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Anthony J.A. Molina
Researcher at University of California, San Diego
Publications - 54
Citations - 5309
Anthony J.A. Molina is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Mitochondrion & mitochondrial fusion. The author has an hindex of 21, co-authored 47 publications receiving 4461 citations. Previous affiliations of Anthony J.A. Molina include University of Illinois at Chicago & Boston University.
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Journal ArticleDOI
Fission and selective fusion govern mitochondrial segregation and elimination by autophagy
Gilad Twig,Alvaro A. Elorza,Anthony J.A. Molina,Anthony J.A. Molina,Hibo Mohamed,Jakob D. Wikstrom,Gil Walzer,Linsey Stiles,Sarah E. Haigh,Steve Katz,Guy Las,Joseph Alroy,Min Wu,Bénédicte F. Py,Junying Yuan,Jude T. Deeney,Barbara E. Corkey,Orian S. Shirihai +17 more
TL;DR: Pulse chase and arrest of autophagy at the pre‐proteolysis stage reveal that fission followed by selective fusion segregates dysfunctional mitochondria and permits their removal by autophagic.
Journal ArticleDOI
Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells
Sameer Kalghatgi,Catherine S. Spina,Catherine S. Spina,Catherine S. Spina,James C. Costello,Marc Liesa,J. Ruben Morones-Ramirez,Shimyn Slomovic,Anthony J.A. Molina,Anthony J.A. Molina,Orian S. Shirihai,James J. Collins,James J. Collins,James J. Collins +13 more
TL;DR: Clinical relevant doses of bactericidal antibiotics—quinolones, aminoglycosides, and β-lactams—cause mitochondrial dysfunction and ROS overproduction in mammalian cells and these bactericidal antibiotic–induced effects lead to oxidative damage to DNA, proteins, and membrane lipids.
Journal ArticleDOI
Mitochondrial Networking Protects β-Cells From Nutrient-Induced Apoptosis
Anthony J.A. Molina,Jakob D. Wikstrom,Jakob D. Wikstrom,Linsey Stiles,Linsey Stiles,Guy Las,Hibo Mohamed,Alvaro A. Elorza,Gil Walzer,Gilad Twig,Steve Katz,Barbara E. Corkey,Orian S. Shirihai +12 more
TL;DR: Data suggest that alterations in mitochondrial fusion and fission play a critical role in nutrient-induced β-cell apoptosis and may be involved in the pathophysiology of type 2 diabetes.
Journal ArticleDOI
Dual role of proapoptotic BAD in insulin secretion and beta cell survival
Nika N. Danial,Loren D. Walensky,Chen-Yu Zhang,Cheol Soo Choi,Jill K. Fisher,Anthony J.A. Molina,Sandeep Robert Datta,Sandeep Robert Datta,Kenneth L. Pitter,Gregory H. Bird,Jakob D. Wikstrom,Jude T. Deeney,Kirsten Robertson,Joel Morash,Ameya Kulkarni,Susanne Neschen,Sheene Kim,Michael E. Greenberg,Barbara E. Corkey,Orian S. Shirihai,Gerald I. Shulman,Bradford B. Lowell,Stanley J. Korsmeyer,Stanley J. Korsmeyer +23 more
TL;DR: In this article, the proapoptotic BCL-2 family member BAD resides in a glucokinase-containing complex that regulates glucose-driven mitochondrial respiration, which is specifically dependent upon the phosphorylation of its BH3 sequence, previously defined as an essential death domain.
Journal ArticleDOI
Skeletal Muscle Mitochondrial Content, Oxidative Capacity, and Mfn2 Expression Are Reduced in Older Patients With Heart Failure and Preserved Ejection Fraction and Are Related to Exercise Intolerance
Anthony J.A. Molina,Manish S. Bharadwaj,Cynthia G. Van Horn,Barbara J. Nicklas,Mary F. Lyles,Joel Eggebeen,Mark J. Haykowsky,Peter H. Brubaker,Dalane W. Kitzman +8 more
TL;DR: These findings suggest that skeletal muscle oxidative capacity, mitochondrial content, and mitochondrial fusion are abnormal in older patients with HFpEF and might contribute to their severe exercise intolerance.