H
Hagai Shorer
Researcher at Weizmann Institute of Science
Publications - 5
Citations - 2281
Hagai Shorer is an academic researcher from Weizmann Institute of Science. The author has contributed to research in topics: Golgi apparatus & Cysteine protease. The author has an hindex of 5, co-authored 5 publications receiving 2101 citations.
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Journal ArticleDOI
Reactive oxygen species are essential for autophagy and specifically regulate the activity of Atg4
TL;DR: The role of reactive oxygen species (ROS) as signaling molecules in starvation‐induced autophagy is described and a cysteine residue located near the HsAtg4 catalytic site is specified as a critical for this regulation.
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Phosphorylation of Insulin Receptor Substrate-1 (IRS-1) by Protein Kinase B Positively Regulates IRS-1 Function
Keren Paz,Yan-Fang Liu,Hagai Shorer,Rina Hemi,Derek LeRoith,Michael Quan,Hannah Kanety,Rony Seger,Yehiel Zick +8 more
TL;DR: Results implicate a wortmannin-sensitive Ser/Thr kinase, different from PKB, as the kinase that phosphorylates IRS-1 and acts as the feedback control regulator that turns off insulin signals by inducting the dissociation of IRS proteins from IR.
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The COOH terminus of GATE-16, an intra-Golgi transport modulator, is cleaved by the human cysteine protease HsApg4A.
TL;DR: It is shown that GATE-16 undergoes COOH-terminal cleavage both in vivo and in vitro, only when the conserved glycine 116 is present, and pure HsApg4A is sufficient to cleave GGate-16.
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Involvement of LMA1 and GATE-16 family members in intracellular membrane dynamics
TL;DR: LMA1 and GATE-16 are suggested to keep the dissociated cis-SNAREs apart from each other, allowing multiple fusion processes to take place, and the involvement of this family in multiple intracellular trafficking pathways is discussed.
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Modulation of N-ethylmaleimide-sensitive factor activity upon amino acid deprivation.
TL;DR: Investigation of the relationship between the general secretory machinery and the autophagic pathway in Chinese hamster ovary cells grown in the absence of amino acid finds that secretion is attenuated in cells growing in media lacking amino acid.