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Cytosolic retention of HtrA2 during mitochondrial protein import stress triggers the DELE1-HRI pathway.

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第一作者： Paul Y,Bi

第一单位： Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, M5S 1A8, Canada.

作者： Paul Y,Bi ^[1] ; Samuel A,Killackey ^[1] ; Linus,Schweizer ^[1] ; Damien,Arnoult ^[2] ; Dana J,Philpott ^[3] ; Stephen E,Girardin ^[4]

作者单位： Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, M5S 1A8, Canada. ^[1] INSERM U1197, Hôpital Paul Brousse, Bâtiment Lavoisier, Villejuif, Cedex, 94807, France. ^[2] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, M5S 1A8, Canada.;Department of Immunology, University of Toronto, Toronto, ON, M5S 1A8, Canada. ^[3] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, M5S 1A8, Canada. stephen.girardin@utoronto.ca.;Department of Immunology, University of Toronto, Toronto, ON, M5S 1A8, Canada. stephen.girardin@utoronto.ca. ^[4]

医学主题词人类(Humans);胞质溶胶(Cytosol);HEK293细胞(HEK293 Cells);线粒体(Mitochondria);线粒体蛋白质类(Mitochondrial Proteins)

DOI 10.1038/s42003-024-06107-7

PMID 38555279

发布时间 2024-12-13

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Communications biology

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Communications biology

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Cytosolic retention of HtrA2 during mitochondrial protein import stress triggers the DELE1-HRI pathway.

Communications biology

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Cytosolic retention of HtrA2 during mitochondrial protein import stress triggers the DELE1-HRI pathway.

Communications biology

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Communications biology

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