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Arvind Ramanathan
Researcher at Buck Institute for Research on Aging
Publications - 34
Citations - 5328
Arvind Ramanathan is an academic researcher from Buck Institute for Research on Aging. The author has contributed to research in topics: Biology & Medicine. The author has an hindex of 19, co-authored 26 publications receiving 4616 citations. Previous affiliations of Arvind Ramanathan include Oak Ridge National Laboratory & Howard Hughes Medical Institute.
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Journal ArticleDOI
The M2 splice isoform of pyruvate kinase is important for cancer metabolism and tumour growth
Heather R. Christofk,Matthew G. Vander Heiden,Marian H. Harris,Arvind Ramanathan,Robert E. Gerszten,Robert E. Gerszten,Ru Wei,Mark D. Fleming,Stuart L. Schreiber,Stuart L. Schreiber,Lewis C. Cantley,Lewis C. Cantley +11 more
TL;DR: It is demonstrated that M2 expression is necessary for aerobic glycolysis and that this metabolic phenotype provides a selective growth advantage for tumour cells in vivo.
Journal ArticleDOI
Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype
Christopher D. Wiley,Michael C. Velarde,Pacome Lecot,Su Liu,Ethan A. Sarnoski,Adam Freund,Kotaro Shirakawa,Hyung W. Lim,Sonnet S. Davis,Arvind Ramanathan,Akos A. Gerencser,Eric Verdin,Judith Campisi,Judith Campisi +13 more
TL;DR: It is shown that several manipulations that compromise mitochondrial function in proliferating human cells induce a senescence growth arrest with a modified SASP that lacks the IL-1-dependent inflammatory arm, providing a mechanism by which mitochondrial dysfunction can drive aging phenotypes.
Journal ArticleDOI
Perturbational profiling of a cell-line model of tumorigenesis by using metabolic measurements
TL;DR: Insight is gained into the relationship between two models of carcinogenesis, one (the Warburg hypothesis) based on increased energy production by glycolysis in cancer cells in response to aberrant respiration, and one based on cancer-causing genes, rather than being opposing models.
Journal ArticleDOI
Direct control of mitochondrial function by mTOR
TL;DR: Inhibiting the FKBP12/rapamycin-sensitive subset of mTOR functions in leukemic cells enhanced aerobic glycolysis and decreased uncoupled mitochondrial respiration within 25 min, as shown by the synergy between the glycoleytic inhibitor 2-deoxyglucose and rapamycin in decreasing cell viability.
Journal ArticleDOI
Metabolite profiling of blood from individuals undergoing planned myocardial infarction reveals early markers of myocardial injury
Gregory D. Lewis,Ru Wei,Emerson Liu,Elaine Yang,Xu Shi,Maryann E. Martinovic,Laurie A. Farrell,Aarti Asnani,Marcoli Cyrille,Arvind Ramanathan,Oded Shaham,Gabriel F. Berriz,Patricia A. Lowry,Igor F. Palacios,Murat Tasan,Frederick P. Roth,Jiangyong Min,Christian Baumgartner,Hasmik Keshishian,Terri Addona,Vamsi K. Mootha,Anthony Rosenzweig,Steven A. Carr,Michael A. Fifer,Marc S. Sabatine,Robert E. Gerszten +25 more
TL;DR: A role for metabolic profiling is identified in the early detection of myocardial injury and it is suggested that similar approaches may be used for detection or prediction of other disease states.