P
Pinar Coskun
Researcher at University of California, Irvine
Publications - 29
Citations - 5961
Pinar Coskun is an academic researcher from University of California, Irvine. The author has contributed to research in topics: Mitochondrion & Mitochondrial DNA. The author has an hindex of 23, co-authored 28 publications receiving 5570 citations. Previous affiliations of Pinar Coskun include Emory University.
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Journal ArticleDOI
Extension of murine life span by overexpression of catalase targeted to mitochondria.
Samuel E. Schriner,Nancy J. Linford,George M. Martin,Piper M. Treuting,Charles E. Ogburn,Mary J. Emond,Pinar Coskun,Warren Ladiges,Norman S. Wolf,Holly Van Remmen,Douglas C. Wallace,Peter S. Rabinovitch +11 more
TL;DR: Transgenic mice that overexpress human catalase localized to the peroxisome, the nucleus, or mitochondria were generated and the importance of mitochondria as a source of radicals was reinforced.
Journal ArticleDOI
Mitochondrial disease in superoxide dismutase 2 mutant mice
Simon Melov,Pinar Coskun,Manisha Patel,Robbyn L. Tuinstra,Barbara A. Cottrell,Albert S. Jun,Tomsz H. Zastawny,Miral Dizdaroglu,Stephen I. Goodman,Ting-Ting Huang,Henry M. Miziorko,Charles J. Epstein,Douglas C. Wallace +12 more
TL;DR: Results indicate that the increase in mitochondrial reactive oxygen species can result in biochemical aberrations with features reminiscent of mitochondrial myopathy, Friedreich ataxia, and 3-hydroxy-3-methylglutaryl-CoA lyase deficiency.
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Alzheimer's brains harbor somatic mtDNA control-region mutations that suppress mitochondrial transcription and replication
TL;DR: Investigation of the sequence of the mtDNA control region (CR) from AD brains for possible disease-causing mutations revealed that all AD brains had an average 63% increase in heteroplasmic mtDNA CR mutations and that AD brains from patients 80 years and older had a 130% increase.
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A novel neurological phenotype in mice lacking mitochondrial manganese superoxide dismutase
Simon Melov,Julie A. Schneider,Brian J. Day,Douglas Hinerfeld,Pinar Coskun,Suzanne S. Mirra,James D. Crapo,Douglas C. Wallace +7 more
TL;DR: In this article, the superoxide dismutase (SOD) mimetic Manganese 5, 10, 15, 20, 20-tetrakis (4-benzoic acid) porphyrin (MnTBAP) was used to save mice from systemic pathology and dramatically prolong their survival.
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Increased mitochondrial oxidative stress in the Sod2 (+/-) mouse results in the age-related decline of mitochondrial function culminating in increased apoptosis.
TL;DR: In this article, the authors analyzed changes in mitochondrial function with age in mice with partial or complete deficiencies in the mitochondrial antioxidant enzyme manganese superoxide dismutase (MnSOD).