Fundamentals of cancer metabolism

Science Advances, Journal Year: 2016, Volume and Issue: 2(5)

Published: May 6, 2016

Researchers provide a conceptual framework to understand current knowledge of the fundamentals cancer metabolism.

Language: Английский

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Cellular Fatty Acid Metabolism and Cancer

Cell Metabolism, Journal Year: 2013, Volume and Issue: 18(2), P. 153 - 161

Published: June 20, 2013

Language: Английский

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Drugging the undruggable RAS: Mission Possible?

Nature Reviews Drug Discovery, Journal Year: 2014, Volume and Issue: 13(11), P. 828 - 851

Published: Oct. 17, 2014

Language: Английский

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Defective fatty acid oxidation in renal tubular epithelial cells has a key role in kidney fibrosis development

Nature Medicine, Journal Year: 2014, Volume and Issue: 21(1), P. 37 - 46

Published: Nov. 24, 2014

Language: Английский

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Fueling Immunity: Insights into Metabolism and Lymphocyte Function

Science, Journal Year: 2013, Volume and Issue: 342(6155)

Published: Oct. 10, 2013

Lymphocytes face major metabolic challenges upon activation. They must meet the bioenergetic and biosynthetic demands of increased cell proliferation also adapt to changing environmental conditions, in which nutrients oxygen may be limiting. An emerging theme immunology is that reprogramming lymphocyte activation are intricately linked. However, why T cells adopt specific programs impact these have on function and, ultimately, immunological outcome remain unclear. Research tumor metabolism has provided valuable insight into pathways important for influence metabolites themselves signal transduction epigenetic programming. In this Review, we highlight concepts regarding proliferating discuss their potential fate function.

Language: Английский

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Predicting Network Activity from High Throughput Metabolomics

PLoS Computational Biology, Journal Year: 2013, Volume and Issue: 9(7), P. e1003123 - e1003123

Published: July 4, 2013

The functional interpretation of high throughput metabolomics by mass spectrometry is hindered the identification metabolites, a tedious and challenging task. We present set computational algorithms which, leveraging collective power metabolic pathways networks, predict activity directly from spectral feature tables without priori metabolites. were experimentally validated on activation innate immune cells.

Language: Английский

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Molecular mechanisms of diabetic kidney disease

Journal of Clinical Investigation, Journal Year: 2014, Volume and Issue: 124(6), P. 2333 - 2340

Published: June 2, 2014

Diabetic kidney disease (DKD) is the leading cause of failure worldwide and single strongest predictor mortality in patients with diabetes. DKD a prototypical gene environmental interactions. Tight glucose control significantly decreases incidence, indicating that hyperglycemia-induced metabolic alterations, including changes energy utilization mitochondrial dysfunction, play critical roles initiation. Blood pressure control, especially medications inhibit angiotensin system, only effective way to slow progression. While considered microvascular complication diabetes, growing evidence indicates podocyte loss epithelial dysfunction important roles. Inflammation, cell hypertrophy, dedifferentiation by activation classic pathways regeneration further contribute Concerted clinical basic research efforts will be needed understand pathogenesis identify novel drug targets.

Language: Английский

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Toward Merging Untargeted and Targeted Methods in Mass Spectrometry-Based Metabolomics and Lipidomics

Analytical Chemistry, Journal Year: 2015, Volume and Issue: 88(1), P. 524 - 545

Published: Dec. 4, 2015

ADVERTISEMENT RETURN TO ISSUEPREVReviewNEXTToward Merging Untargeted and Targeted Methods in Mass Spectrometry-Based Metabolomics LipidomicsTomas Cajka† Oliver Fiehn*†‡View Author Information† UC Davis Genome Center−Metabolomics, University of California Davis, 451 Health Sciences Drive, 95616, United States‡ King Abdulaziz University, Faculty Science, Biochemistry Department, P.O. Box 80203, Jeddah 21589, Saudi Arabia*Phone: +1-530-754-8258. Fax: +1-530-754-9658. E-mail: [email protected]Cite this: Anal. Chem. 2016, 88, 1, 524–545Publication Date (Web):December 4, 2015Publication History Published online16 December 2015Published inissue 5 January 2016https://pubs.acs.org/doi/10.1021/acs.analchem.5b04491https://doi.org/10.1021/acs.analchem.5b04491review-articleACS PublicationsCopyright © 2015 American Chemical SocietyRequest reuse permissionsArticle Views20448Altmetric-Citations571LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum full text article downloads since November 2008 (both PDF HTML) across all institutions individuals. These metrics regularly updated to reflect usage leading up last few days.Citations number other articles citing this article, calculated by Crossref daily. Find more information about citation counts.The Altmetric Attention Score is a quantitative measure attention that research has received online. Clicking on donut icon will load page at altmetric.com with additional details score social media presence for given article. how calculated. Share Add toView InAdd Full Text ReferenceAdd Description ExportRISCitationCitation abstractCitation referencesMore Options onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose SUBJECTS:Ions,Lipidomics,Lipids,Metabolism,Metabolomics Get e-Alerts

Language: Английский

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A roadmap for interpreting 13 C metabolite labeling patterns from cells

Current Opinion in Biotechnology, Journal Year: 2015, Volume and Issue: 34, P. 189 - 201

Published: Feb. 28, 2015

Language: Английский

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Metabolic reprogramming during neuronal differentiation from aerobic glycolysis to neuronal oxidative phosphorylation

eLife, Journal Year: 2016, Volume and Issue: 5

Published: June 10, 2016

How metabolism is reprogrammed during neuronal differentiation unknown. We found that the loss of hexokinase (HK2) and lactate dehydrogenase (LDHA) expression, together with a switch in pyruvate kinase gene splicing from PKM2 to PKM1, marks transition aerobic glycolysis neural progenitor cells (NPC) oxidative phosphorylation. The protein levels c-MYC N-MYC, transcriptional activators HK2 LDHA genes, decrease dramatically. Constitutive expression leads cell death, indicating shut-off essential for survival. metabolic regulators PGC-1α ERRγ increase significantly upon sustain transcription mitochondrial whose are unchanged compared NPCs, revealing distinct regulation genes proliferation post-mitotic states. Mitochondrial mass increases proportionally growth, an unknown mechanism linking biogenesis size.

Language: Английский

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