KBM (생물, 의학, 약학관련 연구 모임) 1월 학술 세미나 안내 [1/18 Tue 6 pm] > 자유게시판

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KBM (생물, 의학, 약학관련 연구 모임) 1월 학술 세미나 안내 [1/18 Tue 6 pm]

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작성자 Science (35.♡.139.226) 댓글 0건 조회 95회 작성일 2022-01-06 17:07



KBM (Korean Biological Research Group in Michigan)은 의학, 약학, 생물학 관련 연구를 수행하는 연구자들의 모임입니다 [홈페이지]. 

매달 셋째 주 화요일 저녁 6시에 온라인으로 학술 세미나 및 네트워킹을 진행하고 있으며, 현재 UofM 뿐만 아니라 다른 학교와의 교류도 도모하고 있습니다. 

KBM Science Series.


2022년 1월 세미나 안내입니다.

Biological Chemistry 소속으로 계시는 유원진 박사님께서 “Impact on vesicular trafficking of the E3 Ubiquitin ligase MARCH2 and the LMP-inducing drug JS-K” 란 주제로 발표해 주십니다.


l  Abstract:

Vesicles trafficking including secretory vesicles and autophagy have an essential role of numerous biological functions such as cell growth, cellular communication, cell metabolism, and intracellular homeostasis. The E3 ubiquitin ligase membrane-associated ring-CH-type finger 2 (MARCH2) is well known to regulate the vesicular trafficking of its substrates such as DLG1, beta2-adrenergic receptors, Cystic fibrosis transmembrane conductance regulator (CFTR), and Dishevelled. However, its role of secretory pathway between endoplasmic reticulum (ER) and Golgi compartments have not been reported yet. Here I examined novel substrate of MARCH2 using proximity-dependent biotinylation assay and identified the ER-Golgi intermediate compartment protein 3 (ERGIC3).

MARCH2 degrades ERGIC3 by ubiquitination, proteasome, and lysosome dependent manner. I further found that α1-antitrypsin and haptoglobin interact with ERGIC3 and that ERGIC3 regulates their secretion. Furthermore, MARCH2-mediated ERGIC3 ubiquitination is the key role in trafficking of ERGIC3-binding secretory proteins. These results reveal that ERGIC3 is a novel cargo receptor for secretion of α1-antitrypsin and haptoglobin and its ubiquitination by MARCH2 is a crucial role in the early secretory pathway of α1-antitrypsin and haptoglobin.

Lysosome-dependent degradation such as autophagy and endocytosis is crucial role for recycling cellular components to maintain intracellular homeostasis. Recently, Study on regulation of lysosomal function is important to develop clinical drug for cancer, crohn’s, and neurodegenerative diseases. In this study, I also found that JS-K as a Nitric oxide-releasing prodrug affected to autophagy process through the lysosomal dysfunction. JS-K impaired degradation of autophagosome and endocytosis-mediated degradation of epidermal growth factor receptors (EGFR). JS-K increased reactive oxygen species (ROS) stress by glutathione (GSH) depletion and releasing NO. In addition, JS-K promoted lysosomal membrane permeabilization by GSH depletion-mediated ROS stress. Surprisingly, blocking the fusion of autophagosome-lysosome fusion prevented JS-K-mediated LMP. These my findings suggest that depletion of GSH-mediated LMP possibly can be useful to develop the therapeutic target for anti-cancer drug and autophagosome-lysosome fusion is essential for LDCD caused by LMP.



l  장소: Biological Sciences Building (BSB), Room 5150

l  주소: 1105 N University Ave, Ann Arbor, MI 48109

l  시간: 1 18(오후 6

l  Zoom link: https://umich.zoom.us/j/2016101518 (passcode:3mDLiz)


세미나는 In-person ZOOM 으로 동시 진행되오니편하신 방법으로 참석해 주세요더불어세미나 이후 식사가 예정되어 있습니다.

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