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1. Acidic Methanol Treatment Facilitates Matrix-Assisted Laser Desorption Ionization-Mass Spectrometry Imaging of Energy Metabolism.

Author

Jankowski, Connor, Samarah, Laith, McReynolds, Melanie, Xing, Xi, Schembri, Jessica, Woolf, Morgan, Rabinowitz, Joshua, Davidson, Shawn, Lu, Wenyun, Park, Noel, and Teslaa, Tara

Subjects
Mice, Animals, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization, Methanol, Glycolysis, Glucose, Lipids, Solvents, Isotopes, Phosphates, Lasers
Abstract

Detection of small molecule metabolites (SMM), particularly those involved in energy metabolism using MALDI-mass spectrometry imaging (MSI), is challenging due to factors including ion suppression from other analytes present (e.g., proteins and lipids). One potential solution to enhance SMM detection is to remove analytes that cause ion suppression from tissue sections before matrix deposition through solvent washes. Here, we systematically investigated solvent treatment conditions to improve SMM signal and preserve metabolite localization. Washing with acidic methanol significantly enhances the detection of phosphate-containing metabolites involved in energy metabolism. The improved detection is due to removing lipids and highly polar metabolites that cause ion suppression and denaturing proteins that release bound phosphate-containing metabolites. Stable isotope infusions of [13C6]nicotinamide coupled to MALDI-MSI (Iso-imaging) in the kidney reveal patterns that indicate blood vessels, medulla, outer stripe, and cortex. We also observed different ATP:ADP raw signals across mouse kidney regions, consistent with regional differences in glucose metabolism favoring either gluconeogenesis or glycolysis. In mouse muscle, Iso-imaging using [13C6]glucose shows high glycolytic flux from infused circulating glucose in type 1 and 2a fibers (soleus) and relatively lower glycolytic flux in type 2b fiber type (gastrocnemius). Thus, improved detection of phosphate-containing metabolites due to acidic methanol treatment combined with isotope tracing provides an improved way to probe energy metabolism with spatial resolution in vivo.

Published
2023

2. Multi-omic analysis of Huntington’s disease reveals a compensatory astrocyte state

Author

Paryani, Fahad, Kwon, Ji-Sun, Ng, Christopher W., Jakubiak, Kelly, Madden, Nacoya, Ofori, Kenneth, Tang, Alice, Lu, Hong, Xia, Shengnan, Li, Juncheng, Mahajan, Aayushi, Davidson, Shawn M., Basile, Anna O., McHugh, Caitlin, Vonsattel, Jean Paul, Hickman, Richard, Zody, Michael C., Housman, David E., Goldman, James E., Yoo, Andrew S., Menon, Vilas, and Al-Dalahmah, Osama

Published
2024
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3. Developmental basis of SHH medulloblastoma heterogeneity

Author

Gold, Maxwell P., Ong, Winnie, Masteller, Andrew M., Ghasemi, David R., Galindo, Julie Anne, Park, Noel R., Huynh, Nhan C., Donde, Aneesh, Pister, Veronika, Saurez, Raul A., Vladoiu, Maria C., Hwang, Grace H., Eisemann, Tanja, Donovan, Laura K., Walker, Adam D., Benetatos, Joseph, Dufour, Christelle, Garzia, Livia, Segal, Rosalind A., Wechsler-Reya, Robert J., Mesirov, Jill P., Korshunov, Andrey, Pajtler, Kristian W., Pomeroy, Scott L., Ayrault, Olivier, Davidson, Shawn M., Cotter, Jennifer A., Taylor, Michael D., and Fraenkel, Ernest

Published
2024
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4. Slow TCA flux and ATP production in primary solid tumours but not metastases

Author

Bartman, Caroline R, Weilandt, Daniel R, Shen, Yihui, Lee, Won Dong, Han, Yujiao, TeSlaa, Tara, Jankowski, Connor SR, Samarah, Laith, Park, Noel R, da Silva-Diz, Victoria, Aleksandrova, Maya, Gultekin, Yetis, Marishta, Argit, Wang, Lin, Yang, Lifeng, Roichman, Asael, Bhatt, Vrushank, Lan, Taijin, Hu, Zhixian, Xing, Xi, Lu, Wenyun, Davidson, Shawn, Wühr, Martin, Vander Heiden, Matthew G, Herranz, Daniel, Guo, Jessie Yanxiang, Kang, Yibin, and Rabinowitz, Joshua D

Subjects
Cancer, Animals, Mice, Adenosine Triphosphate, Breast Neoplasms, Citric Acid Cycle, Deceleration, Energy Metabolism, Glycolysis, Lung Neoplasms, Neoplasm Metastasis, Organ Specificity, Pancreatic Neoplasms, Protein Biosynthesis, General Science & Technology
Abstract

Tissues derive ATP from two pathways-glycolysis and the tricarboxylic acid (TCA) cycle coupled to the electron transport chain. Most energy in mammals is produced via TCA metabolism1. In tumours, however, the absolute rates of these pathways remain unclear. Here we optimize tracer infusion approaches to measure the rates of glycolysis and the TCA cycle in healthy mouse tissues, Kras-mutant solid tumours, metastases and leukaemia. Then, given the rates of these two pathways, we calculate total ATP synthesis rates. We find that TCA cycle flux is suppressed in all five primary solid tumour models examined and is increased in lung metastases of breast cancer relative to primary orthotopic tumours. As expected, glycolysis flux is increased in tumours compared with healthy tissues (the Warburg effect2,3), but this increase is insufficient to compensate for low TCA flux in terms of ATP production. Thus, instead of being hypermetabolic, as commonly assumed, solid tumours generally produce ATP at a slower than normal rate. In mouse pancreatic cancer, this is accommodated by the downregulation of protein synthesis, one of this tissue's major energy costs. We propose that, as solid tumours develop, cancer cells shed energetically expensive tissue-specific functions, enabling uncontrolled growth despite a limited ability to produce ATP.

Published
2023

5. Autophagy in PDGFRα+ mesenchymal cells is essential for intestinal stem cell survival

Author

Yang, Yang, Gomez, Maria, Marsh, Timothy, Poillet-Perez, Laura, Sawant, Akshada, Chen, Lei, Park, Noel R, Jackson, S RaElle, Hu, Zhixian, Alon, Noa, Liu, Chen, Debnath, Jayanta, Guan, Jun-Lin, Davidson, Shawn, Verzi, Michael, and White, Eileen

Subjects
Biochemistry and Cell Biology, Chemical Sciences, Biological Sciences, Stem Cell Research, Digestive Diseases, Regenerative Medicine, Stem Cell Research - Nonembryonic - Non-Human, 2.1 Biological and endogenous factors, Aetiology, Generic health relevance, Animals, Autophagy, Autophagy-Related Protein 5, Autophagy-Related Protein 7, Autophagy-Related Proteins, Cell Survival, Intestines, Mice, Receptor, Platelet-Derived Growth Factor alpha, Stem Cells, autophagy, intestine, stem cells, IBD, metabolism
Abstract

Autophagy defects are a risk factor for inflammatory bowel diseases (IBDs) through unknown mechanisms. Whole-body conditional deletion of autophagy-related gene (Atg) Atg7 in adult mice (Atg7Δ/Δ) causes tissue damage and death within 3 mo due to neurodegeneration without substantial effect on intestine. In contrast, we report here that whole-body conditional deletion of other essential Atg genes Atg5 or Fip200/Atg17 in adult mice (Atg5Δ/Δ or Fip200Δ/Δ) caused death within 5 d due to rapid autophagy inhibition, elimination of ileum stem cells, and loss of barrier function. Atg5Δ/Δ mice lost PDGFRα+ mesenchymal cells (PMCs) and Wnt signaling essential for stem cell renewal, which were partially rescued by exogenous Wnt. Matrix-assisted laser desorption ionization coupled to mass spectrometry imaging (MALDI-MSI) of Atg5Δ/Δ ileum revealed depletion of aspartate and nucleotides, consistent with metabolic insufficiency underlying PMC loss. The difference in the autophagy gene knockout phenotypes is likely due to distinct kinetics of autophagy loss, as deletion of Atg5 more gradually extended lifespan phenocopying deletion of Atg7 or Atg12. Thus, autophagy is required for PMC metabolism and ileum stem cell and mammalian survival. Failure to maintain PMCs through autophagy may therefore contribute to IBD.

Published
2022

6. Huntington disease oligodendrocyte maturation deficits revealed by single-nucleus RNAseq are rescued by thiamine-biotin supplementation

Author

Lim, Ryan G, Al-Dalahmah, Osama, Wu, Jie, Gold, Maxwell P, Reidling, Jack C, Tang, Guomei, Adam, Miriam, Dansu, David K, Park, Hye-Jin, Casaccia, Patrizia, Miramontes, Ricardo, Reyes-Ortiz, Andrea M, Lau, Alice, Hickman, Richard A, Khan, Fatima, Paryani, Fahad, Tang, Alice, Ofori, Kenneth, Miyoshi, Emily, Michael, Neethu, McClure, Nicolette, Flowers, Xena E, Vonsattel, Jean Paul, Davidson, Shawn, Menon, Vilas, Swarup, Vivek, Fraenkel, Ernest, Goldman, James E, and Thompson, Leslie M

Subjects
Biological Sciences, Genetics, Rare Diseases, Brain Disorders, Neurodegenerative, Neurosciences, Stem Cell Research - Nonembryonic - Non-Human, Stem Cell Research, Huntington's Disease, 2.1 Biological and endogenous factors, Aetiology, Neurological, Animals, Humans, Mice, Biotin, Dietary Supplements, Disease Models, Animal, Huntington Disease, Mice, Transgenic, Nerve Tissue Proteins, Oligodendroglia, Solitary Nucleus, Thiamine
Abstract

The complexity of affected brain regions and cell types is a challenge for Huntington's disease (HD) treatment. Here we use single nucleus RNA sequencing to investigate molecular pathology in the cortex and striatum from R6/2 mice and human HD post-mortem tissue. We identify cell type-specific and -agnostic signatures suggesting oligodendrocytes (OLs) and oligodendrocyte precursors (OPCs) are arrested in intermediate maturation states. OL-lineage regulators OLIG1 and OLIG2 are negatively correlated with CAG length in human OPCs, and ATACseq analysis of HD mouse NeuN-negative cells shows decreased accessibility regulated by OL maturation genes. The data implicates glucose and lipid metabolism in abnormal cell maturation and identify PRKCE and Thiamine Pyrophosphokinase 1 (TPK1) as central genes. Thiamine/biotin treatment of R6/1 HD mice to compensate for TPK1 dysregulation restores OL maturation and rescues neuronal pathology. Our insights into HD OL pathology spans multiple brain regions and link OL maturation deficits to abnormal thiamine metabolism.

Published
2022

7. Convergent and complementary selection shaped gains and losses of eusociality in sweat bees

Author

Jones, Beryl M., Rubin, Benjamin E. R., Dudchenko, Olga, Kingwell, Callum J., Traniello, Ian M., Wang, Z. Yan, Kapheim, Karen M., Wyman, Eli S., Adastra, Per A., Liu, Weijie, Parsons, Lance R., Jackson, S. RaElle, Goodwin, Katharine, Davidson, Shawn M., McBride, Matthew J., Webb, Andrew E., Omufwoko, Kennedy S., Van Dorp, Nikki, Otárola, Mauricio Fernández, Pham, Melanie, Omer, Arina D., Weisz, David, Schraiber, Joshua, Villanea, Fernando, Wcislo, William T., Paxton, Robert J., Hunt, Brendan G., Aiden, Erez Lieberman, and Kocher, Sarah D.

Published
2023
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9. APOE4 impairs myelination via cholesterol dysregulation in oligodendrocytes

Author

Blanchard, Joel W., Akay, Leyla Anne, Davila-Velderrain, Jose, von Maydell, Djuna, Mathys, Hansruedi, Davidson, Shawn M., Effenberger, Audrey, Chen, Chih-Yu, Maner-Smith, Kristal, Hajjar, Ihab, Ortlund, Eric A., Bula, Michael, Agbas, Emre, Ng, Ayesha, Jiang, Xueqiao, Kahn, Martin, Blanco-Duque, Cristina, Lavoie, Nicolas, Liu, Liwang, Reyes, Ricardo, Lin, Yuan-Ta, Ko, Tak, R’Bibo, Lea, Ralvenius, William T., Bennett, David A., Cam, Hugh P., Kellis, Manolis, and Tsai, Li-Huei

Published
2022
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10. NAD precursors cycle between host tissues and the gut microbiome

Author

Chellappa, Karthikeyani, McReynolds, Melanie R., Lu, Wenyun, Zeng, Xianfeng, Makarov, Mikhail, Hayat, Faisal, Mukherjee, Sarmistha, Bhat, Yashaswini R., Lingala, Siddharth R., Shima, Rafaella T., Descamps, Hélène C., Cox, Timothy, Ji, Lixin, Jankowski, Connor, Chu, Qingwei, Davidson, Shawn M., Thaiss, Christoph A., Migaud, Marie E., Rabinowitz, Joshua D., and Baur, Joseph A.

Published
2022
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12. Single cell metabolism: current and future trends

Author

Ali, Ahmed, Davidson, Shawn, Fraenkel, Ernest, Gilmore, Ian, Hankemeier, Thomas, Kirwan, Jennifer A., Lane, Andrew N., Lanekoff, Ingela, Larion, Mioara, McCall, Laura-Isobel, Murphy, Michael, Sweedler, Jonathan V., and Zhu, Caigang

Published
2022
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14. Glutamine antagonist DRP-104 suppresses tumor growth and enhances response to checkpoint blockade in KEAP1 mutant lung cancer

Author

Pillai, Ray, primary, LeBoeuf, Sarah E., additional, Hao, Yuan, additional, New, Connie, additional, Blum, Jenna L. E., additional, Rashidfarrokhi, Ali, additional, Huang, Shih Ming, additional, Bahamon, Christian, additional, Wu, Warren L., additional, Karadal-Ferrena, Burcu, additional, Herrera, Alberto, additional, Ivanova, Ellie, additional, Cross, Michael, additional, Bossowski, Jozef P., additional, Ding, Hongyu, additional, Hayashi, Makiko, additional, Rajalingam, Sahith, additional, Karakousi, Triantafyllia, additional, Sayin, Volkan I., additional, Khanna, Kamal M., additional, Wong, Kwok-Kin, additional, Wild, Robert, additional, Tsirigos, Aristotelis, additional, Poirier, John T., additional, Rudin, Charles M., additional, Davidson, Shawn M., additional, Koralov, Sergei B., additional, and Papagiannakopoulos, Thales, additional

Published
2024
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15. Fatty acid synthesis is required for breast cancer brain metastasis

Author

Ferraro, Gino B., Ali, Ahmed, Luengo, Alba, Kodack, David P., Deik, Amy, Abbott, Keene L., Bezwada, Divya, Blanc, Landry, Prideaux, Brendan, Jin, Xin, Posada, Jessica M., Chen, Jiang, Chin, Christopher R., Amoozgar, Zohreh, Ferreira, Raphael, Chen, Ivy X., Naxerova, Kamila, Ng, Christopher, Westermark, Anna M., Duquette, Mark, Roberge, Sylvie, Lindeman, Neal I., Lyssiotis, Costas A., Nielsen, Jens, Housman, David E., Duda, Dan G., Brachtel, Elena, Golub, Todd R., Cantley, Lewis C., Asara, John M., Davidson, Shawn M., Fukumura, Dai, Dartois, Véronique A., Clish, Clary B., Jain, Rakesh K., and Vander Heiden, Matthew G.

Published
2021
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17. EGLN1 Inhibition and Rerouting of α-Ketoglutarate Suffice for Remote Ischemic Protection.

Author

Olenchock, Benjamin, Moslehi, Javid, Baik, Alan, Davidson, Shawn, Williams, Jeremy, Gibson, William, Chakraborty, Abhishek, Pierce, Kerry, Miller, Christine, Hanse, Eric, Kelekar, Ameeta, Sullivan, Lucas, Wagers, Amy, Clish, Clary, Vander Heiden, Matthew, and Kaelin, William

Subjects
Animals, Hypoxia-Inducible Factor-Proline Dioxygenases, Ischemia, Ischemic Preconditioning, Ketoglutaric Acids, Kynurenic Acid, Liver, Mice, Models, Animal, Myocardial Reperfusion Injury, Parabiosis
Abstract

Ischemic preconditioning is the phenomenon whereby brief periods of sublethal ischemia protect against a subsequent, more prolonged, ischemic insult. In remote ischemic preconditioning (RIPC), ischemia to one organ protects others organs at a distance. We created mouse models to ask if inhibition of the alpha-ketoglutarate (αKG)-dependent dioxygenase Egln1, which senses oxygen and regulates the hypoxia-inducible factor (HIF) transcription factor, could suffice to mediate local and remote ischemic preconditioning. Using somatic gene deletion and a pharmacological inhibitor, we found that inhibiting Egln1 systemically or in skeletal muscles protects mice against myocardial ischemia-reperfusion (I/R) injury. Parabiosis experiments confirmed that RIPC in this latter model was mediated by a secreted factor. Egln1 loss causes accumulation of circulating αKG, which drives hepatic production and secretion of kynurenic acid (KYNA) that is necessary and sufficient to mediate cardiac ischemic protection in this setting.

Published
2016

18. Deletion or Inhibition of the Oxygen Sensor PHD1 Protects against Ischemic Stroke via Reprogramming of Neuronal Metabolism

Author

Quaegebeur, Annelies, Segura, Inmaculada, Schmieder, Roberta, Verdegem, Dries, Decimo, Ilaria, Bifari, Francesco, Dresselaers, Tom, Eelen, Guy, Ghosh, Debapriva, Davidson, Shawn M, Schoors, Sandra, Broekaert, Dorien, Cruys, Bert, Govaerts, Kristof, De Legher, Carla, Bouché, Ann, Schoonjans, Luc, Ramer, Matt S, Hung, Gene, Bossaert, Goele, Cleveland, Don W, Himmelreich, Uwe, Voets, Thomas, Lemmens, Robin, Bennett, C Frank, Robberecht, Wim, De Bock, Katrien, Dewerchin, Mieke, Ghesquière, Bart, Fendt, Sarah-Maria, and Carmeliet, Peter

Subjects
Biochemistry and Cell Biology, Biological Sciences, Stroke, Neurosciences, Nutrition, Brain Disorders, 2.1 Biological and endogenous factors, Aetiology, Underpinning research, 1.1 Normal biological development and functioning, Neurological, Animals, Brain, Brain Ischemia, Carbon, Cellular Reprogramming, Free Radical Scavengers, Gene Deletion, Hydroxylation, Hypoxia-Inducible Factor 1, alpha Subunit, Injections, Intraventricular, Mice, Knockout, Neurons, Neuroprotection, Oligonucleotides, Oxidation-Reduction, Oxygen, Pentose Phosphate Pathway, Phenotype, Procollagen-Proline Dioxygenase, Reactive Oxygen Species, Medical Biochemistry and Metabolomics, Endocrinology & Metabolism, Biochemistry and cell biology, Medical biochemistry and metabolomics
Abstract

The oxygen-sensing prolyl hydroxylase domain proteins (PHDs) regulate cellular metabolism, but their role in neuronal metabolism during stroke is unknown. Here we report that PHD1 deficiency provides neuroprotection in a murine model of permanent brain ischemia. This was not due to an increased collateral vessel network. Instead, PHD1(-/-) neurons were protected against oxygen-nutrient deprivation by reprogramming glucose metabolism. Indeed, PHD1(-/-) neurons enhanced glucose flux through the oxidative pentose phosphate pathway by diverting glucose away from glycolysis. As a result, PHD1(-/-) neurons increased their redox buffering capacity to scavenge oxygen radicals in ischemia. Intracerebroventricular injection of PHD1-antisense oligonucleotides reduced the cerebral infarct size and neurological deficits following stroke. These data identify PHD1 as a regulator of neuronal metabolism and a potential therapeutic target in ischemic stroke.

Published
2016

19. Optofluidic real-time cell sorter for longitudinal CTC studies in mouse models of cancer

Author

Hamza, Bashar, Ng, Sheng Rong, Prakadan, Sanjay M., Delgado, Francisco Feijó, Chin, Christopher R., King, Emily M., Yang, Lucy F., Davidson, Shawn M., DeGouveia, Kelsey L., Cermak, Nathan, Navia, Andrew W., Winter, Peter S., Drake, Riley S., Tammela, Tuomas, Li, Carman Man-Chung, Papagiannakopoulos, Thales, Gupta, Alejandro J., Bagnall, Josephine Shaw, Knudsen, Scott M., Vander Heiden, Matthew G., Wasserman, Steven C., Jacks, Tyler, Shalek, Alex K., and Manalis, Scott R.

Published
2019

20. IDH1 mutations alter citric acid cycle metabolism and increase dependence on oxidative mitochondrial metabolism.

Author

Green, Courtney, Zhang, Xiamei, Slocum, Kelly, Pu, Minying, Lin, Fallon, Vickers, Chad, Joud-Caldwell, Carol, Chung, Franklin, Yin, Hong, Handly, Erika, Straub, Christopher, Growney, Joseph, Vander Heiden, Matthew, Murphy, Anne, Pagliarini, Raymond, Grassian, Alexandra, Parker, Seth, Davidson, Shawn, Metallo, Christian, and Divakaruni, Ajit

Subjects
Animals, Antineoplastic Agents, Cell Hypoxia, Citric Acid Cycle, Enzyme Inhibitors, Glutamine, HCT116 Cells, Humans, Isocitrate Dehydrogenase, Mice, Mitochondria, Mutation, Missense, Oxidation-Reduction, Stress, Physiological, Xenograft Model Antitumor Assays
Abstract

Oncogenic mutations in isocitrate dehydrogenase 1 and 2 (IDH1/2) occur in several types of cancer, but the metabolic consequences of these genetic changes are not fully understood. In this study, we performed (13)C metabolic flux analysis on a panel of isogenic cell lines containing heterozygous IDH1/2 mutations. We observed that under hypoxic conditions, IDH1-mutant cells exhibited increased oxidative tricarboxylic acid metabolism along with decreased reductive glutamine metabolism, but not IDH2-mutant cells. However, selective inhibition of mutant IDH1 enzyme function could not reverse the defect in reductive carboxylation activity. Furthermore, this metabolic reprogramming increased the sensitivity of IDH1-mutant cells to hypoxia or electron transport chain inhibition in vitro. Lastly, IDH1-mutant cells also grew poorly as subcutaneous xenografts within a hypoxic in vivo microenvironment. Together, our results suggest therapeutic opportunities to exploit the metabolic vulnerabilities specific to IDH1 mutation.

Published
2014

21. IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism

Author

Grassian, Alexandra R, Parker, Seth J, Davidson, Shawn M, Divakaruni, Ajit S, Green, Courtney R, Zhang, Xiamei, Slocum, Kelly L, Pu, Minying, Lin, Fallon, Vickers, Chad, Joud-Caldwell, Carol, Chung, Franklin, Yin, Hong, Handly, Erika D, Straub, Christopher, Growney, Joseph D, Heiden, Matthew G Vander, Murphy, Anne N, Pagliarini, Raymond, and Metallo, Christian M

Subjects
Cancer, Genetics, 2.1 Biological and endogenous factors, Aetiology, Animals, Antineoplastic Agents, Cell Hypoxia, Citric Acid Cycle, Enzyme Inhibitors, Glutamine, HCT116 Cells, Humans, Isocitrate Dehydrogenase, Mice, Mitochondria, Mutation, Missense, Oxidation-Reduction, Stress, Physiological, Xenograft Model Antitumor Assays, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Oncogenic mutations in isocitrate dehydrogenase 1 and 2 (IDH1/2) occur in several types of cancer, but the metabolic consequences of these genetic changes are not fully understood. In this study, we performed (13)C metabolic flux analysis on a panel of isogenic cell lines containing heterozygous IDH1/2 mutations. We observed that under hypoxic conditions, IDH1-mutant cells exhibited increased oxidative tricarboxylic acid metabolism along with decreased reductive glutamine metabolism, but not IDH2-mutant cells. However, selective inhibition of mutant IDH1 enzyme function could not reverse the defect in reductive carboxylation activity. Furthermore, this metabolic reprogramming increased the sensitivity of IDH1-mutant cells to hypoxia or electron transport chain inhibition in vitro. Lastly, IDH1-mutant cells also grew poorly as subcutaneous xenografts within a hypoxic in vivo microenvironment. Together, our results suggest therapeutic opportunities to exploit the metabolic vulnerabilities specific to IDH1 mutation.

Published
2014

22. PKM1 Exerts Critical Roles in Cardiac Remodeling Under Pressure Overload in the Heart

Author

Li, Qinfeng, Li, Chao, Elnwasany, Abdallah, Sharma, Gaurav, An, Yu A., Zhang, Guangyu, Elhelaly, Waleed M., Lin, Jun, Gong, Yingchao, Chen, Guihao, Wang, Meihui, Zhao, Shangang, Dai, Chongshan, Smart, Charles D., Liu, Juan, Luo, Xiang, Deng, Yingfeng, Tan, Lin, Lv, Shuang-Jie, Davidson, Shawn M., Locasale, Jason W., Lorenzi, Philip L., Malloy, Craig R., Gillette, Thomas G., Vander Heiden, Matthew G., Scherer, Philipp E., Szweda, Luke I., Fu, Guosheng, and Wang, Zhao V.

Published
2021
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23. Acidic Methanol Treatment Facilitates Matrix-Assisted Laser Desorption Ionization-Mass Spectrometry Imaging of Energy Metabolism

Author

Lu, Wenyun, primary, Park, Noel R., additional, TeSlaa, Tara, additional, Jankowski, Connor S.R., additional, Samarah, Laith, additional, McReynolds, Melanie, additional, Xing, Xi, additional, Schembri, Jessica, additional, Woolf, Morgan T., additional, Rabinowitz, Joshua D., additional, and Davidson, Shawn M., additional

Published
2023
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24. Multi-OMIC analysis of Huntington disease reveals a neuroprotective astrocyte state

Author

Paryani, Fahad, primary, Kwon, Ji-Sun, additional, Ng, Chris W, additional, Madden, Nacoya, additional, Ofori, Kenneth, additional, Tang, Alice, additional, Lu, Hong, additional, Li, Juncheng, additional, Mahajan, Aayushi, additional, Davidson, Shawn M., additional, Basile, Anna, additional, McHugh, Caitlin, additional, Vonsattel, Jean Paul, additional, Hickman, Richard, additional, Zody, Michael, additional, Houseman, David E., additional, Goldman, James E., additional, Yoo, Andrew E., additional, Menon, Vilas, additional, and Al-Dalahmah, Osama, additional

Published
2023
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25. Intratumoral drug-releasing microdevices allow in situ high-throughput pharmaco phenotyping in patients with gliomas

Author

Peruzzi, Pierpaolo, primary, Dominas, Christine, additional, Fell, Geoffrey, additional, Bernstock, Joshua D., additional, Blitz, Sarah, additional, Mazzetti, Debora, additional, Zdioruk, Mykola, additional, Dawood, Hassan Y., additional, Triggs, Daniel V., additional, Ahn, Sebastian W., additional, Bhagavatula, Sharath K., additional, Davidson, Shawn M., additional, Tatarova, Zuzana, additional, Pannell, Michael, additional, Truman, Kyla, additional, Ball, Anna, additional, Gold, Maxwell P., additional, Pister, Veronika, additional, Fraenkel, Ernest, additional, Chiocca, E. Antonio, additional, Ligon, Keith L., additional, Wen, Patrick Y., additional, and Jonas, Oliver, additional

Published
2023
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26. Pyruvate kinase M2 activators promote tetramer formation and suppress tumorigenesis

Author

Anastasiou, Dimitrios, Yu, Yimin, Israelsen, William J, Jiang, Jian-Kang, Boxer, Matthew B, Hong, Bum Soo, Tempel, Wolfram, Dimov, Svetoslav, Shen, Min, Jha, Abhishek, Yang, Hua, Mattaini, Katherine R, Metallo, Christian M, Fiske, Brian P, Courtney, Kevin D, Malstrom, Scott, Khan, Tahsin M, Kung, Charles, Skoumbourdis, Amanda P, Veith, Henrike, Southall, Noel, Walsh, Martin J, Brimacombe, Kyle R, Leister, William, Lunt, Sophia Y, Johnson, Zachary R, Yen, Katharine E, Kunii, Kaiko, Davidson, Shawn M, Christofk, Heather R, Austin, Christopher P, Inglese, James, Harris, Marian H, Asara, John M, Stephanopoulos, Gregory, Salituro, Francesco G, Jin, Shengfang, Dang, Lenny, Auld, Douglas S, Park, Hee-Won, Cantley, Lewis C, Thomas, Craig J, and Vander Heiden, Matthew G

Subjects
Biochemistry and Cell Biology, Biological Sciences, Cancer, Animals, Biopolymers, Blotting, Western, Cell Proliferation, Cell Transformation, Neoplastic, Enzyme Activators, Humans, Mice, Neoplasms, Pyruvate Kinase, Medicinal and Biomolecular Chemistry, Biochemistry & Molecular Biology, Biochemistry and cell biology, Medicinal and biomolecular chemistry
Abstract

Cancer cells engage in a metabolic program to enhance biosynthesis and support cell proliferation. The regulatory properties of pyruvate kinase M2 (PKM2) influence altered glucose metabolism in cancer. The interaction of PKM2 with phosphotyrosine-containing proteins inhibits enzyme activity and increases the availability of glycolytic metabolites to support cell proliferation. This suggests that high pyruvate kinase activity may suppress tumor growth. We show that expression of PKM1, the pyruvate kinase isoform with high constitutive activity, or exposure to published small-molecule PKM2 activators inhibits the growth of xenograft tumors. Structural studies reveal that small-molecule activators bind PKM2 at the subunit interaction interface, a site that is distinct from that of the endogenous activator fructose-1,6-bisphosphate (FBP). However, unlike FBP, binding of activators to PKM2 promotes a constitutively active enzyme state that is resistant to inhibition by tyrosine-phosphorylated proteins. These data support the notion that small-molecule activation of PKM2 can interfere with anabolic metabolism.

Published
2012

27. Author Correction: Fatty acid synthesis is required for breast cancer brain metastasis

Author

Ferraro, Gino B., Ali, Ahmed, Luengo, Alba, Kodack, David P., Deik, Amy, Abbott, Keene L., Bezwada, Divya, Blanc, Landry, Prideaux, Brendan, Jin, Xin, Posada, Jessica M., Chen, Jiang, Chin, Christopher R., Amoozgar, Zohreh, Ferreira, Raphael, Chen, Ivy X., Naxerova, Kamila, Ng, Christopher, Westermark, Anna M., Duquette, Mark, Roberge, Sylvie, Lindeman, Neal I., Lyssiotis, Costas A., Nielsen, Jens, Housman, David E., Duda, Dan G., Brachtel, Elena, Golub, Todd R., Cantley, Lewis C., Asara, John M., Davidson, Shawn M., Fukumura, Dai, Dartois, Véronique A., Clish, Clary B., Jain, Rakesh K., and Vander Heiden, Matthew G.

Published
2021
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28. Glutamine antagonist DRP-104 suppresses tumor growth and enhances response to checkpoint blockade inKEAP1mutant lung cancer

Author

Pillai, Ray, primary, LeBoeuf, Sarah E., additional, Hao, Yuan, additional, New, Connie, additional, Blum, Jenna L. E., additional, Rashidfarrokhi, Ali, additional, Huang, Shih Ming, additional, Bahamon, Christian, additional, Wu, Warren L., additional, Karadal-Ferrena, Burcu, additional, Herrera, Alberto, additional, Ivanova, Ellie, additional, Cross, Michael, additional, Bossowski, Jozef P., additional, Ding, Hongyu, additional, Hayashi, Makiko, additional, Rajalingam, Sahith, additional, Karakousi, Triantafyllia, additional, Sayin, Volkan I., additional, Khanna, Kamal M., additional, Wong, Kwok-Kin, additional, Wild, Robert, additional, Tsirigos, Aristotelis, additional, Poirier, John T., additional, Rudin, Charles M., additional, Davidson, Shawn M., additional, Koralov, Sergei B., additional, and Papagiannakopoulos, Thales, additional

Published
2023
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30. Supplementary Data from Translational Activation of ATF4 through Mitochondrial Anaplerotic Metabolic Pathways Is Required for DLBCL Growth and Survival

Author

Li, Meng, primary, Teater, Matthew R., primary, Hong, Jun Young, primary, Park, Noel R., primary, Duy, Cihangir, primary, Shen, Hao, primary, Wang, Ling, primary, Chen, Zhengming, primary, Cerchietti, Leandro, primary, Davidson, Shawn M., primary, Lin, Hening, primary, and Melnick, Ari M., primary

Published
2023
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31. Data from Limited Environmental Serine and Glycine Confer Brain Metastasis Sensitivity to PHGDH Inhibition

Author

Ngo, Bryan, primary, Kim, Eugenie, primary, Osorio-Vasquez, Victoria, primary, Doll, Sophia, primary, Bustraan, Sophia, primary, Liang, Roger J., primary, Luengo, Alba, primary, Davidson, Shawn M., primary, Ali, Ahmed, primary, Ferraro, Gino B., primary, Fischer, Grant M., primary, Eskandari, Roozbeh, primary, Kang, Diane S., primary, Ni, Jing, primary, Plasger, Ariana, primary, Rajasekhar, Vinagolu K., primary, Kastenhuber, Edward R., primary, Bacha, Sarah, primary, Sriram, Roshan K., primary, Stein, Benjamin D., primary, Bakhoum, Samuel F., primary, Snuderl, Matija, primary, Cotzia, Paolo, primary, Healey, John H., primary, Mainolfi, Nello, primary, Suri, Vipin, primary, Friedman, Adam, primary, Manfredi, Mark, primary, Sabatini, David M., primary, Jones, Drew R., primary, Yu, Min, primary, Zhao, Jean J., primary, Jain, Rakesh K., primary, Keshari, Kayvan R., primary, Davies, Michael A., primary, Vander Heiden, Matthew G., primary, Hernando, Eva, primary, Mann, Matthias, primary, Cantley, Lewis C., primary, and Pacold, Michael E., primary

Published
2023
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32. Supplementary Figures S1-S9, Supplementary Table S1 from Limited Environmental Serine and Glycine Confer Brain Metastasis Sensitivity to PHGDH Inhibition

Author

Ngo, Bryan, primary, Kim, Eugenie, primary, Osorio-Vasquez, Victoria, primary, Doll, Sophia, primary, Bustraan, Sophia, primary, Liang, Roger J., primary, Luengo, Alba, primary, Davidson, Shawn M., primary, Ali, Ahmed, primary, Ferraro, Gino B., primary, Fischer, Grant M., primary, Eskandari, Roozbeh, primary, Kang, Diane S., primary, Ni, Jing, primary, Plasger, Ariana, primary, Rajasekhar, Vinagolu K., primary, Kastenhuber, Edward R., primary, Bacha, Sarah, primary, Sriram, Roshan K., primary, Stein, Benjamin D., primary, Bakhoum, Samuel F., primary, Snuderl, Matija, primary, Cotzia, Paolo, primary, Healey, John H., primary, Mainolfi, Nello, primary, Suri, Vipin, primary, Friedman, Adam, primary, Manfredi, Mark, primary, Sabatini, David M., primary, Jones, Drew R., primary, Yu, Min, primary, Zhao, Jean J., primary, Jain, Rakesh K., primary, Keshari, Kayvan R., primary, Davies, Michael A., primary, Vander Heiden, Matthew G., primary, Hernando, Eva, primary, Mann, Matthias, primary, Cantley, Lewis C., primary, and Pacold, Michael E., primary

Published
2023
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35. Keap1 loss promotes Kras-driven lung cancer and results in dependence on glutaminolysis

Author

Romero, Rodrigo, Sayin, Volkan I, Davidson, Shawn M, Bauer, Matthew R, Singh, Simranjit X, LeBoeuf, Sarah E, Karakousi, Triantafyllia R, Ellis, Donald C, Bhutkar, Arjun, Sánchez-Rivera, Francisco J, Subbaraj, Lakshmipriya, Martinez, Britney, Bronson, Roderick T, Prigge, Justin R, Schmidt, Edward E, Thomas, Craig J, Goparaju, Chandra, Davies, Angela, Dolgalev, Igor, Heguy, Adriana, Allaj, Viola, Poirier, John T, Moreira, Andre L, Rudin, Charles M, Pass, Harvey I, Vander Heiden, Matthew G, Jacks, Tyler, and Papagiannakopoulos, Thales

Subjects
Gene mutations -- Research -- Usage, Cell proliferation -- Research -- Usage, Cancer -- Diagnosis, Lung cancer -- Care and treatment -- Diagnosis -- Research, CT imaging -- Usage -- Research, Biological sciences, Health
Abstract

Author(s): Rodrigo Romero [1, 2]; Volkan I Sayin [3]; Shawn M Davidson [1, 2]; Matthew R Bauer [1]; Simranjit X Singh [3]; Sarah E LeBoeuf [3]; Triantafyllia R Karakousi [3]; [...]

Published
2017
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36. Supplementary Tables 1-6 from Genome-Wide Interrogation of Human Cancers Identifies EGLN1 Dependency in Clear Cell Ovarian Cancers

Author

Price, Colles, primary, Gill, Stanley, primary, Ho, Zandra V., primary, Davidson, Shawn M., primary, Merkel, Erin, primary, McFarland, James M., primary, Leung, Lisa, primary, Tang, Andrew, primary, Kost-Alimova, Maria, primary, Tsherniak, Aviad, primary, Jonas, Oliver, primary, Vazquez, Francisca, primary, and Hahn, William C., primary

Published
2023
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37. Supplementary Table from Pyruvate Kinase M1 Suppresses Development and Progression of Prostate Adenocarcinoma

Author

Davidson, Shawn M., primary, Schmidt, Daniel R., primary, Heyman, Julia E., primary, O'Brien, James P., primary, Liu, Amy C., primary, Israelsen, William J., primary, Dayton, Talya L., primary, Sehgal, Raghav, primary, Bronson, Roderick T., primary, Freinkman, Elizaveta, primary, Mak, Howard H., primary, Fanelli, Giuseppe Nicolò, primary, Malstrom, Scott, primary, Bellinger, Gary, primary, Carracedo, Arkaitz, primary, Pandolfi, Pier Paolo, primary, Courtney, Kevin D., primary, Jha, Abhishek, primary, DePinho, Ronald A., primary, Horner, James W., primary, Thomas, Craig J., primary, Cantley, Lewis C., primary, Loda, Massimo, primary, and Vander Heiden, Matthew G., primary

Published
2023
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38. Supplementary Figure from Pyruvate Kinase M1 Suppresses Development and Progression of Prostate Adenocarcinoma

Author

Davidson, Shawn M., primary, Schmidt, Daniel R., primary, Heyman, Julia E., primary, O'Brien, James P., primary, Liu, Amy C., primary, Israelsen, William J., primary, Dayton, Talya L., primary, Sehgal, Raghav, primary, Bronson, Roderick T., primary, Freinkman, Elizaveta, primary, Mak, Howard H., primary, Fanelli, Giuseppe Nicolò, primary, Malstrom, Scott, primary, Bellinger, Gary, primary, Carracedo, Arkaitz, primary, Pandolfi, Pier Paolo, primary, Courtney, Kevin D., primary, Jha, Abhishek, primary, DePinho, Ronald A., primary, Horner, James W., primary, Thomas, Craig J., primary, Cantley, Lewis C., primary, Loda, Massimo, primary, and Vander Heiden, Matthew G., primary

Published
2023
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39. Data from Genome-Wide Interrogation of Human Cancers Identifies EGLN1 Dependency in Clear Cell Ovarian Cancers

Author

Price, Colles, primary, Gill, Stanley, primary, Ho, Zandra V., primary, Davidson, Shawn M., primary, Merkel, Erin, primary, McFarland, James M., primary, Leung, Lisa, primary, Tang, Andrew, primary, Kost-Alimova, Maria, primary, Tsherniak, Aviad, primary, Jonas, Oliver, primary, Vazquez, Francisca, primary, and Hahn, William C., primary

Published
2023
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40. Supplementary Figures 1-7 from Genome-Wide Interrogation of Human Cancers Identifies EGLN1 Dependency in Clear Cell Ovarian Cancers

Author

Price, Colles, primary, Gill, Stanley, primary, Ho, Zandra V., primary, Davidson, Shawn M., primary, Merkel, Erin, primary, McFarland, James M., primary, Leung, Lisa, primary, Tang, Andrew, primary, Kost-Alimova, Maria, primary, Tsherniak, Aviad, primary, Jonas, Oliver, primary, Vazquez, Francisca, primary, and Hahn, William C., primary

Published
2023
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41. Supplementary Data from Pyruvate Kinase M1 Suppresses Development and Progression of Prostate Adenocarcinoma

Author

Davidson, Shawn M., primary, Schmidt, Daniel R., primary, Heyman, Julia E., primary, O'Brien, James P., primary, Liu, Amy C., primary, Israelsen, William J., primary, Dayton, Talya L., primary, Sehgal, Raghav, primary, Bronson, Roderick T., primary, Freinkman, Elizaveta, primary, Mak, Howard H., primary, Fanelli, Giuseppe Nicolò, primary, Malstrom, Scott, primary, Bellinger, Gary, primary, Carracedo, Arkaitz, primary, Pandolfi, Pier Paolo, primary, Courtney, Kevin D., primary, Jha, Abhishek, primary, DePinho, Ronald A., primary, Horner, James W., primary, Thomas, Craig J., primary, Cantley, Lewis C., primary, Loda, Massimo, primary, and Vander Heiden, Matthew G., primary

Published
2023
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42. Data from Pyruvate Kinase M1 Suppresses Development and Progression of Prostate Adenocarcinoma

Author

Davidson, Shawn M., primary, Schmidt, Daniel R., primary, Heyman, Julia E., primary, O'Brien, James P., primary, Liu, Amy C., primary, Israelsen, William J., primary, Dayton, Talya L., primary, Sehgal, Raghav, primary, Bronson, Roderick T., primary, Freinkman, Elizaveta, primary, Mak, Howard H., primary, Fanelli, Giuseppe Nicolò, primary, Malstrom, Scott, primary, Bellinger, Gary, primary, Carracedo, Arkaitz, primary, Pandolfi, Pier Paolo, primary, Courtney, Kevin D., primary, Jha, Abhishek, primary, DePinho, Ronald A., primary, Horner, James W., primary, Thomas, Craig J., primary, Cantley, Lewis C., primary, Loda, Massimo, primary, and Vander Heiden, Matthew G., primary

Published
2023
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43. Data from Metformin Decreases Glucose Oxidation and Increases the Dependency of Prostate Cancer Cells on Reductive Glutamine Metabolism

Author

Fendt, Sarah-Maria, primary, Bell, Eric L., primary, Keibler, Mark A., primary, Davidson, Shawn M., primary, Wirth, Gregory J., primary, Fiske, Brian, primary, Mayers, Jared R., primary, Schwab, Matthias, primary, Bellinger, Gary, primary, Csibi, Alfredo, primary, Patnaik, Akash, primary, Blouin, Marie Jose, primary, Cantley, Lewis C., primary, Guarente, Leonard, primary, Blenis, John, primary, Pollak, Michael N., primary, Olumi, Aria F., primary, Vander Heiden, Matthew G., primary, and Stephanopoulos, Gregory, primary

Published
2023
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44. Supplementary Methods, Figure Legends from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism

Author

Grassian, Alexandra R., primary, Parker, Seth J., primary, Davidson, Shawn M., primary, Divakaruni, Ajit S., primary, Green, Courtney R., primary, Zhang, Xiamei, primary, Slocum, Kelly L., primary, Pu, Minying, primary, Lin, Fallon, primary, Vickers, Chad, primary, Joud-Caldwell, Carol, primary, Chung, Franklin, primary, Yin, Hong, primary, Handly, Erika D., primary, Straub, Christopher, primary, Growney, Joseph D., primary, Vander Heiden, Matthew G., primary, Murphy, Anne N., primary, Pagliarini, Raymond, primary, and Metallo, Christian M., primary

Published
2023
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45. Supplementary Figures 1 - 5 from Metformin Decreases Glucose Oxidation and Increases the Dependency of Prostate Cancer Cells on Reductive Glutamine Metabolism

Author

Fendt, Sarah-Maria, primary, Bell, Eric L., primary, Keibler, Mark A., primary, Davidson, Shawn M., primary, Wirth, Gregory J., primary, Fiske, Brian, primary, Mayers, Jared R., primary, Schwab, Matthias, primary, Bellinger, Gary, primary, Csibi, Alfredo, primary, Patnaik, Akash, primary, Blouin, Marie Jose, primary, Cantley, Lewis C., primary, Guarente, Leonard, primary, Blenis, John, primary, Pollak, Michael N., primary, Olumi, Aria F., primary, Vander Heiden, Matthew G., primary, and Stephanopoulos, Gregory, primary

Published
2023
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46. Supplementary Figures 1 - 6 from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism

Author

Grassian, Alexandra R., primary, Parker, Seth J., primary, Davidson, Shawn M., primary, Divakaruni, Ajit S., primary, Green, Courtney R., primary, Zhang, Xiamei, primary, Slocum, Kelly L., primary, Pu, Minying, primary, Lin, Fallon, primary, Vickers, Chad, primary, Joud-Caldwell, Carol, primary, Chung, Franklin, primary, Yin, Hong, primary, Handly, Erika D., primary, Straub, Christopher, primary, Growney, Joseph D., primary, Vander Heiden, Matthew G., primary, Murphy, Anne N., primary, Pagliarini, Raymond, primary, and Metallo, Christian M., primary

Published
2023
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47. Data from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism

Author

Grassian, Alexandra R., primary, Parker, Seth J., primary, Davidson, Shawn M., primary, Divakaruni, Ajit S., primary, Green, Courtney R., primary, Zhang, Xiamei, primary, Slocum, Kelly L., primary, Pu, Minying, primary, Lin, Fallon, primary, Vickers, Chad, primary, Joud-Caldwell, Carol, primary, Chung, Franklin, primary, Yin, Hong, primary, Handly, Erika D., primary, Straub, Christopher, primary, Growney, Joseph D., primary, Vander Heiden, Matthew G., primary, Murphy, Anne N., primary, Pagliarini, Raymond, primary, and Metallo, Christian M., primary

Published
2023
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48. Supplementary Tables 1 - 4 from IDH1 Mutations Alter Citric Acid Cycle Metabolism and Increase Dependence on Oxidative Mitochondrial Metabolism

Author

Grassian, Alexandra R., primary, Parker, Seth J., primary, Davidson, Shawn M., primary, Divakaruni, Ajit S., primary, Green, Courtney R., primary, Zhang, Xiamei, primary, Slocum, Kelly L., primary, Pu, Minying, primary, Lin, Fallon, primary, Vickers, Chad, primary, Joud-Caldwell, Carol, primary, Chung, Franklin, primary, Yin, Hong, primary, Handly, Erika D., primary, Straub, Christopher, primary, Growney, Joseph D., primary, Vander Heiden, Matthew G., primary, Murphy, Anne N., primary, Pagliarini, Raymond, primary, and Metallo, Christian M., primary

Published
2023
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49. Environment Impacts the Metabolic Dependencies of Ras-Driven Non-Small Cell Lung Cancer

Author

Davidson, Shawn M., Papagiannakopoulos, Thales, Olenchock, Benjamin A., Heyman, Julia E., Keibler, Mark A., Luengo, Alba, Bauer, Matthew R., Jha, Abhishek K., O’Brien, James P., Pierce, Kerry A., Gui, Dan Y., Sullivan, Lucas B., Wasylenko, Thomas M., Subbaraj, Lakshmipriya, Chin, Christopher R., Stephanopolous, Gregory, Mott, Bryan T., Jacks, Tyler, Clish, Clary B., and Vander Heiden, Matthew G.

Published
2016
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50. Mutations in mitochondrial enzyme GPT2 cause metabolic dysfunction and neurological disease with developmental and progressive features

Author

Ouyang, Qing, Nakayama, Tojo, Baytas, Ozan, Davidson, Shawn M., Yang, Chendong, Schmidt, Michael, Lizarraga, Sofia B., Mishra, Sasmita, EI-Quessny, Malak, Niaz, Saima, Butt, Mirrat Gul, Murtaza, Syed Imran, Javed, Afzal, Chaudhry, Haroon Rashid, Vaughan, Dylan J., Hill, R. Sean, Partlow, Jennifer N., Yoo, Seung-Yun, Lam, Anh-Thu N., Nasir, Ramzi, Al-Saffar, Muna, Barkovich, A. James, Schwede, Matthew, Nagpal, Shailender, Rajab, Anna, DeBerardinis, Ralph J., Housman, David E., Mochida, Ganeshwaran H., and Morrow, Eric M.

Published
2016

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