• 한국식품영양과학회지
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• 제26권5호
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• pp.914-919
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• 1997

We investigated the effects of vitamin E supplementation on the protein glycosylation in vivo. Weaned KK-mice were fed high fat diet containing 20% corn oil(wt/wt), and sacrificed at 4, 6, and 0 months of age. High vitamin E diet was the high fat diet supplemented with an excess amount of 이-$\alpha$-tocopheryl acetate(2080IU/kg diet). We measured $HbA_{1C}$ as a glycosylation early product, and collagen-linked fluorescence (CLF) of skin as a glycosylation and product. We found that diabetic group had increased levels of $HbA_{1C}$ within 2 months after onset of diabetes and during the experiments. The skin CLF increased dramatically 5 months after onset of diabetics. Treatment with vitamin E did not modify the level of blood glucose. However, we observed a significant lowering in CLF and $HbA_{1C}$ in diabetic mice.

• Journal of Nutrition and Health
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• 제31권6호
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• pp.1024-1030
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• 1998

KK마우스에 고지방 식이를 섭취시켜 당뇨를 유발하고, Maillard 반응의 초기산물인 Hb $A_{IC}$와 후기 산물인 신장조직의 CLF가 증가되는지를 확인하고. 당뇨병에 의해 증가되는 Maillard 반응이 비타민 I의 투여로 억제되는지 관찰하였다. 또 신장조직의 광학 현미경 관찰을 통하여 신장병변을 검사하였다. 이유즉시 KK마우스를 1개월간 pellet diet로 적응시킨 후 저비타민 E 식이(corn oil 20%, wt/wt)를 먹여 당뇨를 유도하였다. 비타민 E 보강은 2080IU/kg diet 수준으로 하였으며. 생후 4개월 , 6개월 . 9개월(당뇨 0개월. 2개월, 5개월)에 희생시켰다. 정상 KK-마우스에서는 월령이 증가하였을 때. 혈당과 Hb $A_{IC}$는 유의적인 변화를 보이지 않았으나 신장조직의 CLF는 점진적으로 증가되었다. 당뇨군에서 Hb $A_{IC}$는 6개월에서 증가되기 시작하였고 9개월군과 차이가 없었으며 . 신장조직의 CLF는 9개월 군에서 급격히 증가하였다. 또 고비타민 E 식이를 섭취시킨 경우 당뇨군에서 초기 및 후기 Maillard 반응생성물의 감소가 관찰되었다. 이상의 결과로부터 KK마우스에서는 월령이 증가함에 따라 초기 및 후기 당화산물의 축적과 신장 병변의 변화가 관찰되었고, 또한 당뇨 유발에 의해 이 변화들은 더욱 촉진되었으나, 2080IU/kg diet 수준의 고비타민 E 식이를 섭취시켰을 때 이런 변들이 억제되었음을 확인하였다.확인하였다.

• Genomics & Informatics
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• 제11권4호
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• pp.224-229
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• 2013

Receptor for advanced glycation endproducts (RAGE) is a multi-ligand receptor that is able to bind several different ligands, including advanced glycation endproducts, high-mobility group protein (B)1 (HMGB1), S-100 calcium-binding protein, amyloid-${\beta}$-protein, Mac-1, and phosphatidylserine. Its interaction is engaged in critical cellular processes, such as inflammation, proliferation, apoptosis, autophagy, and migration, and dysregulation of RAGE and its ligands leads to the development of numerous human diseases. In this review, we summarize the signaling pathways regulated by RAGE and its ligands identified up to date and demonstrate the effects of hyper-activation of RAGE signals on human diseases, focused mainly on renal disorders. Finally, we propose that RAGE and its ligands are the potential targets for the diagnosis, monitoring, and treatment of numerous renal diseases.

• Journal of Applied Biological Chemistry
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• 제64권3호
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• pp.225-236
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• 2021

The epipyrone (EPN) biosynthetic gene cluster of Epicoccum nigrum is composed of epnC, epnB, and epnA, which encode cytochrome P450 oxidase, glycosyltransferase, and highly reducing polyketide synthase, respectively. Gene inactivation mutants for epnA, epnB, and epnC were previously generated, and it was found that all of them were incapable of producing EPN and any of its related compounds. It was also reported that epnB inactivation abolished epnA transcription, generating ΔepnAB. This study shows that the introduction of native epnC readily restored EPN production in ΔepnC, suggesting that epnC is essential for polyketide release from EpnA and implies that EpnC works during the polyketide chain assembly of EpnA. Introduction of epnC promoter-epnA restored EPN production in ΔepnA. The ΔepnB genotype was prepared by introducing the epnA expression vector into ΔepnAB, and it was found that the resulting recombinant strain did not produce any EPN-related compounds. A canonical epnB inactivation strain was also generated by deleting its 5'-end. At the deletion point, an Aspergllus nidulans gpdA promoter was inserted to ensure the transcription of epnA, which is located downstream of epnB. Examination of the metabolite profile of the resulting ΔepnB mutant via LC-mass spectrometry verified that no EPN-related compound was produced in this strain. This substantiates that C-glycosylation by EpnB is a prerequisite for the release of EpnA-tethered product. In conclusion, it is proposed that cytochrome P450 oxidase and glycosyltransferase work in concert with polyketide synthase to generate EPN without the occurrence of any free intermediates.

• Journal of Microbiology and Biotechnology
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• 제28권9호
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• pp.1447-1456
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• 2018

The amylosucrase encoding gene from Deinococcus geothermalis DSM 11300 (DgAS) was codon-optimized and expressed in Escherichia coli. The enzyme was employed for biosynthesis of three different dihydroxybenzene glucosides using sucrose as the source of glucose moiety. The reaction parameters, including temperature, pH, and donor (sucrose) and acceptor substrate concentrations, were optimized to increase the production yield. This study demonstrates the highest ever reported molar yield of hydroquinone glucosides 325.6 mM (88.6 g/l), resorcinol glucosides 130.2 mM (35.4 g/l) and catechol glucosides 284.4 mM (77.4 g/l) when 400 mM hydroquinone, 200 mM resorcinol and 300 mM catechol, respectively, were used as an acceptor substrate. Furthermore, the use of commercially available amyloglucosidase at the end of the transglycosylation reaction minimized the gluco-oligosaccharides, thereby enhancing the target productivity of mono-glucosides. Moreover, the immobilized DgAS on Amicogen LKZ118 beads led to a 278.4 mM (75.8 g/l), 108.8 mM (29.6 g/l) and 211.2 mM (57.5 g/l) final concentration of mono-glycosylated product of hydroquinone, catechol and resorcinol at 35 cycles, respectively, when the same substrate concentration was used as mentioned above. The percent yield of the total glycosides of hydroquinone and catechol varied from 85% to 90% during 35 cycles of reactions in an immobilized system, however, in case of resorcinol the yield was in between 65% to 70%. The immobilized DgAS enhanced the efficiency of the glycosylation reaction and is therefore considered effective for industrial application.