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Shaolin Shi

Researcher at Albert Einstein College of Medicine

Publications -  23
Citations -  1426

Shaolin Shi is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Notch signaling pathway & Medicine. The author has an hindex of 14, co-authored 17 publications receiving 1345 citations. Previous affiliations of Shaolin Shi include University of California, San Diego & Yeshiva University.

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Protein O-fucosyltransferase 1 is an essential component of Notch signaling pathways.

TL;DR: It is shown that mouse embryos lacking protein O-fucosyltransferase 1 die at midgestation with severe defects in somitogenesis, vasculogenesis, cardiogenesis, and neurogenesis, and the phenotype is similar to that of embryos lacking downstream effectors of all Notch signaling pathways such as presenilins or RBP-Jκ.
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Modification of epidermal growth factor-like repeats with O-fucose. Molecular cloning and expression of a novel GDP-fucose protein O-fucosyltransferase.

TL;DR: The isolation of a cDNA that encodes human O-FucT-1 is reported, which contains an open reading frame encoding a protein of 388 amino acids with a predicted N-terminal transmembrane sequence typical of a type II membrane orientation.
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Roles of Pofut1 and O-Fucose in Mammalian Notch Signaling

TL;DR: Mammalian Notch receptors contain 29–36 epidermal growth factor-like repeats that may be modified by protein O-fucosyltransferase 1 (Pofut1), an essential component of the canonical Notch signaling pathway, but, in contrast to Drosophila, P ofut1 is not required for stable cell surface expression of Notch.
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The canonical Notch/RBP-J signaling pathway controls the balance of cell lineages in mammary epithelium during pregnancy

TL;DR: It is proposed that the Notch-RBP-J pathway regulates alveolar development during pregnancy by maintaining luminal cell fate and preventing uncontrolled basal cell proliferation.
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Inactivation of the Mgat1 gene in oocytes impairs oogenesis, but embryos lacking complex and hybrid N-glycans develop and implant.

TL;DR: In this paper, the Mgat1 gene in oocytes was deleted by using a ZP3Cre recombinase transgene to identify roles for complex and hybrid N-glycans in oogenesis and preimplantation development.