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Gil Leibowitz

Researcher at Hebrew University of Jerusalem

Publications -  97
Citations -  10377

Gil Leibowitz is an academic researcher from Hebrew University of Jerusalem. The author has contributed to research in topics: Insulin & Diabetes mellitus. The author has an hindex of 39, co-authored 88 publications receiving 9429 citations. Previous affiliations of Gil Leibowitz include University of California, San Diego & Hadassah Medical Center.

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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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mTOR Inhibition by Rapamycin Prevents β-Cell Adaptation to Hyperglycemia and Exacerbates the Metabolic State in Type 2 Diabetes

TL;DR: The essential role of mTOR/S6K1 in orchestrating β-cell adaptation to hyperglycemia in type 2 diabetes is emphasized and it is likely that treatments based on mTOR inhibition will cause exacerbation of diabetes.
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Effect of Saxagliptin on Renal Outcomes in the SAVOR-TIMI 53 Trial.

TL;DR: Treatment with saxagliptin improved ACR, even in the normoalbuminuric range, without affecting eGFR, and the beneficial effect of saxagLIptin on albuminuria could not be explained by its effect on glycemic control.
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Presenilin 1 Facilitates the Constitutive Turnover of β-Catenin: Differential Activity of Alzheimer’s Disease–Linked PS1 Mutants in the β-Catenin–Signaling Pathway

TL;DR: It is shown that both the full length and the C-terminal fragment of wild-type or FAD mutant PS1 interact with β-catenin from transfected cells and brains of transgenic mice, whereas E-cadherin and adenomatous polyposis coli (APC) are not detected in this complex.
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Glucotoxicity and beta-cell failure in type 2 diabetes mellitus.

TL;DR: The role of glucotoxicity in beta-cell dysfunction in type 2 diabetes mellitus is discussed, which results from decreased insulin gene transcription due to hyperglycemia-induced changes in the activity of beta- cell specific transcription factors.