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2017 Fiscal Year Final Research Report

The mechanism of synthesis of calreticulin, a molecular chaperone, and the cellular function in trophoblasts

Research Project

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Project/Area Number 15K20156
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Obstetrics and gynecology
Research InstitutionWakayama Medical University

Principal Investigator

Yamamoto Madoka  和歌山県立医科大学, 医学部, 助教 (70596973)

Project Period (FY) 2015-04-01 – 2018-03-31
Keywords胎盤 / 絨毛外栄養膜細胞 / カルレティキュリン / 分子シャペロン / 妊娠高血圧症候群
Outline of Final Research Achievements

The expression of Calreticulin (CRT) was detected in four trophoblastic cell lines and human placenta of normal pregnant women which was obtained with informed consent. In the human extravillous trophoblast (EVT) cell line HTR8/SVneo cells, CRT knockdown suppressed the invasion ability and the adhesion to fibronectin, and suppressed the phosphorylation level of Akt on attachment to fibronection. CRT knockdown modulated N-glycosylation of integrin (Itg) β1, and changed the expression level of several glycosyltransferases in the cells. These results showed that CRT, which interacts with the glycosylated protein, promotes cell adhesion and invasion ability of EVTs by regulating N-glycosylation of Itg β1.

Free Research Field

産婦人科学

URL: 

Published: 2019-03-29  

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