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Navdeep S. Chandel

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https://read.qxmd.com/read/30858621/nad-biosynthetic-pathways-regulate-innate-immunity
#1
Leah K Billingham, Navdeep S Chandel
No abstract text is available yet for this article.
March 11, 2019: Nature Immunology
https://read.qxmd.com/read/30773464/serine-metabolism-supports-macrophage-il-1%C3%AE-production
#2
Arianne E Rodriguez, Gregory S Ducker, Leah K Billingham, Carlos A Martinez, Nello Mainolfi, Vipin Suri, Adam Friedman, Mark G Manfredi, Samuel E Weinberg, Joshua D Rabinowitz, Navdeep S Chandel
Serine is a substrate for nucleotide, NADPH, and glutathione (GSH) synthesis. Previous studies in cancer cells and lymphocytes have shown that serine-dependent one-carbon units are necessary for nucleotide production to support proliferation. Presently, it is unknown whether serine metabolism impacts the function of non-proliferative cells, such as inflammatory macrophages. We find that in macrophages, serine is required for optimal lipopolysaccharide (LPS) induction of IL-1β mRNA expression, but not inflammasome activation...
February 7, 2019: Cell Metabolism
https://read.qxmd.com/read/30659235/the-mitochondrial-retrograde-signaling-regulates-wnt-signaling-to-promote-tumorigenesis-in-colon-cancer
#3
Yang-An Wen, Xiaopeng Xiong, Timothy Scott, Austin T Li, Chi Wang, Heidi L Weiss, Li Tan, Emily Bradford, Teresa W M Fan, Navdeep S Chandel, Terrence A Barrett, Tianyan Gao
Cancer cells are known to upregulate aerobic glycolysis to promote growth, proliferation, and survival. However, the role of mitochondrial respiration in tumorigenesis remains elusive. Here we report that inhibition of mitochondrial function by silencing TFAM, a key transcription factor essential for mitochondrial DNA (mtDNA) replication and the transcription of mtDNA-encoded genes, markedly reduced tumor-initiating potential of colon cancer cells. Knockdown of TFAM significantly decreased mitochondrial respiration in colon cancer cells; however, the cellular levels of ATP remained largely unchanged as a result of increased glycolysis...
January 18, 2019: Cell Death and Differentiation
https://read.qxmd.com/read/30626970/mitochondrial-complex-iii-is-essential-for-suppressive-function-of-regulatory-t-cells
#4
Samuel E Weinberg, Benjamin D Singer, Elizabeth M Steinert, Carlos A Martinez, Manan M Mehta, Inmaculada Martínez-Reyes, Peng Gao, Kathryn A Helmin, Hiam Abdala-Valencia, Laura A Sena, Paul T Schumacker, Laurence A Turka, Navdeep S Chandel
Regulatory T cells (Treg cells), a distinct subset of CD4+ T cells, are necessary for the maintenance of immune self-tolerance and homeostasis1,2 . Recent studies have demonstrated that Treg cells exhibit a unique metabolic profile, characterized by an increase in mitochondrial metabolism relative to other CD4+ effector subsets3,4 . Furthermore, the Treg cell lineage-defining transcription factor, Foxp3, has been shown to promote respiration5,6 ; however, it remains unknown whether the mitochondrial respiratory chain is required for the T cell-suppression capacity, stability and survival of Treg cells...
January 9, 2019: Nature
https://read.qxmd.com/read/30613765/idh3%C3%AE-regulates-one-carbon-metabolism-in-glioblastoma
#5
Jasmine L May, Fotini M Kouri, Lisa A Hurley, Juan Liu, Serena Tommasini-Ghelfi, Yanrong Ji, Peng Gao, Andrea E Calvert, Andrew Lee, Navdeep S Chandel, Ramana V Davuluri, Craig M Horbinski, Jason W Locasale, Alexander H Stegh
Mutation or transcriptional up-regulation of isocitrate dehydrogenases 1 and 2 ( IDH1 and IDH2 ) promotes cancer progression through metabolic reprogramming and epigenetic deregulation of gene expression. Here, we demonstrate that IDH3α, a subunit of the IDH3 heterotetramer, is elevated in glioblastoma (GBM) patient samples compared to normal brain tissue and promotes GBM progression in orthotopic glioma mouse models. IDH3α loss of function reduces tricarboxylic acid (TCA) cycle turnover and inhibits oxidative phosphorylation...
January 2019: Science Advances
https://read.qxmd.com/read/30595481/efferocytosis-fuels-requirements-of-fatty-acid-oxidation-and-the-electron-transport-chain-to-polarize-macrophages-for-tissue-repair
#6
Shuang Zhang, Samuel Weinberg, Matthew DeBerge, Anastasiia Gainullina, Matthew Schipma, Jason M Kinchen, Issam Ben-Sahra, David R Gius, Laurent Yvan-Charvet, Navdeep S Chandel, Paul T Schumacker, Edward B Thorp
During wound injury, efferocytosis fills the macrophage with a metabolite load nearly equal to the phagocyte itself. A timely question pertains to how metabolic phagocytic signaling regulates the signature anti-inflammatory macrophage response. Here we report the metabolome of activated macrophages during efferocytosis to reveal an interleukin-10 (IL-10) cytokine escalation that was independent of glycolysis yet bolstered by apoptotic cell fatty acids and mitochondrial β-oxidation, the electron transport chain, and heightened coenzyme NAD+ ...
February 5, 2019: Cell Metabolism
https://read.qxmd.com/read/30563855/probing-mitochondrial-metabolism-in-vivo
#7
Gregory S McElroy, Navdeep S Chandel
No abstract text is available yet for this article.
December 18, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://read.qxmd.com/read/30517626/hepatic-hkdc1-expression-contributes-to-liver-metabolism
#8
Carolina M Pusec, Adam De Jesus, Md Wasim Khan, Alexander R Terry, Anton E Ludvik, Kai Xu, Nicholas Giancola, Haaris Pervaiz, Emily Daviau Smith, Xianzhong Ding, Stephen Harrison, Navdeep S Chandel, Thomas C Becker, Nissim Hay, Hossein Ardehali, Jose Cordoba-Chacon, Brian T Layden
Glucokinase (GCK) is the principal hexokinase (HK) in the liver, operating as a glucose sensor to regulate glucose metabolism and lipid homeostasis. Recently, we proposed Hexokinase Domain Containing-1 (HKDC1) to be a novel 5th HK with expression in the liver. Here, we reveal HKDC1 to have low glucose-phosphorylating ability and demonstrate its association with the mitochondria in hepatocytes. As we have shown previously that genetic deletion of HKDC1 leads to altered hepatic triglyceride levels, we also explored the influence of overexpression of HKDC1 in hepatocytes on cellular metabolism observing reduced glycolytic capacity and maximal mitochondrial respiration with concurrent reductions in glucose oxidation and mitochondrial membrane potential...
December 3, 2018: Endocrinology
https://read.qxmd.com/read/30383397/there-is-no-smoke-without-mitochondria
#9
SeungHye Han, Navdeep S Chandel
No abstract text is available yet for this article.
November 1, 2018: American Journal of Respiratory Cell and Molecular Biology
https://read.qxmd.com/read/30318339/metformin-targets-mitochondrial-electron-transport-to-reduce-air-pollution-induced-thrombosis
#10
Saul Soberanes, Alexander V Misharin, Amit Jairaman, Luisa Morales-Nebreda, Alexandra C McQuattie-Pimentel, Takugo Cho, Robert B Hamanaka, Angelo Y Meliton, Paul A Reyfman, James M Walter, Ching-I Chen, Monica Chi, Stephen Chiu, Francisco J Gonzalez-Gonzalez, Matthew Antalek, Hiam Abdala-Valencia, Sergio E Chiarella, Kaitlyn A Sun, Parker S Woods, Andrew J Ghio, Manu Jain, Harris Perlman, Karen M Ridge, Richard I Morimoto, Jacob I Sznajder, William E Balch, Sangeeta M Bhorade, Ankit Bharat, Murali Prakriya, Navdeep S Chandel, Gökhan M Mutlu, G R Scott Budinger
Urban particulate matter air pollution induces the release of pro-inflammatory cytokines including interleukin-6 (IL-6) from alveolar macrophages, resulting in an increase in thrombosis. Here, we report that metformin provides protection in this murine model. Treatment of mice with metformin or exposure of murine or human alveolar macrophages to metformin prevented the particulate matter-induced generation of complex III mitochondrial reactive oxygen species, which were necessary for the opening of calcium release-activated channels (CRAC) and release of IL-6...
October 11, 2018: Cell Metabolism
https://read.qxmd.com/read/30140438/hexokinase-2-is-dispensable-for-t-cell-dependent-immunity
#11
Manan M Mehta, Samuel E Weinberg, Elizabeth M Steinert, Krishan Chhiba, Carlos Alberto Martinez, Peng Gao, Harris R Perlman, Paul Bryce, Nissim Hay, Navdeep S Chandel
Background: T cells and cancer cells utilize glycolysis for proliferation. The hexokinase (1-4) family of enzymes catalyze the first step of glycolysis. Hexokinase 2 (HK2) is one of the most highly upregulated metabolic enzymes in both cancer and activated T cells. HK2 is required for the development and/or growth of cancer in several cancer models, but the necessity of HK2 in T cells is not fully understood. The clinical applicability of HK2 inhibition in cancer may be significantly limited by any potential negative effects of HK2 inhibition on T cells...
2018: Cancer & Metabolism
https://read.qxmd.com/read/29894695/ros-promotes-cancer-cell-survival-through-calcium-signaling
#12
Colleen R Reczek, Navdeep S Chandel
To avoid reactive oxygen species (ROS)-induced cell death, cancer cells increase their antioxidant defense system. In this issue of Cancer Cell, Takahashi et al. identify a novel, non-canonical oxidative stress defense mechanism involving TRPA1, a redox-sensitive Ca2+ channel, and the upregulation of anti-apoptotic pathways to promote cancer cell survival.
June 11, 2018: Cancer Cell
https://read.qxmd.com/read/29727615/to-claim-growth-turf-mtor-says-sod-off
#13
Hyewon Kong, Navdeep S Chandel
Maintaining redox balance in cancer cells is essential for tumor development and progression. In this issue of Molecular Cell, Tsang et al. (2018) identify an evolutionarily conserved mTORC1-dependent mechanism by which cancer cells control redox homeostasis in ischemic tumor microenvironment.
May 3, 2018: Molecular Cell
https://read.qxmd.com/read/29692354/acetyl-coa-directed-gene-transcription-in-cancer-cells
#14
REVIEW
Inmaculada Martínez-Reyes, Navdeep S Chandel
Fluctuations in acetyl-coenzyme A (acetyl-CoA) levels have been previously associated with changes in global histone acetylation and gene expression. The study by Lee and colleagues (pp. 497-511) in this issue of Genes & Development demonstrates that acetyl-CoA can promote the up-regulation of cell migration- and adhesion-related genes in glioblastoma by controlling Ca2+ -NFAT (nuclear factor of activated T cells) signaling.
April 1, 2018: Genes & Development
https://read.qxmd.com/read/29617673/mitochondrial-complex-i-inhibitors-expose-a-vulnerability-for-selective-killing-of-pten-null-cells
#15
Adam Naguib, Grinu Mathew, Colleen R Reczek, Kaitlin Watrud, Alexandra Ambrico, Tali Herzka, Irene Casanova Salas, Matthew F Lee, Nour El-Amine, Wu Zheng, M Emilia Di Francesco, Joseph R Marszalek, Darryl J Pappin, Navdeep S Chandel, Lloyd C Trotman
A hallmark of advanced prostate cancer (PC) is the concomitant loss of PTEN and p53 function. To selectively eliminate such cells, we screened cytotoxic compounds on Pten-/- ;Trp53-/- fibroblasts and their Pten-WT reference. Highly selective killing of Pten-null cells can be achieved by deguelin, a natural insecticide. Deguelin eliminates Pten-deficient cells through inhibition of mitochondrial complex I (CI). Five hundred-fold higher drug doses are needed to obtain the same killing of Pten-WT cells, even though deguelin blocks their electron transport chain equally well...
April 3, 2018: Cell Reports
https://read.qxmd.com/read/29562198/mitochondria-er-pas-de-deux-controls-memory-t-cell-function
#16
COMMENT
Elizabeth M Steinert, Navdeep S Chandel
Memory CD8+ T cells mediate protective secondary immune responses. In this issue, Bantug et al. (2018) demonstrate that mTORC2-AKT-GSK3β signaling at mitochondria-ER contact sites enables the TCA cycle flux that is necessary for memory CD8+ T cells to produce IFN-γ.
March 20, 2018: Immunity
https://read.qxmd.com/read/29362479/molecular-mechanisms-of-cell-death-recommendations-of-the-nomenclature-committee-on-cell-death-2018
#17
REVIEW
Lorenzo Galluzzi, Ilio Vitale, Stuart A Aaronson, John M Abrams, Dieter Adam, Patrizia Agostinis, Emad S Alnemri, Lucia Altucci, Ivano Amelio, David W Andrews, Margherita Annicchiarico-Petruzzelli, Alexey V Antonov, Eli Arama, Eric H Baehrecke, Nickolai A Barlev, Nicolas G Bazan, Francesca Bernassola, Mathieu J M Bertrand, Katiuscia Bianchi, Mikhail V Blagosklonny, Klas Blomgren, Christoph Borner, Patricia Boya, Catherine Brenner, Michelangelo Campanella, Eleonora Candi, Didac Carmona-Gutierrez, Francesco Cecconi, Francis K-M Chan, Navdeep S Chandel, Emily H Cheng, Jerry E Chipuk, John A Cidlowski, Aaron Ciechanover, Gerald M Cohen, Marcus Conrad, Juan R Cubillos-Ruiz, Peter E Czabotar, Vincenzo D'Angiolella, Ted M Dawson, Valina L Dawson, Vincenzo De Laurenzi, Ruggero De Maria, Klaus-Michael Debatin, Ralph J DeBerardinis, Mohanish Deshmukh, Nicola Di Daniele, Francesco Di Virgilio, Vishva M Dixit, Scott J Dixon, Colin S Duckett, Brian D Dynlacht, Wafik S El-Deiry, John W Elrod, Gian Maria Fimia, Simone Fulda, Ana J García-Sáez, Abhishek D Garg, Carmen Garrido, Evripidis Gavathiotis, Pierre Golstein, Eyal Gottlieb, Douglas R Green, Lloyd A Greene, Hinrich Gronemeyer, Atan Gross, Gyorgy Hajnoczky, J Marie Hardwick, Isaac S Harris, Michael O Hengartner, Claudio Hetz, Hidenori Ichijo, Marja Jäättelä, Bertrand Joseph, Philipp J Jost, Philippe P Juin, William J Kaiser, Michael Karin, Thomas Kaufmann, Oliver Kepp, Adi Kimchi, Richard N Kitsis, Daniel J Klionsky, Richard A Knight, Sharad Kumar, Sam W Lee, John J Lemasters, Beth Levine, Andreas Linkermann, Stuart A Lipton, Richard A Lockshin, Carlos López-Otín, Scott W Lowe, Tom Luedde, Enrico Lugli, Marion MacFarlane, Frank Madeo, Michal Malewicz, Walter Malorni, Gwenola Manic, Jean-Christophe Marine, Seamus J Martin, Jean-Claude Martinou, Jan Paul Medema, Patrick Mehlen, Pascal Meier, Sonia Melino, Edward A Miao, Jeffery D Molkentin, Ute M Moll, Cristina Muñoz-Pinedo, Shigekazu Nagata, Gabriel Nuñez, Andrew Oberst, Moshe Oren, Michael Overholtzer, Michele Pagano, Theocharis Panaretakis, Manolis Pasparakis, Josef M Penninger, David M Pereira, Shazib Pervaiz, Marcus E Peter, Mauro Piacentini, Paolo Pinton, Jochen H M Prehn, Hamsa Puthalakath, Gabriel A Rabinovich, Markus Rehm, Rosario Rizzuto, Cecilia M P Rodrigues, David C Rubinsztein, Thomas Rudel, Kevin M Ryan, Emre Sayan, Luca Scorrano, Feng Shao, Yufang Shi, John Silke, Hans-Uwe Simon, Antonella Sistigu, Brent R Stockwell, Andreas Strasser, Gyorgy Szabadkai, Stephen W G Tait, Daolin Tang, Nektarios Tavernarakis, Andrew Thorburn, Yoshihide Tsujimoto, Boris Turk, Tom Vanden Berghe, Peter Vandenabeele, Matthew G Vander Heiden, Andreas Villunger, Herbert W Virgin, Karen H Vousden, Domagoj Vucic, Erwin F Wagner, Henning Walczak, David Wallach, Ying Wang, James A Wells, Will Wood, Junying Yuan, Zahra Zakeri, Boris Zhivotovsky, Laurence Zitvogel, Gerry Melino, Guido Kroemer
Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes...
March 2018: Cell Death and Differentiation
https://read.qxmd.com/read/29282291/regulation-of-redox-balance-in-cancer-and-t-cells
#18
REVIEW
Hyewon Kong, Navdeep S Chandel
Reactive oxygen species (ROS) mediate redox signaling necessary for numerous cellular functions. Yet, high levels of ROS in cells and tissues can cause damage and cell death. Therefore, regulation of redox homeostasis is essential for ROS-dependent signaling that does not incur cellular damage. Cells achieve this optimal balance by coordinating ROS production and elimination. In this Minireview, we discuss the mechanisms by which proliferating cancer and T cells maintain a carefully controlled redox balance...
May 18, 2018: Journal of Biological Chemistry
https://read.qxmd.com/read/29259335/mitochondria-back-to-the-future
#19
Navdeep S Chandel
No abstract text is available yet for this article.
February 2018: Nature Reviews. Molecular Cell Biology
https://read.qxmd.com/read/29211977/waste-not-want-not-lactate-oxidation-fuels-the-tca-cycle
#20
Inmaculada Martínez-Reyes, Navdeep S Chandel
Previous studies have demonstrated that mitochondrial respiration is essential for tumorigenesis. Hui et al. (2017) and Faubert et al. (2017) demonstrate that lactate, traditionally viewed as a waste product of anaerobic and aerobic glycolysis, is a major carbon source to fuel the mitochondrial TCA cycle in normal tissue and in tumors.
December 5, 2017: Cell Metabolism
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