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Navdeep S. Chandel

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https://www.readbyqxmd.com/read/30517626/hepatic-hkdc1-expression-contributes-to-liver-metabolism
#1
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://www.readbyqxmd.com/read/30383397/there-is-no-smoke-without-mitochondria
#2
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://www.readbyqxmd.com/read/30318339/metformin-targets-mitochondrial-electron-transport-to-reduce-air-pollution-induced-thrombosis
#3
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://www.readbyqxmd.com/read/30140438/hexokinase-2-is-dispensable-for-t-cell-dependent-immunity
#4
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://www.readbyqxmd.com/read/29894695/ros-promotes-cancer-cell-survival-through-calcium-signaling
#5
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://www.readbyqxmd.com/read/29727615/to-claim-growth-turf-mtor-says-sod-off
#6
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://www.readbyqxmd.com/read/29692354/acetyl-coa-directed-gene-transcription-in-cancer-cells
#7
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://www.readbyqxmd.com/read/29617673/mitochondrial-complex-i-inhibitors-expose-a-vulnerability-for-selective-killing-of-pten-null-cells
#8
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://www.readbyqxmd.com/read/29562198/mitochondria-er-pas-de-deux-controls-memory-t-cell-function
#9
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://www.readbyqxmd.com/read/29362479/molecular-mechanisms-of-cell-death-recommendations-of-the-nomenclature-committee-on-cell-death-2018
#10
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://www.readbyqxmd.com/read/29282291/regulation-of-redox-balance-in-cancer-and-t-cells
#11
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://www.readbyqxmd.com/read/29259335/mitochondria-back-to-the-future
#12
Navdeep S Chandel
No abstract text is available yet for this article.
February 2018: Nature Reviews. Molecular Cell Biology
https://www.readbyqxmd.com/read/29211977/waste-not-want-not-lactate-oxidation-fuels-the-tca-cycle
#13
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
https://www.readbyqxmd.com/read/29118187/jnk2-up-regulates-hypoxia-inducible-factors-and-contributes-to-hypoxia-induced-erythropoiesis-and-pulmonary-hypertension
#14
Marc A Sala, Cong Chen, Qiao Zhang, Hanh Chi Do-Umehara, Wenjiao Wu, Alexander V Misharin, Gregory B Waypa, Deyu Fang, G R Scott Budinger, Shuwen Liu, Navdeep S Chandel, Paul T Schumacker, Jacob I Sznajder, Jing Liu
The hypoxic response is a stress response triggered by low oxygen tension. Hypoxia-inducible factors (HIFs) play a prominent role in the pathobiology of hypoxia-associated conditions, including pulmonary hypertension (PH) and polycythemia. The c-Jun N-terminal protein kinase (JNK), a stress-activated protein kinase that consists of two ubiquitously expressed isoforms, JNK1 and JNK2, and a tissue-specific isoform, JNK3, has been shown to be activated by hypoxia. However, the physiological role of JNK1 and JNK2 in the hypoxic response remains elusive...
January 5, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29058724/a-crispr-screen-identifies-a-pathway-required-for-paraquat-induced-cell-death
#15
Colleen R Reczek, Kıvanç Birsoy, Hyewon Kong, Inmaculada Martínez-Reyes, Tim Wang, Peng Gao, David M Sabatini, Navdeep S Chandel
Paraquat, a herbicide linked to Parkinson's disease, generates reactive oxygen species (ROS), which causes cell death. Because the source of paraquat-induced ROS production remains unknown, we conducted a CRISPR-based positive-selection screen to identify metabolic genes essential for paraquat-induced cell death. Our screen uncovered three genes, POR (cytochrome P450 oxidoreductase), ATP7A (copper transporter), and SLC45A4 (sucrose transporter), required for paraquat-induced cell death. Furthermore, our results revealed POR as the source of paraquat-induced ROS production...
December 2017: Nature Chemical Biology
https://www.readbyqxmd.com/read/28874604/mitochondrial-redox-signaling-enables-repair-of-injured-skeletal-muscle-cells
#16
Adam Horn, Jack H Van der Meulen, Aurelia Defour, Marshall Hogarth, Sen Chandra Sreetama, Aaron Reed, Luana Scheffer, Navdeep S Chandel, Jyoti K Jaiswal
Strain and physical trauma to mechanically active cells, such as skeletal muscle myofibers, injures their plasma membranes, and mitochondrial function is required for their repair. We found that mitochondrial function was also needed for plasma membrane repair in myoblasts as well as nonmuscle cells, which depended on mitochondrial uptake of calcium through the mitochondrial calcium uniporter (MCU). Calcium uptake transiently increased the mitochondrial production of reactive oxygen species (ROS), which locally activated the guanosine triphosphatase (GTPase) RhoA, triggering F-actin accumulation at the site of injury and facilitating membrane repair...
September 5, 2017: Science Signaling
https://www.readbyqxmd.com/read/28694385/monocyte-derived-alveolar-macrophages-drive-lung-fibrosis-and-persist-in-the-lung-over-the-life-span
#17
Alexander V Misharin, Luisa Morales-Nebreda, Paul A Reyfman, Carla M Cuda, James M Walter, Alexandra C McQuattie-Pimentel, Ching-I Chen, Kishore R Anekalla, Nikita Joshi, Kinola J N Williams, Hiam Abdala-Valencia, Tyrone J Yacoub, Monica Chi, Stephen Chiu, Francisco J Gonzalez-Gonzalez, Khalilah Gates, Anna P Lam, Trevor T Nicholson, Philip J Homan, Saul Soberanes, Salina Dominguez, Vince K Morgan, Rana Saber, Alexander Shaffer, Monique Hinchcliff, Stacy A Marshall, Ankit Bharat, Sergejs Berdnikovs, Sangeeta M Bhorade, Elizabeth T Bartom, Richard I Morimoto, William E Balch, Jacob I Sznajder, Navdeep S Chandel, Gökhan M Mutlu, Manu Jain, Cara J Gottardi, Benjamin D Singer, Karen M Ridge, Neda Bagheri, Ali Shilatifard, G R Scott Budinger, Harris Perlman
Little is known about the relative importance of monocyte and tissue-resident macrophages in the development of lung fibrosis. We show that specific genetic deletion of monocyte-derived alveolar macrophages after their recruitment to the lung ameliorated lung fibrosis, whereas tissue-resident alveolar macrophages did not contribute to fibrosis. Using transcriptomic profiling of flow-sorted cells, we found that monocyte to alveolar macrophage differentiation unfolds continuously over the course of fibrosis and its resolution...
August 7, 2017: Journal of Experimental Medicine
https://www.readbyqxmd.com/read/28669986/mitochondrial-control-of-immunity-beyond-atp
#18
REVIEW
Manan M Mehta, Samuel E Weinberg, Navdeep S Chandel
Mitochondria are important signalling organelles, and they dictate immunological fate. From T cells to macrophages, mitochondria form the nexus of the various metabolic pathways that define each immune cell subset. In this central position, mitochondria help to control the various metabolic decision points that determine immune cell function. In this Review, we discuss how mitochondrial metabolism varies across different immune cell subsets, how metabolic signalling dictates cell fate and how this signalling could potentially be targeted therapeutically...
October 2017: Nature Reviews. Immunology
https://www.readbyqxmd.com/read/28564604/cancer-associated-idh1-promotes-growth-and-resistance-to-targeted-therapies-in-the-absence-of-mutation
#19
Andrea E Calvert, Alexandra Chalastanis, Yongfei Wu, Lisa A Hurley, Fotini M Kouri, Yingtao Bi, Maureen Kachman, Jasmine L May, Elizabeth Bartom, Youjia Hua, Rama K Mishra, Gary E Schiltz, Oleksii Dubrovskyi, Andrew P Mazar, Marcus E Peter, Hongwu Zheng, C David James, Charles F Burant, Navdeep S Chandel, Ramana V Davuluri, Craig Horbinski, Alexander H Stegh
Oncogenic mutations in two isocitrate dehydrogenase (IDH)-encoding genes (IDH1 and IDH2) have been identified in acute myelogenous leukemia, low-grade glioma, and secondary glioblastoma (GBM). Our in silico and wet-bench analyses indicate that non-mutated IDH1 mRNA and protein are commonly overexpressed in primary GBMs. We show that genetic and pharmacologic inactivation of IDH1 decreases GBM cell growth, promotes a more differentiated tumor cell state, increases apoptosis in response to targeted therapies, and prolongs the survival of animal subjects bearing patient-derived xenografts (PDXs)...
May 30, 2017: Cell Reports
https://www.readbyqxmd.com/read/28504707/regulation-of-mitochondrial-biogenesis-in-erythropoiesis-by-mtorc1-mediated-protein-translation
#20
COMPARATIVE STUDY
Xin Liu, Yuannyu Zhang, Min Ni, Hui Cao, Robert A J Signer, Dan Li, Mushan Li, Zhimin Gu, Zeping Hu, Kathryn E Dickerson, Samuel E Weinberg, Navdeep S Chandel, Ralph J DeBerardinis, Feng Zhou, Zhen Shao, Jian Xu
Advances in genomic profiling present new challenges of explaining how changes in DNA and RNA are translated into proteins linking genotype to phenotype. Here we compare the genome-scale proteomic and transcriptomic changes in human primary haematopoietic stem/progenitor cells and erythroid progenitors, and uncover pathways related to mitochondrial biogenesis enhanced through post-transcriptional regulation. Mitochondrial factors including TFAM and PHB2 are selectively regulated through protein translation during erythroid specification...
June 2017: Nature Cell Biology
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