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Penny E. Lovat

Researcher at Newcastle University

Publications -  106
Citations -  9733

Penny E. Lovat is an academic researcher from Newcastle University. The author has contributed to research in topics: Melanoma & Fenretinide. The author has an hindex of 36, co-authored 94 publications receiving 8002 citations. Previous affiliations of Penny E. Lovat include Sapienza University of Rome & University of Newcastle.

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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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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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Increasing melanoma cell death using inhibitors of protein disulfide isomerases to abrogate survival responses to endoplasmic reticulum stress

TL;DR: In this paper, the authors show that inhibition of PDI activity increases apoptosis in response to agents which induce ER stress and suggest that the development of potent, small-molecule PDI inhibitors has significant potential as a powerful tool for enhancing the efficacy of chemotherapy in melanoma.
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Regulation of Endoplasmic Reticulum Stress-induced Cell Death by ATF4 in Neuroectodermal Tumor Cells

TL;DR: It is demonstrated that ATF4 mediates ER stress-induced cell death of neuroectodermal tumor cells in response to fenretinide or bortezomib.
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Oncogenic BRAF induces chronic ER stress condition resulting in increased basal autophagy and apoptotic resistance of cutaneous melanoma

TL;DR: Enhanced basal autophagy, typically observed in BRAFV600E melanomas, is a consequence of a chronic ER stress status, which ultimately results in the chemoresistance of such tumours, and targeted therapies that attenuate ER stress may represent a novel and more effective therapeutic strategy for BRAF mutant melanoma.