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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1999-03-05
    Description: Long interspersed nuclear elements (LINE-1s or L1s) are the most abundant retrotransposons in the human genome, and they serve as major sources of reverse transcriptase activity. Engineered L1s retrotranspose at high frequency in cultured human cells. Here it is shown that L1s insert into transcribed genes and retrotranspose sequences derived from their 3' flanks to new genomic locations. Thus, retrotransposition-competent L1s provide a vehicle to mobilize non-L1 sequences, such as exons or promoters, into existing genes and may represent a general mechanism for the evolution of new genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moran, J V -- DeBerardinis, R J -- Kazazian, H H Jr -- GM45398/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1999 Mar 5;283(5407):1530-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA, 19104-6145 USA. moranj@umich.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10066175" target="_blank"〉PubMed〈/a〉
    Keywords: Codon, Initiator ; Exons/*genetics ; Expressed Sequence Tags ; Gene Expression ; *Genome, Human ; Gentamicins/pharmacology ; HeLa Cells ; Humans ; Introns ; Long Interspersed Nucleotide Elements/*genetics ; Poly A/metabolism ; Promoter Regions, Genetic ; *Recombination, Genetic ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 2013-05-04
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4324171/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4324171/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jiyeon -- DeBerardinis, Ralph J -- R01 CA157996/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2013 May 3;340(6132):558-9. doi: 10.1126/science.1238523.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23641103" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzeneacetamides/*pharmacology ; *Cell Differentiation ; Cell Transformation, Neoplastic/*metabolism ; Enzyme Inhibitors/*pharmacology ; Glioma/*enzymology/*pathology ; Glutarates/*metabolism ; Hematopoiesis/*drug effects ; Humans ; Imidazoles/*pharmacology ; Isocitrate Dehydrogenase/antagonists & inhibitors/genetics/*metabolism ; Leukemia/*enzymology ; Leukemia, Myeloid, Acute/*enzymology ; Phenylurea Compounds/*pharmacology ; Procollagen-Proline Dioxygenase/*antagonists & inhibitors ; Sulfonamides/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2011-11-22
    Description: Mitochondrial metabolism provides precursors to build macromolecules in growing cancer cells. In normally functioning tumour cell mitochondria, oxidative metabolism of glucose- and glutamine-derived carbon produces citrate and acetyl-coenzyme A for lipid synthesis, which is required for tumorigenesis. Yet some tumours harbour mutations in the citric acid cycle (CAC) or electron transport chain (ETC) that disable normal oxidative mitochondrial function, and it is unknown how cells from such tumours generate precursors for macromolecular synthesis. Here we show that tumour cells with defective mitochondria use glutamine-dependent reductive carboxylation rather than oxidative metabolism as the major pathway of citrate formation. This pathway uses mitochondrial and cytosolic isoforms of NADP(+)/NADPH-dependent isocitrate dehydrogenase, and subsequent metabolism of glutamine-derived citrate provides both the acetyl-coenzyme A for lipid synthesis and the four-carbon intermediates needed to produce the remaining CAC metabolites and related macromolecular precursors. This reductive, glutamine-dependent pathway is the dominant mode of metabolism in rapidly growing malignant cells containing mutations in complex I or complex III of the ETC, in patient-derived renal carcinoma cells with mutations in fumarate hydratase, and in cells with normal mitochondria subjected to acute pharmacological ETC inhibition. Our findings reveal the novel induction of a versatile glutamine-dependent pathway that reverses many of the reactions of the canonical CAC, supports tumour cell growth, and explains how cells generate pools of CAC intermediates in the face of impaired mitochondrial metabolism.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3262117/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3262117/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mullen, Andrew R -- Wheaton, William W -- Jin, Eunsook S -- Chen, Pei-Hsuan -- Sullivan, Lucas B -- Cheng, Tzuling -- Yang, Youfeng -- Linehan, W Marston -- Chandel, Navdeep S -- DeBerardinis, Ralph J -- 5T32GM083831/GM/NIGMS NIH HHS/ -- DK078933/DK/NIDDK NIH HHS/ -- K01 DK078933/DK/NIDDK NIH HHS/ -- K01 DK078933-03/DK/NIDDK NIH HHS/ -- K08 DK072565/DK/NIDDK NIH HHS/ -- K08 DK072565-06/DK/NIDDK NIH HHS/ -- K08DK072565/DK/NIDDK NIH HHS/ -- P41 RR002584/RR/NCRR NIH HHS/ -- P41 RR002584-22/RR/NCRR NIH HHS/ -- R01 CA123067/CA/NCI NIH HHS/ -- R01 CA123067-05/CA/NCI NIH HHS/ -- R01 CA157996/CA/NCI NIH HHS/ -- R01 CA157996-01/CA/NCI NIH HHS/ -- R01CA123067/CA/NCI NIH HHS/ -- R01CA157996/CA/NCI NIH HHS/ -- RR02584/RR/NCRR NIH HHS/ -- T32 CA009560/CA/NCI NIH HHS/ -- T32 CA009560-20/CA/NCI NIH HHS/ -- T32 GM008061/GM/NIGMS NIH HHS/ -- T32 GM008061-30/GM/NIGMS NIH HHS/ -- T32 GM083831/GM/NIGMS NIH HHS/ -- T32 GM083831-04/GM/NIGMS NIH HHS/ -- T32CA009560/CA/NCI NIH HHS/ -- T32GM008061/GM/NIGMS NIH HHS/ -- Intramural NIH HHS/ -- England -- Nature. 2011 Nov 20;481(7381):385-8. doi: 10.1038/nature10642.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, University of Texas - Southwestern Medical Center at Dallas, Dallas, Texas 75390-9063, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22101431" target="_blank"〉PubMed〈/a〉
    Keywords: Acetyl Coenzyme A/metabolism ; Animals ; Carcinoma, Renal Cell/genetics/metabolism/pathology ; Cell Hypoxia ; Cell Line, Tumor ; Citric Acid/metabolism ; Electron Transport ; Electron Transport Complex I/metabolism ; Electron Transport Complex III/metabolism ; Fumarate Hydratase/genetics/metabolism ; Glucose/metabolism ; Glutamine/metabolism ; Humans ; Isocitrate Dehydrogenase/metabolism ; Kidney Neoplasms/genetics/metabolism/pathology ; Mice ; Mitochondria/*metabolism/*pathology ; NADP/metabolism ; Neoplasms/*metabolism/*pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2011-08-19
    Description: Fumarate hydratase (FH) is an enzyme of the tricarboxylic acid cycle (TCA cycle) that catalyses the hydration of fumarate into malate. Germline mutations of FH are responsible for hereditary leiomyomatosis and renal-cell cancer (HLRCC). It has previously been demonstrated that the absence of FH leads to the accumulation of fumarate, which activates hypoxia-inducible factors (HIFs) at normal oxygen tensions. However, so far no mechanism that explains the ability of cells to survive without a functional TCA cycle has been provided. Here we use newly characterized genetically modified kidney mouse cells in which Fh1 has been deleted, and apply a newly developed computer model of the metabolism of these cells to predict and experimentally validate a linear metabolic pathway beginning with glutamine uptake and ending with bilirubin excretion from Fh1-deficient cells. This pathway, which involves the biosynthesis and degradation of haem, enables Fh1-deficient cells to use the accumulated TCA cycle metabolites and permits partial mitochondrial NADH production. We predicted and confirmed that targeting this pathway would render Fh1-deficient cells non-viable, while sparing wild-type Fh1-containing cells. This work goes beyond identifying a metabolic pathway that is induced in Fh1-deficient cells to demonstrate that inhibition of haem oxygenation is synthetically lethal when combined with Fh1 deficiency, providing a new potential target for treating HLRCC patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frezza, Christian -- Zheng, Liang -- Folger, Ori -- Rajagopalan, Kartik N -- MacKenzie, Elaine D -- Jerby, Livnat -- Micaroni, Massimo -- Chaneton, Barbara -- Adam, Julie -- Hedley, Ann -- Kalna, Gabriela -- Tomlinson, Ian P M -- Pollard, Patrick J -- Watson, Dave G -- Deberardinis, Ralph J -- Shlomi, Tomer -- Ruppin, Eytan -- Gottlieb, Eyal -- 090532/Wellcome Trust/United Kingdom -- DK072565-05/DK/NIDDK NIH HHS/ -- WT091112MA/Wellcome Trust/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2011 Aug 17;477(7363):225-8. doi: 10.1038/nature10363.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Research UK, Beatson Institute for Cancer Research, Switchback Road, Glasgow G61 1BD, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21849978" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bilirubin/metabolism ; Cell Line ; Cells, Cultured ; Citric Acid Cycle ; Computer Simulation ; Fumarate Hydratase/deficiency/*genetics/*metabolism ; Fumarates/metabolism ; Genes, Lethal/*genetics ; *Genes, Tumor Suppressor ; Glutamine/metabolism ; Heme/metabolism ; Heme Oxygenase (Decyclizing)/antagonists & inhibitors/*genetics/*metabolism ; Kidney Neoplasms/drug therapy/enzymology/genetics/metabolism ; Leiomyomatosis/congenital/drug therapy/enzymology/genetics/metabolism ; Mice ; Mitochondria/metabolism ; Mutation/*genetics ; NAD/metabolism ; Neoplastic Syndromes, Hereditary ; Skin Neoplasms ; Uterine Neoplasms
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2012-09-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, Lei -- Deberardinis, Ralph J -- England -- Nature. 2012 Sep 27;489(7417):511-2. doi: 10.1038/489511a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23018962" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Cell Division/drug effects ; Disease Progression ; Enzyme Activation/drug effects ; Glucose/*metabolism ; *Glycolysis/drug effects ; Isoenzymes/antagonists & inhibitors/metabolism ; Models, Biological ; Neoplasms/drug therapy/enzymology/*metabolism/*pathology ; Pyruvate Kinase/antagonists & inhibitors/classification/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2015-10-16
    Description: Solid cancer cells commonly enter the blood and disseminate systemically, but are highly inefficient at forming distant metastases for poorly understood reasons. Here we studied human melanomas that differed in their metastasis histories in patients and in their capacity to metastasize in NOD-SCID-Il2rg(-/-) (NSG) mice. We show that melanomas had high frequencies of cells that formed subcutaneous tumours, but much lower percentages of cells that formed tumours after intravenous or intrasplenic transplantation, particularly among inefficiently metastasizing melanomas. Melanoma cells in the blood and visceral organs experienced oxidative stress not observed in established subcutaneous tumours. Successfully metastasizing melanomas underwent reversible metabolic changes during metastasis that increased their capacity to withstand oxidative stress, including increased dependence on NADPH-generating enzymes in the folate pathway. Antioxidants promoted distant metastasis in NSG mice. Folate pathway inhibition using low-dose methotrexate, ALDH1L2 knockdown, or MTHFD1 knockdown inhibited distant metastasis without significantly affecting the growth of subcutaneous tumours in the same mice. Oxidative stress thus limits distant metastasis by melanoma cells in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4644103/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4644103/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Piskounova, Elena -- Agathocleous, Michalis -- Murphy, Malea M -- Hu, Zeping -- Huddlestun, Sara E -- Zhao, Zhiyu -- Leitch, A Marilyn -- Johnson, Timothy M -- DeBerardinis, Ralph J -- Morrison, Sean J -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 Nov 12;527(7577):186-91. doi: 10.1038/nature15726. Epub 2015 Oct 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Research Institute and the Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Department of Surgery, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Department of Dermatology, University of Michigan, Ann Arbor, Michigan 48109-2216, USA. ; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26466563" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antioxidants/metabolism ; Female ; Folic Acid/metabolism ; Gene Knockdown Techniques ; Humans ; Male ; Melanoma/blood/*metabolism/*pathology ; Methotrexate/pharmacology ; Methylenetetrahydrofolate Dehydrogenase (NADP)/deficiency/metabolism ; Mice ; Mice, Inbred NOD ; Mice, SCID ; NADP/metabolism ; Neoplasm Metastasis/*prevention & control ; Neoplasm Transplantation ; *Oxidative Stress ; Oxidoreductases Acting on CH-NH Group Donors/deficiency/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2014-12-20
    Description: Multivalent molecules with repetitive structures including bacterial capsular polysaccharides and viral capsids elicit antibody responses through B cell receptor (BCR) crosslinking in the absence of T cell help. We report that immunization with these T cell-independent type 2 (TI-2) antigens causes up-regulation of endogenous retrovirus (ERV) RNAs in antigen-specific mouse B cells. These RNAs are detected via a mitochondrial antiviral signaling protein (MAVS)-dependent RNA sensing pathway or reverse-transcribed and detected via the cGAS-cGAMP-STING pathway, triggering a second, sustained wave of signaling that promotes specific immunoglobulin M production. Deficiency of both MAVS and cGAS, or treatment of MAVS-deficient mice with reverse transcriptase inhibitors, dramatically inhibits TI-2 antibody responses. These findings suggest that ERV and two innate sensing pathways that detect them are integral components of the TI-2 B cell signaling apparatus.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391621/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4391621/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zeng, Ming -- Hu, Zeping -- Shi, Xiaolei -- Li, Xiaohong -- Zhan, Xiaoming -- Li, Xiao-Dong -- Wang, Jianhui -- Choi, Jin Huk -- Wang, Kuan-wen -- Purrington, Tiana -- Tang, Miao -- Fina, Maggy -- DeBerardinis, Ralph J -- Moresco, Eva Marie Y -- Pedersen, Gabriel -- McInerney, Gerald M -- Karlsson Hedestam, Gunilla B -- Chen, Zhijian J -- Beutler, Bruce -- P01 AI070167/AI/NIAID NIH HHS/ -- R01 AI093967/AI/NIAID NIH HHS/ -- R01 CA157996/CA/NCI NIH HHS/ -- U19 AI100627/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Dec 19;346(6216):1486-92. doi: 10.1126/science.346.6216.1486.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Genetics of Host Defense, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8502, USA. ; Department of Pediatrics and Children's Medical Center Research Institute, and McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8502, USA. ; Center for the Genetics of Host Defense, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8502, USA. Howard Hughes Medical Institute, Department of Molecular Biology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9148, USA. ; Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Nobels vag 16, SE-171 77 Stockholm, Sweden. ; Center for the Genetics of Host Defense, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8502, USA. Bruce.Beutler@UTSouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25525240" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/genetics/*immunology ; Animals ; Antibody Formation ; Antigens, T-Independent/*immunology ; B-Lymphocytes/*immunology ; Cytosol/immunology ; DNA/immunology ; Endogenous Retroviruses/genetics/*immunology ; Lymphocyte Activation ; Membrane Proteins/immunology ; Mice ; Mice, Inbred C57BL ; NF-kappa B/metabolism ; Nucleotides, Cyclic/immunology ; Nucleotidyltransferases/genetics/*immunology ; RNA, Viral/genetics/*immunology ; Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2016-04-07
    Description: Cells receive growth and survival stimuli through their attachment to an extracellular matrix (ECM). Overcoming the addiction to ECM-induced signals is required for anchorage-independent growth, a property of most malignant cells. Detachment from ECM is associated with enhanced production of reactive oxygen species (ROS) owing to altered glucose metabolism. Here we identify an unconventional pathway that supports redox homeostasis and growth during adaptation to anchorage independence. We observed that detachment from monolayer culture and growth as anchorage-independent tumour spheroids was accompanied by changes in both glucose and glutamine metabolism. Specifically, oxidation of both nutrients was suppressed in spheroids, whereas reductive formation of citrate from glutamine was enhanced. Reductive glutamine metabolism was highly dependent on cytosolic isocitrate dehydrogenase-1 (IDH1), because the activity was suppressed in cells homozygous null for IDH1 or treated with an IDH1 inhibitor. This activity occurred in absence of hypoxia, a well-known inducer of reductive metabolism. Rather, IDH1 mitigated mitochondrial ROS in spheroids, and suppressing IDH1 reduced spheroid growth through a mechanism requiring mitochondrial ROS. Isotope tracing revealed that in spheroids, isocitrate/citrate produced reductively in the cytosol could enter the mitochondria and participate in oxidative metabolism, including oxidation by IDH2. This generates NADPH in the mitochondria, enabling cells to mitigate mitochondrial ROS and maximize growth. Neither IDH1 nor IDH2 was necessary for monolayer growth, but deleting either one enhanced mitochondrial ROS and reduced spheroid size, as did deletion of the mitochondrial citrate transporter protein. Together, the data indicate that adaptation to anchorage independence requires a fundamental change in citrate metabolism, initiated by IDH1-dependent reductive carboxylation and culminating in suppression of mitochondrial ROS.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860952/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860952/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jiang, Lei -- Shestov, Alexander A -- Swain, Pamela -- Yang, Chendong -- Parker, Seth J -- Wang, Qiong A -- Terada, Lance S -- Adams, Nicholas D -- McCabe, Michael T -- Pietrak, Beth -- Schmidt, Stan -- Metallo, Christian M -- Dranka, Brian P -- Schwartz, Benjamin -- DeBerardinis, Ralph J -- R01 CA157996/CA/NCI NIH HHS/ -- R01 CA188652/CA/NCI NIH HHS/ -- R01CA157996/CA/NCI NIH HHS/ -- R01CA188652/CA/NCI NIH HHS/ -- England -- Nature. 2016 Apr 14;532(7598):255-8. doi: 10.1038/nature17393. Epub 2016 Apr 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Medical Center Research Institute, UT Southwestern Medical Center, Dallas, Texas 75390-8502, USA. ; Department of Radiology, University of Pennsylvania School of Medicine, 3620 Hamilton Walk, Philadelphia, Pennsylvania 19104, USA. ; Seahorse Bioscience, 16 Esquire Road, North Billerica, Massachusetts 01862, USA. ; Department of Bioengineering, University of California, San Diego, La Jolla, California 92093, USA. ; Touchstone Diabetes Center, UT Southwestern Medical Center, Dallas, Texas 75390, USA. ; Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas 75390, USA. ; GlaxoSmithKline, 1250 South Collegeville Road, Collegeville, Pennsylvania 19426, USA. ; Department of Pediatrics, UT Southwestern Medical Center, Dallas, Texas 75390, USA. ; McDermott Center for Human Growth and Development, UT Southwestern Medical Center, Dallas, Texas 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27049945" target="_blank"〉PubMed〈/a〉
    Keywords: Cell Adhesion ; Cell Hypoxia ; Cell Line, Tumor ; Cell Proliferation ; Citric Acid/*metabolism ; Contact Inhibition ; Cytosol/enzymology/metabolism ; Extracellular Matrix/metabolism ; Glucose/metabolism ; Glutamic Acid/metabolism ; Glutamine/metabolism ; *Homeostasis ; Humans ; Isocitrate Dehydrogenase/antagonists & inhibitors/deficiency/genetics/*metabolism ; Isocitrates/metabolism ; Mitochondria/*metabolism ; NADP/biosynthesis ; Neoplasms/enzymology/*metabolism/*pathology ; Oxidation-Reduction ; Oxidative Stress ; Reactive Oxygen Species/*metabolism ; Spheroids, Cellular/metabolism/pathology
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2015-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egnatchik, Robert A -- DeBerardinis, Ralph J -- England -- Nature. 2015 Apr 9;520(7546):165-6. doi: 10.1038/nature14375. Epub 2015 Apr 1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Medical Center Research Institute, UT Southwestern Medical Center, Dallas, Texas 75390-8502, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25830890" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon/*metabolism ; Endothelial Cells/*metabolism ; Fatty Acids/*chemistry/*metabolism ; Humans ; Nucleotides/*biosynthesis
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2011-05-09
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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