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3. High-calorie diets uncouple hypothalamic oxytocin neurons from a gut-to-brain satiation pathway via κ-opioid signaling

Author

Gruber, Tim, Lechner, Franziska, Murat, Cahuê, Contreras, Raian E., Sanchez-Quant, Eva, Miok, Viktorian, Makris, Konstantinos, Le Thuc, Ophélia, González-García, Ismael, García-Clave, Elena, Althammer, Ferdinand, Krabichler, Quirin, DeCamp, Lisa M., Jones, Russell G., Lutter, Dominik, Williams, Rhiannan H., Pfluger, Paul T., Müller, Timo D., Woods, Stephen C., Pospisilik, John Andrew, Martinez-Jimenez, Celia P., Tschöp, Matthias H., Grinevich, Valery, and García-Cáceres, Cristina

Published
2023
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5. Itaconate confers tolerance to late NLRP3 inflammasome activation

Author

Bambouskova, Monika, primary, Potuckova, Lucie, additional, Paulenda, Tomas, additional, Kerndl, Martina, additional, Mogilenko, Denis A., additional, Lizotte, Kate, additional, Swain, Amanda, additional, Hayes, Sebastian, additional, Sheldon, Ryan D., additional, Kim, Hyeryun, additional, Kapadnis, Unnati, additional, Ellis, Abigail E., additional, Isaguirre, Christine, additional, Burdess, Samantha, additional, Laha, Anwesha, additional, Amarasinghe, Gaya K., additional, Chubukov, Victor, additional, Roddy, Thomas P., additional, Diamond, Michael S., additional, Jones, Russell G., additional, Simons, Donald M., additional, and Artyomov, Maxim N., additional

Published
2021
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6. MicroRNA-9 Fine-Tunes Dendritic Cell Function by Suppressing Negative Regulators in a Cell-Type-Specific Manner

Author

Cordeiro, Brendan, primary, Jeon, Peter, additional, Boukhaled, Giselle M., additional, Corrado, Mario, additional, Lapohos, Orsolya, additional, Roy, Dominic G., additional, Williams, Kelsey, additional, Jones, Russell G., additional, Gruenheid, Samantha, additional, Sagan, Selena M., additional, and Krawczyk, Connie M., additional

Published
2020
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7. Immature Low-Density Neutrophils Exhibit Metabolic Flexibility that Facilitates Breast Cancer Liver Metastasis

Author

Hsu, Brian E., primary, Tabariès, Sébastien, additional, Johnson, Radia M., additional, Andrzejewski, Sylvia, additional, Senecal, Julien, additional, Lehuédé, Camille, additional, Annis, Matthew G., additional, Ma, Eric H., additional, Völs, Sandra, additional, Ramsay, LeeAnn, additional, Froment, Remi, additional, Monast, Anie, additional, Watson, Ian R., additional, Granot, Zvi, additional, Jones, Russell G., additional, St-Pierre, Julie, additional, and Siegel, Peter M., additional

Published
2019
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8. The Transcription Factors TFEB and TFE3 Link the FLCN-AMPK Signaling Axis to Innate Immune Response and Pathogen Resistance

Author

El-Houjeiri, Leeanna, primary, Possik, Elite, additional, Vijayaraghavan, Tarika, additional, Paquette, Mathieu, additional, Martina, José A., additional, Kazan, Jalal M., additional, Ma, Eric H., additional, Jones, Russell, additional, Blanchette, Paola, additional, Puertollano, Rosa, additional, and Pause, Arnim, additional

Published
2019
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10. The miR-17 ∼ 92 microRNA Cluster Is a Global Regulator of Tumor Metabolism

Author

Izreig, Said, primary, Samborska, Bozena, additional, Johnson, Radia M., additional, Sergushichev, Alexey, additional, Ma, Eric H., additional, Lussier, Carine, additional, Loginicheva, Ekaterina, additional, Donayo, Ariel O., additional, Poffenberger, Maya C., additional, Sagan, Selena M., additional, Vincent, Emma E., additional, Artyomov, Maxim N., additional, Duchaine, Thomas F., additional, and Jones, Russell G., additional

Published
2016
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11. The miR-17∼92 microRNA Cluster Is a Global Regulator of Tumor Metabolism.

Author

Izreig, Said, Samborska, Bozena, Johnson, Radia M., Sergushichev, Alexey, Ma, Eric H., Lussier, Carine, Loginicheva, Ekaterina, Donayo, Ariel O., Poffenberger, Maya C., Sagan, Selena M., Vincent, Emma E., Artyomov, Maxim N., Duchaine, Thomas F., and Jones, Russell G.

Abstract

Summary A central hallmark of cancer cells is the reprogramming of cellular metabolism to meet the bioenergetic and biosynthetic demands of malignant growth. Here, we report that the miR-17 ∼ 92 microRNA (miRNA) cluster is an oncogenic driver of tumor metabolic reprogramming. Loss of miR-17 ∼ 92 in Myc + tumor cells leads to a global decrease in tumor cell metabolism, affecting both glycolytic and mitochondrial metabolism, whereas increased miR-17 ∼ 92 expression is sufficient to drive increased nutrient usage by tumor cells. We mapped the metabolic control element of miR-17 ∼ 92 to the miR-17 seed family, which influences cellular metabolism and mammalian target of rapamycin complex 1 (mTORC1) signaling through negative regulation of the LKB1 tumor suppressor. miR-17 -dependent tuning of LKB1 levels regulates both the metabolic potential of Myc + lymphomas and tumor growth in vivo. Our results establish metabolic reprogramming as a central function of the oncogenic miR-17 ∼ 92 miRNA cluster that drives the progression of MYC-dependent tumors. [ABSTRACT FROM AUTHOR]

Published
2016
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12. The miR-17∼92microRNA Cluster Is a Global Regulator of Tumor Metabolism

Author

Izreig, Said, Samborska, Bozena, Johnson, Radia M., Sergushichev, Alexey, Ma, Eric H., Lussier, Carine, Loginicheva, Ekaterina, Donayo, Ariel O., Poffenberger, Maya C., Sagan, Selena M., Vincent, Emma E., Artyomov, Maxim N., Duchaine, Thomas F., and Jones, Russell G.

Abstract

A central hallmark of cancer cells is the reprogramming of cellular metabolism to meet the bioenergetic and biosynthetic demands of malignant growth. Here, we report that the miR-17∼92microRNA (miRNA) cluster is an oncogenic driver of tumor metabolic reprogramming. Loss of miR-17∼92in Myc+tumor cells leads to a global decrease in tumor cell metabolism, affecting both glycolytic and mitochondrial metabolism, whereas increased miR-17∼92expression is sufficient to drive increased nutrient usage by tumor cells. We mapped the metabolic control element of miR-17∼92to the miR-17seed family, which influences cellular metabolism and mammalian target of rapamycin complex 1 (mTORC1) signaling through negative regulation of the LKB1 tumor suppressor. miR-17-dependent tuning of LKB1 levels regulates both the metabolic potential of Myc+lymphomas and tumor growth in vivo. Our results establish metabolic reprogramming as a central function of the oncogenic miR-17∼92miRNA cluster that drives the progression of MYC-dependent tumors.

Published
2016
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13. Creatine transport and creatine kinase activity is required for CD8+T cell immunity

Author

Samborska, Bozena, Roy, Dominic G., Rahbani, Janane F., Hussain, Mohammed F., Ma, Eric H., Jones, Russell G., and Kazak, Lawrence

Abstract

The factors that promote T cell expansion are not fully known. Creatine is an abundant circulating metabolite that has recently been implicated in T cell function; however, its cell-autonomous role in immune-cell function is unknown. Here, we show that creatine supports cell-intrinsic CD8+T cell homeostasis. We further identify creatine kinase B (CKB) as the creatine kinase isoenzyme that supports these T cell properties. Loss of the creatine transporter (Slc6a8) or Ckbresults in compromised CD8+T cell expansion in response to infection without influencing adenylate energy charge. Rather, loss of Slc6a8or Ckbdisrupts naive T cell homeostasis and weakens TCR-mediated activation of mechanistic target of rapamycin complex 1 (mTORC1) signaling required for CD8+T cell expansion. These data demonstrate a cell-intrinsic role for creatine transport and creatine transphosphorylation, independent of their effects on global cellular energy charge, in supporting CD8+T cell homeostasis and effector function.

Published
2022
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14. Creatine transport and creatine kinase activity is required for CD8 + T cell immunity.

Author

Samborska B, Roy DG, Rahbani JF, Hussain MF, Ma EH, Jones RG, and Kazak L

Subjects
Creatine Kinase metabolism, Phosphorylation, Signal Transduction, CD8-Positive T-Lymphocytes, Creatine metabolism
Abstract

The factors that promote T cell expansion are not fully known. Creatine is an abundant circulating metabolite that has recently been implicated in T cell function; however, its cell-autonomous role in immune-cell function is unknown. Here, we show that creatine supports cell-intrinsic CD8 + T cell homeostasis. We further identify creatine kinase B (CKB) as the creatine kinase isoenzyme that supports these T cell properties. Loss of the creatine transporter (Slc6a8) or Ckb results in compromised CD8 + T cell expansion in response to infection without influencing adenylate energy charge. Rather, loss of Slc6a8 or Ckb disrupts naive T cell homeostasis and weakens TCR-mediated activation of mechanistic target of rapamycin complex 1 (mTORC1) signaling required for CD8 + T cell expansion. These data demonstrate a cell-intrinsic role for creatine transport and creatine transphosphorylation, independent of their effects on global cellular energy charge, in supporting CD8 + T cell homeostasis and effector function., Competing Interests: Declaration of interests R.G.J. is a consultant for Agios Pharmaceuticals and Servier Pharmaceuticals and serves on the Scientific Advisory Board of ImmunoMet Therapeutics., (Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2022
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