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Soo-Youl Kim

Researcher at Cornell University

Publications -  135
Citations -  9604

Soo-Youl Kim is an academic researcher from Cornell University. The author has contributed to research in topics: Tissue transglutaminase & Cancer cell. The author has an hindex of 36, co-authored 130 publications receiving 8683 citations. Previous affiliations of Soo-Youl Kim include National Institutes of Health & Yonsei University.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Tissue transglutaminase-induced aggregation of α-synuclein: Implications for Lewy body formation in Parkinson's disease and dementia with Lewy bodies

TL;DR: Findings suggest that tTGase activity leads to α-synuclein aggregation to form Lewy bodies and perhaps contributes to neurodegeneration.
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Loss of proteolytically processed filaggrin caused by epidermal deletion of Matriptase/MT-SP1

TL;DR: It is shown that epidermal deficiency of the transmembrane serine protease Matriptase/MT-SP1 perturbs lipid matrix formation, cornified envelope morphogenesis, and stratum corneum desquamation.
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Differential expression of multiple transglutaminases in human brain. Increased expression and cross-linking by transglutaminases 1 and 2 in Alzheimer's disease.

TL;DR: The transglutaminase (TGase) family of enzymes participate in many biological processes involving cross-linking proteins into large macromolecular assemblies, including terminal differentiation programs of epithelial cell development and barrier function.
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Transglutaminase 2 Induces Nuclear Factor-κB Activation via a Novel Pathway in BV-2 Microglia

TL;DR: It is found that TGase 2 activates the transcriptional activator nuclear factor (NF)-κB and thereby enhances LPS-induced expression of inducible nitric-oxide synthase and prevents depletion of monomeric I-κBα in the cytosol of cells overexpressingTGase 2.