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Piotr K. Kopinski
Researcher at Howard Hughes Medical Institute
Publications - 12
Citations - 1318
Piotr K. Kopinski is an academic researcher from Howard Hughes Medical Institute. The author has contributed to research in topics: Mitochondrial respiratory chain complex III & Mitochondrial DNA. The author has an hindex of 7, co-authored 10 publications receiving 809 citations. Previous affiliations of Piotr K. Kopinski include Temple University & Children's Hospital of Philadelphia.
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Journal ArticleDOI
Foxp3 Reprograms T Cell Metabolism to Function in Low-Glucose, High-Lactate Environments
Alessia Angelin,Luis Gil-de-Gómez,Satinder Dahiya,Jing Jiao,Lili Guo,Matthew H. Levine,Zhonglin Wang,William J. Quinn,Piotr K. Kopinski,Piotr K. Kopinski,Liqing Wang,Tatiana Akimova,Yujie Liu,Tricia R. Bhatti,Rongxiang Han,Benjamin L. Laskin,Joseph A. Baur,Ian A. Blair,Douglas C. Wallace,Douglas C. Wallace,Wayne W. Hancock,Ulf H. Beier +21 more
TL;DR: It is reported that the Treg transcription factor Foxp3 reprograms T cell metabolism by suppressing Myc and glycolysis, enhancing oxidative phosphorylation, and increasing nicotinamide adenine dinucleotide oxidation, which allows Tregs a metabolic advantage in low-glucose, lactate-rich environments.
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Mitochondrial functions modulate neuroendocrine, metabolic, inflammatory, and transcriptional responses to acute psychological stress
Martin Picard,Meagan J. McManus,Meagan J. McManus,Jason D. Gray,Carla Nasca,Cynthia Moffat,Piotr K. Kopinski,Piotr K. Kopinski,Erin L. Seifert,Bruce S. McEwen,Douglas C. Wallace,Douglas C. Wallace +11 more
TL;DR: The role of mitochondrial energetics and redox balance as modulators of key pathophysiological perturbations previously linked to disease is demonstrated, establishing mitochondria as stress-response modulators, with implications for understanding the mechanisms of stress pathophysiology and mitochondrial diseases.
Journal ArticleDOI
Rac2-MRC-cIII–generated ROS cause genomic instability in chronic myeloid leukemia stem cells and primitive progenitors
Margaret Nieborowska-Skorska,Piotr K. Kopinski,Regina Ray,Grazyna Hoser,Danielle Ngaba,Sylwia Flis,Kimberly Cramer,Mamatha M. Reddy,Mateusz Koptyra,Tyrone Penserga,Eliza Glodkowska-Mrowka,Elisabeth Bolton,Tessa L. Holyoake,Connie J. Eaves,Sabine Cerny-Reiterer,Peter Valent,Andreas Hochhaus,Timothy P. Hughes,Heiko van der Kuip,Martin Sattler,Wieslaw Wiktor-Jedrzejczak,Christine Richardson,Adrienne M. Dorrance,Tomasz Stoklosa,David R. Williams,Tomasz Skorski +25 more
TL;DR: It is postulate that the Rac2-MRC-cIII pathway triggers ROS-mediated genomic instability in LSCs and primitive LPCs, which could be targeted to prevent the relapse and malignant progression of CML.
Journal ArticleDOI
Lactate Limits T Cell Proliferation via the NAD(H) Redox State.
William J. Quinn,Jing Jiao,Tara TeSlaa,Jason Stadanlick,Zhonglin Wang,Liqing Wang,Tatiana Akimova,Alessia Angelin,Patrick M. Schäfer,Michelle D. Cully,Caroline Perry,Piotr K. Kopinski,Lili Guo,Ian A. Blair,Louis R. Ghanem,Michael S. Leibowitz,Wayne W. Hancock,Edmund K. Moon,Matthew H. Levine,Evgeniy Eruslanov,Douglas C. Wallace,Joseph A. Baur,Ulf H. Beier +22 more
TL;DR: It is reported that nicotinamide adenine dinucleotide (NAD+), which is reduced to NADH by lactate dehydrogenase in lactate-rich conditions, is a key point of metabolic control in T cells and directly targeting the redox state may be a useful approach for developing novel immunotherapies in cancer and therapeutic immunosuppression.
Journal ArticleDOI
Regulation of nuclear epigenome by mitochondrial DNA heteroplasmy.
Piotr K. Kopinski,Kevin A. Janssen,Patrick M. Schaefer,Sophie Trefely,Sophie Trefely,Caroline Perry,Prasanth Potluri,Jesus A Tintos-Hernandez,Larry N. Singh,Kelly R. Karch,Sydney L. Campbell,Mary T. Doan,Helen Jiang,Itzhak Nissim,Eiko Nakamaru-Ogiso,Kathryn E. Wellen,Nathaniel W. Snyder,Benjamin A. Garcia,Douglas C. Wallace +18 more
TL;DR: Exhaustive metabolomic and histone posttranscriptional modification analysis of cultivated cybrid cell lines harboring 3243G heteroplasmy revealed that changes in mtDNA heteroplAsmy cause changes in mitochondrial intermediates and redox state, which result in distinctive histone modification changes.