• Korean Journal of Veterinary Research
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• v.39 no.1
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• pp.62-69
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• 1999

Although it has been reported that hormones or chemicals, which increase in intracellular cAMP, produced $Mg^{2+}$ release from the heart, it is not well characterized whether a specific $Mg^{2+}$ exchanger is involved in cAMP-induced $Mg^{2+}$ efflux in the mammalian hearts. In this work, we studied the relationship between the increase in intracellular cAMP and ion transport system on $Mg^{2+}$ regulation in the perfused rat heart and isolated myocytes. The $Mg^{2+}$ content in the perfusate and supernatant were measured by atomic absorption spectrophotometer. The addition of membrane permeable cAMP analogue to the perfused hearts and myocytes induced a $Mg^{2+}$ efflux in the dose dependent manners. $Mg^{2+}$ efflux was stimulated by cAMP modulators (forskolin, IBMX and Ro20-1724) in the perfused hearts and myocytes. cAMP-induced $Mg^{2+}$ efflux was inhibited by $H_7$, benzamil or imipramine in the perfused hearts and myocytes, but not by EIPA. We confirmed that a significant $Mg^{2+}$ efflux was induced by an increase in intracellular cAMP in the hearts and myocytes. The cAMP-induced increase of $Mg^{2+}$ efflux in the hearts may be involved in ion transport system ($Na^+-Ca^{2+}$ and $Na^+-Mg^{2+}$ exchanger).

• Journal of Pharmaceutical Investigation
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• v.22 no.4
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• pp.289-300
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• 1992

The counter-transport phenomena in the hepatic transport of 1-anilino-8-naphthalene sulfonate (ANS) were kinetically investigated by analyzing the plasma disappearance-time profiles and the transport into the isolated hepatocytes. In vivo "counter transport phenomena" were simulated based on the perfusion model which incorporated the carrier-mediated transport and the saturable intracellular binding. The condition that the mobility of carrier-ligand complex is greater than that of free carrier is not essential for the occurrence of counter-transport phenomenon. To examine the inhibitory effects on the initial uptake of a ligand by the liver, it is necessary to judge whether the true counter-transport mechanism (trans-stimulation) is working or not. The initial plasma disappearance curves of ANS were then kinetically analyzed based on a two-compartment model, in which the ligand is eliminated only from the peripheral compartment (liver compartment). No effects on the initial plasma disappearance rates of ANS were observed after preloading of bromophenol blue (BPB) or rose bengal (RB) in the liver. Inhibitory effect of BPB or RB on the initial uptake (or efflux) rates of ANS by the isolated hepatocytes were not observed, suggesting that the true counter transport mechanism is not working. In conclusion, checking the preloading effects of transstimulation on the initial uptake of a ligand by the liver could be a useful criterion for carrier cycling and common use of the same carrier between two ligands. However, one cannot exclude those possibilities even if the preloading effects cannot be observed.

• Korea Journal of Cosmetic Science
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• v.1 no.1
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• pp.31-43
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• 2019

Melanosomes are specific melanin-containing intracellular organelles of epidermal melanocytes. In epidermal melanocytes, there are three kinds of key player proteins. Rab27a, melanophilin or Slac2-a and Myosin 5a form a tripartite complex connects the melanosome. Mature melanosomes make movements through the tripartite protein complex along actin filaments.In this study, we found that the haplamine (6-Methoxyflindersine) induced melanosome aggregation around the nucleus in epidermal melanocyte. In an attempt to elucidate the inhibitory effect of haplamine on melanosome transport, effect of haplamineon the expression level of Rab27a, melanophilin and Myosin 5a was measured. The results indicated that haplamine up to 5��M effectively suppressed mRNA and protein expression level of melanophilin.To determine the upstream regulator of melanophilin regulated by haplamine, we checked the level of MITF, c-JUN and USF1. Those are possible transcription factor of melanophilin. Among them,treatment of USF1 siRNA decreased mRNA and protein expression level of USF1 as well as melanophilin. Also, treatment of haplamine decreased mRNA and protein expression level of melanophilin as well as USF1 in a dose-dependent manner. Consequently, we found the inhibitory effect of haplamine on melanosome transport in melan-a melanocyte. Treatment of haplamine reduced melanophilin expression level which is a key protein of melanosome transport. We identified that USF1 could be a major transcription factor of melanophilin regulated by haplamine.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.5
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• pp.423-431
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• 2001

Some recent investigations revealed that vasodilatory action of adenosine is mainly not mediated by surface A2 receptor and suggested the existence of an intracellular action site. In the present study, we tried to differentiate intracellular from extracellular site of adenosine action in the regulation of coronary flow. In perfused rabbit hearts, concentration-response curve of coronary flow to exogenous adenosine was constructed in the presence or absence of dipyridamole, an inhibitor of transmembrane purine transport. Inhibition of cellular adenosine uptake by dipyridamole suppressed the increase of flow rate while enhancing the decrease in heart rate induced by exogenous adenosine. In another series of experiments, perfused rabbit hearts were subjected to energy deprivation in order to increase the production of endogenous adenosine. Energy deprivation along with dipyridamole administration resulted in higher coronary flow rate. Lower perfusate adenosine concentration was observed along with higher tissue adenosine content in this group. These results implied that coronary flow rate is determined not by interstitial adenosine concentration but by intracellular activity of adenosine. To confirm the effects of dypiridamole in vivo, direct measurement of interstitial adenosine concentration by mycrodialysis along with the assay of intracellular adenosine content was performed after intranenous dipyridamole administration. After dipyridamole infusion, intracellular adenosine content was markedly increased while interstitial adenosine concentration was not altered. In another series of experiments, the right shift of concentration-response curve of adenosine-induced vasodilation by 8-phenyltheophilline, a representative adenosine receptor antagonist, was mostly abolished by prior administration of prazosin, indicating that the influence of 8-PT on the adenosine action is not attributed to the inhibition of A2 receptor but related to the suppression of ${\alpha}-adrenoceptor$ activation. From these results, we concluded that adenosine acts intracellularly to regulate the coronary blood flow.

• BMB Reports
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• v.34 no.4
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• pp.285-292
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• 2001

Insulin stimulates glucose uptake in muscle and adipose tissue and thus maintains normal blood glucose level in our body. Derangement of this process causes many grave health problems. Insulin stimulates glucose transport primarily by recruiting GLUT4 from its intracellular storage sites to the plasma membrane. The process is complex and involves GLUT4 trafficking through multiple subcellular compartments (organelles) and many protein functions, details of which are poorly understood. This review summarizes a recent development to isolate and characterize the individual intracellular GLUT4 compartments and to illustrate how this compartmental analysis will help to identify the insulin-sensitive step or steps in the insulin-induced GLUT4 recruitment in rat adipocytes. The review does not cover the recent exciting development in identification of many proteins implicated in this process.

• Journal of Microbiology
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• v.41 no.1
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• pp.41-45
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• 2003

N crassa mutant strain nap showed reduced growth rate, decreased electric membrane potential, and elevated intracellular ATP content in comparison to the wild type. Blue light induced a hyperpolarization of the membrane potential in both strains. The analysis of oxidative and phosphorylation activities of mitochondria isolated from the two strains has revealed that nap utilized more efficient oxidative pathways. The higher intracellular ATP content in the nap was presumably due to impaired transport systems of the plasma membrane, and to a lesser extent to the functioning of the fully competent respiratory chain. The excess ATP possibly accounts for carotenoid accumulation in the mutant.

• Asian-Australasian Journal of Animal Sciences
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• v.14 no.5
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• pp.710-719
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• 2001

Several amino acid transport systems in mammary gland have been characterized during the last few years. These systems may be divided into two broad categories based on whether they are sodium-dependent or $Na^{+}$-independent, and each of these categories is subdivided into 3 groups depending on whether the systems prefer zwitterionic, cationic or anionic substrates. The zwitterion preferring transport processes in mammary gland are $Na^{+}$-dependent system A and $Na^{+}$-independent systems L and T. System $y^{+}$ is a $Na^{+}$-independent transporter of cationic amino acids and $X_{AG^{-}}$ is a $Na^{+}$-dependent system for anionic amino acids. A ($Na^{+}+Cl^{-}$)-dependent system, selective for $\beta$-amino acids has been reported in rat mammary tissue. In addition, there is yet another class of transporters that have still broader specificity. The $Na^{+}$-dependent systems $BCl^{-}$-dependent and $BCl^{-}$-independent and $Na^{+}$-independent system $y^{+}L$ have been reported to mediate the transport of zwitterionic as well as cationic amino acids. Each system has been characterized with respect to its substrate specificity, affinity, kinetics and ion-dependence. Transport of amino acids by mammary tissue is regulated by i) the intracellular substrate concentration, ii) lactogenic hormones and iii) milk stasis. Four of the above transport systems (i.e. A, L, $y^{+}$ and $BCl^{-}$-independent) are up-regulated by lactogenic hormones (insulin, cortisol and prolactin) in mammary gland.

• Korean Journal of Veterinary Research
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• v.40 no.2
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• pp.291-299
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• 2000

Magnesium ($Mg^{2+}$) transport across the plasma membrane of cardiac myocytes appears to be under hormonal control. Repeated stimulations with adrenergic or histaminergic agonist produced a progressive decrease in $Mg^{2+}$ efflux from hearts. Thus we hypothesized that the $Mg^{2+}$ efflux may be resulted from a down-regulation of receptors or from a depletion of $Mg^{2+}$ from intracellular pool(s) in the hearts. In the present study, the regulation of $Mg^{2+}$ homeostasis by receptor stimulation was studied in perfused rat and guinea pig hearts. The successive short addition of norepinephrine (NE) to rat and guinea pig, and of histamine (HT) to perfused guinea pig hearts induced a progressive decrease in $Mg^{2+}$ efflux. These $Mg^{2+}$ effluxes were blocked by propranolol or ranitidine, respectively. These decrease in $Mg^{2+}$ efflux were inhibited by sodium cyanide (NaCN), which increases intracellular $Mg^{2+}$ ($[Mg^{2+}]_i$) levels. When NE (or HT) was added after HT (or NE), this efflux was also decreased in the guinea pig hearts. In the rat hearts and myocytes, HT did not stimulate $Mg^{2+}$ efflux. But NE produced a large $Mg^{2+}$ efflux after stimulation with HT. 8-(4-Chlorophenylthio)-adenosine cAMP (cAMP), like NE and HT, also induced a progressive decrease in $Mg^{2+}$ efflux in guinea pig hearts. This effect was inhibited by NaCN. These data provide evidence that the progressive decrease in receptor-stimulated $Mg^{2+}$ efflux is considered to be due to a decrease in $[Mg^{2+}]_i$ levels rather than receptor down-regulation.

• Journal of Plant Biology
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• v.34 no.4
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• pp.325-330
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• 1991

The ability of several auxin analogs to induce ethylene production was tested in the corn coleoptile. The synthetic auxins 1-naphthaleneacetic acid (1-NAA) and 2, 4-dichlorophenoxyacetic acid (2, 4-D) had strong stimulatory effects on ethylene induction surpassing that of IAA. Both 2-naphthalaneacetic acid (2-NAA) and 2, 6-dichlorophenoxy acetic acid (2, 6-D), structural analogs of these auxins, respectively, were found to be inactive. Treatment with NPA, a strong inhibitor of polar auxin transport, led to drastic increase in IAA-induced ethylene production while it has bo effect on ethylene production induced by 1-NAA. A positive correlative existed between intracellular auxin level and ethylene production.

• BMB Reports
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• v.39 no.3
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• pp.335-338
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• 2006

Methylglyoxal (MG) is an endogenous physiological metabolite which is present in increased concentrations in diabetics. MG reacts with the amino acids of proteins to form advanced glycation end products. In this in vitro study, we investigated the effect of MG on the structure and function of ceruloplasmin (CP) a serum oxidase carrier of copper ions in the human. When CP was incubated with MG, the protein showed increased electrophoretic mobility which represented the aggregates at a high concentration of MG (100 mM). MG-mediated CP aggregation led to the loss of enzymatic activity and the release of copper ions from the protein. Radical scavengers and copper ion chelators significantly prevented CP aggregation. CP is an important protein that circulates in plasma as a major copper transport protein. It is suggested that oxidative damage of CP by MG may induce perturbations of the copper transport system and subsequently lead to harmful intracellular condition. The proposed mechanism, in part, may provide an explanation for the deterioration of organs in the diabetic patient.