplifying MTs in the spindle. We will review here our current understanding on the molecular mechanism, the physiological function and the cell-cycle regulation of MT amplification.

• BMB Reports
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• v.30 no.4
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• pp.246-252
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• 1997

Malonate decarboxylase from Acinetobacter calcoaceticus is shown to have malonyl-CoA: acetate CoA transferase. acetyl-CoA: malonate CoA transferase, and malonyl-CoA decarboxylase activity. These enzyme activities were elucidated by isotope exchange reactions. The enzyme modified by N-ethylmaleimide completely lost its malonate decarboxylase activity, whereas it still kept CoA transferases and malonyl-CoA decarboxylase activities. The existence of CoA transferases and malonyl-CoA decarboxylase activity is clear, but their physiological significance is obscure. The catalytic reactions for two eoA transfers and malonyl-CoA decarboxylation proceed via a cyclic mechanism, which is through two covalent intermediates, enzyme-Smalonyl and enzyme-S-acetyL proposed for malonate decarboxylation of the enzyme.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.3
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• pp.624-628
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• 2003

JebyeongwonhuronㆍYobaebyeonjehu is well organized and detailed is stated of classification and cause, mechanism of lumbago. That is divided into nine classes according to cause and symptoms of lumbago and described those respectively. Although there is some different, classification of lumbago after ages is based on this method in the main. The outbreak mechanism of lumbago can be stated that wicked germ invade into the body in condition that spirit and energy, especially the kidney energy is poor through various reason. That is stressed on interior factors. In the relation to organs, it is inferred that outbreak of lumbago have connection with the kidney deeply.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.2
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• pp.480-487
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• 2009

Atherosclerosis, slow progressing inflammatory lesion in arteries, is one of the major causes of cardiovascular diseases. As mortality due to cardiovascular disease keeps increasing in Korea, researches on pathological mechanism of atherosclerosis may be beneficial in fighting against cardiovascular diseases. It is known that migration and MMP-9 secretion of Vascular Smooth Muscle Cell(VSMC) play a significant part in pathogenesis of atherosclerosis, although detailed mechanism of entire process is not clarified. We investigated whether the seeds of Trichosanthes kirilowii maxim (TS), inhibit migration and MMP-9 production of HASMC(human aortic SMC), which were induced by TNF-${\alpha}$ treatment. Migration assay showed that TS inhibited the migration of HASMC induced by TNF-${\alpha}$, in dose dependent manner. Also by Zymography MMP-9 production of HASMC was found to be reduced by TS, both in time and in dose dependent manner. Western blotting results suggest TS suppress activity of MAPkinases.

• Journal of Physiology & Pathology in Korean Medicine
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• v.28 no.2
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• pp.195-199
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• 2014

Although the Herba Cirsii is known to posses beneficial health effects, the anti-diabetic effects and the mechanism of action have not been elucidated. In the present study we have shown that Herba Cirsii Extract (HCE) can stimulate glucose uptake in OP9 adipocytes. Unlike insulin, HCE did not stimulate the Ser473 phosphorylation and activation of Akt. The increasing effects of HCE on glucose uptake were inhibited by PD680509 and compound C pretreatment, which means that the glucose uptake effects by HCE were carried out by extracelluar signal-regulated kinase1/2(ERK1/2) and AMP-activated protein kinase (AMPK) activation. Further studies revealed that HCE stimulated glucose transport occurs through a mechanism involving ERK1/2 activation and AMPK activation.

• BMB Reports
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• v.51 no.3
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• pp.106-118
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• 2018

How the organ size is adjusted to the proper size during development and how organs know that they reach the original size during regeneration remain long-standing questions. Based on studies using multiple model organisms and approaches for over 20 years, a consensus has been established that the Hippo pathway plays crucial roles in controlling organ size and maintaining tissue homeostasis. Given the significance of these processes, the dysregulation of the Hippo pathway has also implicated various diseases, such as tissue degeneration and cancer. By regulating the downstream transcriptional coactivators YAP and TAZ, the Hippo pathway coordinates cell proliferation and apoptosis in response to a variety of signals including cell contact inhibition, polarity, mechanical sensation and soluble factors. Since the core components and their functions of the Hippo pathway are evolutionarily conserved, this pathway serves as a global regulator of organ size control. Therefore, further investigation of the regulatory mechanisms will provide physiological insights to better understand tissue homeostasis. In this review, the historical developments and current understandings of the regulatory mechanism of Hippo signaling pathway are discussed.

• The Korean Journal of Physiology
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• v.11 no.2
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• pp.17-22
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• 1977

By the intravenous infusion of saline solution through the postcaval vein, the effects of increasing the venous return on the heart rate were studied in the water turtle (Amyda japonica). The following results were obtained: 1) Prior to saline infusion, when the initial heart rate was below $50{\sim}55/min$ the heart rate was increased by the infusion. When the initial rate was above this value no changes in heart rate were observed following the infusion. 2) When the heart rate was decreased by vagal stimulation, the infusion elicited a remarkable increase in the heart rate. 3) Increased heart rate caused by tile infusion was not affected by vagotomy or sympathectomy. 4) These results suggest that the increase in heart rate secondary to increased venous return is under the control of a myogenic regulatory mechanism, not a neural mechanism.

• BMB Reports
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• v.52 no.1
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• pp.64-69
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• 2019

The loss of skeletal muscle, called sarcopenia, is an inevitable event during the aging process, and significantly impacts quality of life. Autophagy is known to reduce muscle atrophy caused by dysfunctional organelles, even though the molecular mechanism remains unclear. Here, we have discuss the current understanding of exercise-induced autophagy activation in skeletal muscle regeneration and remodeling, leading to sarcopenia intervention. With aging, dysregulation of autophagy flux inhibits lysosomal storage processes involved in muscle biogenesis. AMPK-ULK1 and the $FoxO/PGC-1{\alpha}$ signaling pathways play a critical role in the induction of autophagy machinery in skeletal muscle, thus these pathways could be targets for therapeutics development. Autophagy has been also shown to be a critical regulator of stem cell fate, which determines satellite cell differentiation into muscle fiber, thereby increasing muscle mass. This review aims to provide a comprehensive understanding of the physiological role of autophagy in skeletal muscle aging and sarcopenia.

• Biomolecules & Therapeutics
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• v.30 no.6
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• pp.490-500
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• 2022

Aging is defined as physiological dysfunction of the body and a key risk factor for human diseases. During the aging process, cellular senescence occurs in response to various extrinsic and intrinsic factors such as radiation-induced DNA damage, the activation of oncogenes, and oxidative stress. These senescent cells accumulate in many tissues and exhibit diverse phenotypes, such as resistance to apoptosis, production of senescence-associated secretory phenotype, cellular flattening, and cellular hypertrophy. They also induce abnormal dysfunction of the microenvironment and damage neighboring cells, eventually causing harmful effects in the development of various chronic diseases such as diabetes, cancer, and neurodegenerative diseases. Thus, pharmacological interventions targeting senescent cells, called senotherapeutics, have been extensively studied. These senotherapeutics provide a novel strategy for extending the health span and improving age-related diseases. In this review, we discuss the current progress in understanding the molecular mechanisms of senotherapeutics and provide insights for developing senotherapeutics.