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Michael J. Morgan

Researcher at University of Colorado Denver

Publications -  54
Citations -  12250

Michael J. Morgan is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Programmed cell death & Autophagy. The author has an hindex of 34, co-authored 51 publications receiving 10554 citations. Previous affiliations of Michael J. Morgan include University of Colorado Boulder & National Institutes of Health.

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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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Crosstalk of reactive oxygen species and NF-κB signaling.

Michael J. Morgan, +1 more
- 01 Jan 2011 - 
TL;DR: The regulation of ROS levels by NF-κB targets and various ways in which ROS have been proposed to impact NF-σκB signaling pathways are reviewed.
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TNF-induced activation of the Nox1 NADPH oxidase and its role in the induction of necrotic cell death

You-Sun Kim, +3 more
- 08 Jun 2007 - 
TL;DR: It is shown that TNF also activates the Nox1 NADPH oxidase in mouse fibroblasts when cells undergo necrosis, suggesting that activation of Nox 1 through forming a complex with TNF signaling components plays a key role in TNF-induced necrotic cell death.
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Chloroquine sensitizes breast cancer cells to chemotherapy independent of autophagy

Paola Maycotte, +5 more
- 01 Feb 2012 - 
TL;DR: It is proposed that although CQ might be helpful in combination with cancer therapeutic drugs, its sensitizing effects can occur independently of autophagy inhibition, and this possibility should be considered in the ongoing clinical trials where CQ or HCQ are used in the treatment of cancer.
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Methylation-dependent loss of RIP3 expression in cancer represses programmed necrosis in response to chemotherapeutics

Gi Bang Koo, +21 more
- 08 May 2015 - 
TL;DR: This work shows that programmed necrosis is activated in response to many chemotherapeutic agents and contributes to chemotherapy-induced cell death, and proposes that RIP3-deficient cancer patients may benefit from receiving hypomethylating agents to induce RIP3 expression prior to treatment with conventional Chemotherapeutics.