M
Melissa N. Quinsay
Researcher at University of Montana
Publications - 9
Citations - 1917
Melissa N. Quinsay is an academic researcher from University of Montana. The author has contributed to research in topics: Mitochondrion & Mitochondrial permeability transition pore. The author has an hindex of 8, co-authored 9 publications receiving 1581 citations. Previous affiliations of Melissa N. Quinsay include University of California, San Diego.
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Journal ArticleDOI
Microtubule-associated Protein 1 Light Chain 3 (LC3) Interacts with Bnip3 Protein to Selectively Remove Endoplasmic Reticulum and Mitochondria via Autophagy
Rita A. Hanna,Melissa N. Quinsay,Amabel M. Orogo,Kayla Giang,Shivaji Rikka,Åsa B. Gustafsson +5 more
TL;DR: The data indicate that Bnip3 regulates the apoptotic balance as an autophagy receptor that induces removal of both mitochondria and ER and that this process significantly reduced both mitophagy and ERphagy.
Journal ArticleDOI
Parkin Protein Deficiency Exacerbates Cardiac Injury and Reduces Survival following Myocardial Infarction
Dieter A Kubli,Xiaoxue Zhang,Youngil Lee,Rita A. Hanna,Melissa N. Quinsay,Christine K. Nguyen,Rebecca E. Jimenez,Susanna Petrosyan,Anne N. Murphy,Åsa B. Gustafsson +9 more
TL;DR: The results suggest that Parkin plays a critical role in adapting to stress in the myocardium by promoting removal of damaged mitochondria in response to myocardial infarction.
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Bnip3 impairs mitochondrial bioenergetics and stimulates mitochondrial turnover.
Shivaji Rikka,Melissa N. Quinsay,Robert L Thomas,Dieter A Kubli,Xiaoxue Zhang,Anne N. Murphy,Åsa B. Gustafsson +6 more
TL;DR: Bnip3-mediated impairment of mitochondrial respiration induces mitochondrial turnover by activating mitochondrial autophagy, and it is found that this effect caused an increase in mitochondrial protease activity, suggesting that Bnip 3 might promote degradation of proteins in the mitochondria.
Journal ArticleDOI
Loss of MCL-1 leads to impaired autophagy and rapid development of heart failure
Robert L Thomas,David J. Roberts,Dieter A Kubli,Youngil Lee,Melissa N. Quinsay,Jarvis B. Owens,Kimberlee M. Fischer,Mark A. Sussman,Shigeki Miyamoto,Shigeki Miyamoto,Åsa B. Gustafsson,Åsa B. Gustafsson +11 more
TL;DR: It is demonstrated that MCL-1 is essential for mitochondrial homeostasis and induction of autophagy in the heart and raises concerns about potential cardiotoxicity for chemotherapeutics that target M CL-1.
Journal ArticleDOI
Bnip3-mediated mitochondrial autophagy is independent of the mitochondrial permeability transition pore
TL;DR: The results support a model where Bnip3 induces selective removal of the mitochondria in cardiac myocytes, and that BnIP3 triggers induction of autophagy independent of Ca2+, ROS generation, and mPTP opening.