Sialyltransferases add CMP-sialic acid to the terminal portions of the sialylated glycolipids (gangliosides) or to the N- or O-linked sugar chains of glycoproteins. Here, we focused on alpha-2,3 sialyltransferase VI (ST3GAL6) as a transporter that add sialic acid to N-glycan of glycoproteins. Our study showed that amyloid β-peptide 1-42(Aβ1-42)-induced cell death of SK-N-SH human neuroblastoma cells and SB203580, a p38 MAPK inhibitor protect against Aβ1-42 toxicity. During Aβ1-42 induced-apotosis, we found that alpha-2,3 sialyltransferase VI was decreased almost 50% by 20uM Aβ1-42 and alpha-2,3 linked sialic acid on total protein decreased. Also, cell viability was increased by SB203580 in Aβ 1-42-induced cell death for about 30%. Collectively, our findings suggest that p38 MAPK signaling pathway is related with alpha-2,3 sialyltransferase VI expression in beta-amyloid induced apoptosis.
저자
Sung Min Kim [ Department of Biotechnology and Biomaterials Engineering Research Center, The Catholic University of Korea ]
Yong Il Park [ Department of Biotechnology and Biomaterials Engineering Research Center, The Catholic University of Korea ]
본 학회는 화학, 생화학, 분자생물학, 미생물학, 식품공학, 의학, 약학, 유전공학 및 생물공학, 환경 및 기타 공업 등 전 분야의 탄수화물관련 이론과 기술을 연구 발전시키고 산학협동을 통해 이를 보급하여 국내 관련 산업의 발전 및 국민생활의 과학화에 기여하고자 하며, 이러한 목표와 비젼의 실현을 위해 회원들이 적극적인 참여와 활동을 전개하고자 한다.