M
Minchul Seo
Researcher at Kyungpook National University
Publications - 25
Citations - 1272
Minchul Seo is an academic researcher from Kyungpook National University. The author has contributed to research in topics: Autophagy & Hypothermia. The author has an hindex of 15, co-authored 23 publications receiving 994 citations. Previous affiliations of Minchul Seo include Dongguk University & University of Minnesota.
Papers
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Journal ArticleDOI
The ULK1 complex mediates MTORC1 signaling to the autophagy initiation machinery via binding and phosphorylating ATG14
Ji Man Park,Chang Hwa Jung,Minchul Seo,Neil Michael Otto,Douglas Grunwald,Kwan Hyun Kim,Branden S. Moriarity,Young Mi Kim,Colby G. Starker,Richard Seonghun Nho,Daniel F. Voytas,Do Hyung Kim +11 more
TL;DR: A key molecular event is defined for the starvation-induced activation of the ATG14-containing PtdIns3K complex by ULK1, and hierarchical relations between the ULK 1 activation and other autophagy proteins involved in phagophore formation are demonstrated.
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mTORC1 phosphorylates UVRAG to negatively regulate autophagosome and endosome maturation.
TL;DR: It is demonstrated that mTORC1 engages in late stages of autophagy and endosome maturation, defining a broader range of m TORC1 functions in the membrane-associated processes.
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ULK1 inhibits the kinase activity of mTORC1 and cell proliferation.
TL;DR: It is found that ULK1 inhibits the kinase activity of mTORC1 and cell proliferation and is important to coordinately regulate cell growth and autophagy with optimized utilization of cellular energy.
Journal ArticleDOI
ULK1 phosphorylates Ser30 of BECN1 in association with ATG14 to stimulate autophagy induction.
Ji Man Park,Minchul Seo,Chang Hwa Jung,Douglas Grunwald,Matthew D. Stone,Neil Michael Otto,Erik A. Toso,Yeseul Ahn,Michael Kyba,Timothy J. Griffin,LeeAnn Higgins,Do Hyung Kim +11 more
TL;DR: It is demonstrated that BECN1 Ser30 is a ULK1 target site whose phosphorylation activates the ATG14-containing PIK3C3 complex and stimulates autophagosome formation in response to amino acid starvation, hypoxia, and MTORC1 inhibition.
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Lipocalin-2 Protein Deficiency Ameliorates Experimental Autoimmune Encephalomyelitis THE PATHOGENIC ROLE OF LIPOCALIN-2 IN THE CENTRAL NERVOUS SYSTEM AND PERIPHERAL LYMPHOID TISSUES
Youngpyo Nam,Jong Heon Kim,Minchul Seo,Jae-Hong Kim,Myungwon Jin,Sangmin Jeon,Jung Wan Seo,Won-Ha Lee,So Jin Bing,Youngheun Jee,Won Kee Lee,Dong Ho Park,Hyun Kook,Kyoungho Suk +13 more
TL;DR: LCN2 is a critical mediator of autoimmune inflammation and disease development in EAE and it is suggested that LCN2 be regarded a potential therapeutic target in multiple sclerosis.