Ana Maria Cuervo, M.D., Ph.D

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Ana Maria Cuervo, M.D., Ph.D. Professor, Developmental and Molecular Biology Professor, Anatomy and Structural Biology Co-Director, Institute for Aging Research Robert and Renée Belfer Chair for the Study of Neurodegenerative Diseases Dr. Ana Maria Cuervo obtained her M.D. and Ph.D. in Biochemistry and Molecular biology from the University of Valencia (Spain) in 1990 and 1994, respectively, and received postdoctoral training at Tufts University in Boston, MA. In 2002, she started her laboratory at Albert Einstein College of Medicine. She is a recognized leader in the field of protein degradation and the biology of aging. In 2019, she was elected to the National Academy of Sciences. Dr. Cuervo has been the recipient of prestigious awards, including the P. Benson Award in Cell Biology, the Keith Porter Lecture (Award), the Nathan Shock Memorial Lecture Award, the Vincent Cristofalo Aging Award, the Bennett J. Cohen Award in Aging Biology, the Marshall Horwitz Prize, and the Saul Korey Prize in Translational Medicine. Dr. Cuervo has organized and chaired international conferences on protein degradation and aging, has presented lectures at numerous national and international scientific gatherings, and is a member of several research journal editorial boards and co-editor in chief of Aging Cell. Dr. Cuervo was included in the Clarivate Analytics 2018 and 2019 Highly Cited Researchers List (ranking of top 1% cited researchers). She has been a member of the National Institute on Aging (NIA) Scientific Council, the National Institutes of Health (NIH) Council of Councils, the NIA Board of Scientific Counselors, and the Advisory Committee to the NIH Deputy Director. She is an elected member of the Royal Academy of Medicine of the Valencia Community, the Real Academia de Ciencias Exactas, Fisicas y Naturales (the Spanish Royal Academy of Sciences), and the American Academy of Arts and Sciences. .

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Chaperone-Mediated Autophagy: Roles in Disease and Aging Cell Research (2014) 24:92-104
npg Chaperone-mediated autophagy: roles in disease and aging Cell Research (2014) 24:92-104. 92 © 2014 IBCB, SIBS, CAS All rights reserved 1001-0602/14 $ 32.00 npg REVIEW www.nature.com/cr Chaperone-mediated autophagy: roles in disease and aging Ana Maria Cuervo1, Esther Wong2 1Department of Developmental and Molecular Biology, Institute for Aging Studies, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Chanin Building 504, Bronx, NY 10461, USA; 2School of Biological Sci- ences, Nanyang Technological University, SBS-03n-05, 60 Nanyang Drive, Singapore 637551, Singapore This review focuses on chaperone-mediated autophagy (CMA), one of the proteolytic systems that contributes to degradation of intracellular proteins in lysosomes. CMA substrate proteins are selectively targeted to lysosomes and translocated into the lysosomal lumen through the coordinated action of chaperones located at both sides of the membrane and a dedicated protein translocation complex. The selectivity of CMA permits timed degradation of spe- cific proteins with regulatory purposes supporting a modulatory role for CMA in enzymatic metabolic processes and subsets of the cellular transcriptional program. In addition, CMA contributes to cellular quality control through the removal of damaged or malfunctioning proteins. Here, we describe recent advances in the understanding of the mo- lecular dynamics, regulation and physiology of CMA, and discuss the evidence in support of the contribution of CMA dysfunction to severe human disorders such as neurodegeneration and cancer. Keywords: chaperone-mediated autophagy; neurodegeneration; cancer; aging Cell Research (2014) 24:92-104. doi:10.1038/cr.2013.153; published online 26 November 2013 Introduction the lysosomal membrane and then gain access to the lu- men of this organelle by directly crossing its membrane.
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Dopamine-modified α-synuclein blocks chaperone-mediated autophagy Marta Martinez-Vicente, … , David Sulzer, Ana Maria Cuervo J Clin Invest. 2008;118(2):777-788. https://doi.org/10.1172/JCI32806. Research Article Neuroscience Altered degradation of α-synuclein (α-syn) has been implicated in the pathogenesis of Parkinson disease (PD). We have shown that α-syn can be degraded via chaperone-mediated autophagy (CMA), a selective lysosomal mechanism for degradation of cytosolic proteins. Pathogenic mutants of α-syn block lysosomal translocation, impairing their own degradation along with that of other CMA substrates. While pathogenic α-syn mutations are rare, α-syn undergoes posttranslational modifications, which may underlie its accumulation in cytosolic aggregates in most forms of PD. Using mouse ventral medial neuron cultures, SH-SY5Y cells in culture, and isolated mouse lysosomes, we have found that most of these posttranslational modifications of α-syn impair degradation of this protein by CMA but do not affect degradation of other substrates. Dopamine-modified α-syn, however, is not only poorly degraded by CMA but also blocks degradation of other substrates by this pathway. As blockage of CMA increases cellular vulnerability to stressors, we propose that dopamine-induced autophagic inhibition could explain the selective degeneration of PD dopaminergic neurons. Find the latest version: https://jci.me/32806/pdf Research article Dopamine-modified α-synuclein blocks chaperone-mediated autophagy Marta Martinez-Vicente,1,2 Zsolt Talloczy,3,4 Susmita Kaushik,1,2 Ashish C. Massey,1,2 Joseph Mazzulli,5 Eugene V. Mosharov,3,4 Roberto Hodara,5 Ross Fredenburg,6 Du-Chu Wu,4,7 Antonia Follenzi,2 William Dauer,4 Serge Przedborski,4,7 Harry Ischiropoulos,5 Peter T.
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Ana Maria Cuervo MD Phd
Ana Maria Cuervo MD PhD CONTENTS I. C.V. Personal and professional information Awards and Honors Scientific Review Editorial Tasks Organization of meetings Advisory groups Invited presentations II. Publication List III. Teaching and Related Activities IV. Administration V. Research Support (past and active) Wikipedia: #1day#1women initiative: Ana Maria Cuervo February 20 Ana Maria Cuervo, MD PhD CURRICULUM VITAE PERSONAL INFORMATION Date of Birth: July 14, 1966 Place of Birth: Barcelona, Spain Citizenship: American Address: Department of Developmental and Molecular Biology, Chanin Building R. 504, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461 Phone: (718) 430 2689 Fax: (718) 430 8975 e-mail: ana-maria. [email protected] POSITION TITLE Robert and Renee Belfer Chair for the Study of Neurodegenerative Diseases Professor Dept. of Development and Molecular Biology (with tenure) Professor Dept. of Medicine (with tenure) Professor Dept. of Anatomy and Structural Biology (with tenure) Co-Director of the Einstein Institute for Aging Research Member of the Marion Bessin Liver Research Center of the Albert Einstein College of Medicine. Member of the Albert Einstein Cancer Center Member of the Diabetes Research Center EDUCATION/TRAINING Institution and Location Degree Year Field of Study University of Valencia, Spain M.D. 1990 Medicine University of Valencia, Spain Ph.D. 1994 Biochem. & Mol. Biol. Tufts University, Boston, USA Postdoc 1995/8 Physiology Professional employment and Hospital appointments 1985/90 Research Fellow-Medical Student, Department of Physiology, School of Medicine, University of Valencia, Spain. 1991/94 Predoctoral Fellow, Instituto de Investigaciones Citologicas, Valencia, Spain. 1995/97 Postdoctoral Fellow, Department of Physiology, Tufts University, Boston MA, USA.
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When Lysosomes Get Old૾
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The Proteasome and Autophagy
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