Journal articles: 'Cell metabolism Regulation'

1

GAO, Ping, and HaoRan WEI. "Regulation of cancer cell metabolism." SCIENTIA SINICA Vitae 47, no. 1 (January 1, 2017): 132–39. http://dx.doi.org/10.1360/n052016-00334.

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Hagel-Bradway, S., and R. Dziak. "Regulation of bone cell metabolism." Journal of Oral Pathology and Medicine 18, no. 6 (July 1989): 344–51. http://dx.doi.org/10.1111/j.1600-0714.1989.tb01564.x.

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Sun, Xinghui, and Mark W. Feinberg. "Regulation of Endothelial Cell Metabolism." Arteriosclerosis, Thrombosis, and Vascular Biology 35, no. 1 (January 2015): 13–15. http://dx.doi.org/10.1161/atvbaha.114.304869.

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Cairns, Rob A., Isaac S. Harris, and Tak W. Mak. "Regulation of cancer cell metabolism." Nature Reviews Cancer 11, no. 2 (January 24, 2011): 85–95. http://dx.doi.org/10.1038/nrc2981.

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Brynildsen, M. P., W. W. Wong, and J. C. Liao. "Transcriptional regulation and metabolism." Biochemical Society Transactions 33, no. 6 (October 26, 2005): 1423–26. http://dx.doi.org/10.1042/bst0331423.

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Understanding organisms from a systems perspective is essential for predicting cellular behaviour as well as designing gene-metabolic circuits for novel functions. The structure, dynamics and interactions of cellular networks are all vital components of systems biology. To facilitate investigation of these aspects, we have developed an integrative technique called network component analysis, which utilizes mRNA expression and transcriptional network connectivity to determine network component dynamics, functions and interactions. This approach has been applied to elucidate transcription factor dynamics in Saccharomyces cerevisiae cell-cycle regulation, detect cross-talks in Escherichia coli two-component signalling pathways, and characterize E. coli carbon source transition. An ultimate test of system-wide understanding is the ability to design and construct novel gene-metabolic circuits. To this end, artificial feedback regulation, cell–cell communication and oscillatory circuits have been constructed, which demonstrate the design principles of gene-metabolic regulation in the cell.

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Pokotylo, I. V. "Lipoxygenases and plant cell metabolism regulation." Ukrainian Biochemical Journal 87, no. 2 (April 27, 2015): 41–55. http://dx.doi.org/10.15407/ubj87.02.041.

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Spiegel, Sarah, and Alfred H. Merrill. "Sphingolipid metabolism and cell growth regulation." FASEB Journal 10, no. 12 (October 1996): 1388–97. http://dx.doi.org/10.1096/fasebj.10.12.8903509.

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Hough, Kenneth P., Danielle A. Chisolm, and Amy S. Weinmann. "Transcriptional regulation of T cell metabolism." Molecular Immunology 68, no. 2 (December 2015): 520–26. http://dx.doi.org/10.1016/j.molimm.2015.07.038.

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Wang, Yin-Hu, Anthony Y. Tao, Martin Vaeth, and Stefan Feske. "Calcium regulation of T cell metabolism." Current Opinion in Physiology 17 (October 2020): 207–23. http://dx.doi.org/10.1016/j.cophys.2020.07.016.

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Bailey, Shannon M., Uduak S. Udoh, and Martin E. Young. "Circadian regulation of metabolism." Journal of Endocrinology 222, no. 2 (June 13, 2014): R75—R96. http://dx.doi.org/10.1530/joe-14-0200.

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In association with sleep–wake and fasting–feeding cycles, organisms experience dramatic oscillations in energetic demands and nutrient supply. It is therefore not surprising that various metabolic parameters, ranging from the activity status of molecular energy sensors to circulating nutrient levels, oscillate in time-of-day-dependent manners. It has become increasingly clear that rhythms in metabolic processes are not simply in response to daily environmental/behavioral influences, but are driven in part by cell autonomous circadian clocks. By synchronizing the cell with its environment, clocks modulate a host of metabolic processes in a temporally appropriate manner. The purpose of this article is to review current understanding of the interplay between circadian clocks and metabolism, in addition to the pathophysiologic consequences of disruption of this molecular mechanism, in terms of cardiometabolic disease development.

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Plas, David R., and Craig B. Thompson. "Cell metabolism in the regulation of programmed cell death." Trends in Endocrinology & Metabolism 13, no. 2 (March 2002): 75–78. http://dx.doi.org/10.1016/s1043-2760(01)00528-8.

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Jiang, Yajian, and Daisuke Nakada. "Cell intrinsic and extrinsic regulation of leukemia cell metabolism." International Journal of Hematology 103, no. 6 (February 20, 2016): 607–16. http://dx.doi.org/10.1007/s12185-016-1958-6.

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Boutilier, Robert G., and Ralph A. Ferguson. "Nucleated red cell function: metabolism and pH regulation." Canadian Journal of Zoology 67, no. 12 (December 1, 1989): 2986–93. http://dx.doi.org/10.1139/z89-421.

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The full extent and apportionment of aerobic and anaerobic contributions to energy transduction for membrane pumps associated with cellular pH regulation are very poorly understood. One way of approaching this problem at the cellular level is by using the nucleated erythrocyte as a model cell. Indeed, the aerobic and anaerobic capacity of salmonid erythrocytes and their β-adrenergic mediated pH regulation offers a model "pH regulating system" for examining cellular strategies of response to acute and (or) chronic changes in oxygen availability. Much of our work has focused on the balance between metabolic energy production and the maintenance of erythrocytic pH through primarily or secondarily active ionic exchange mechanisms at the cell membrane. Upon adrenergic stimulation, a rise in cyclic AMP activates the Na+–H+ exchanger, leading to cell alkalinization and an elevation of intracellular Na+. The increased Na+ evidently stimulates Na+,K+-ATPase activity and the increased ATP consumption is matched with aerobic energy production. The pHi that is subsequently established appears to be set by levels of poly anionic phosphates.

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Kumar, Ajay, Kalyani Pyaram, Emily Yarosz, Shailendra Giri, and Cheong-Hee Chang. "Regulation of NKT cell metabolism by PLZF." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 167.2. http://dx.doi.org/10.4049/jimmunol.200.supp.167.2.

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Abstract Cellular metabolism and signaling pathways are the key regulators to determine T cell fate, survival and function, particularly during activation. Resting CD4 and CD8 T cells use oxidative phosphorylation as a primary energy source but switches to glycolysis upon activation, which is necessary to produce biomolecules for cell proliferation and function. Failure of this reprogramming is detrimental for T cell mediated immunity. However, little is understood about how NKT cells control their metabolism to survive and function. We found that NKT cells operate distinctly different metabolic programming from CD4 T cells for their survival and function. Supporting evidence includes that, unlike CD4 T cells, oxidative phosphorylation seems to be preferred over glycolysis in NKT cells even after stimulation as revealed by lower level of intracellular lactate produced by NKT cells than CD4 cells after activation. These cells also seem to have high energy as revealed by higher ATP in NKT cells. Although the proper maintenance and functions of stimulated NKT cells need glucose, they are sensitive to the elevated glycolytic potential compared to CD4 T cells resulting in spontaneous cell death accompanied by hyperproliferation. Importantly, PLZF is the essential regulator of NKT cells’ metabolism so that similar changes of glucose metabolism were found in CD4 T cells expressing PLZF. Conversely, NKT cells with haplodeficient PLZF were more tolerant to increased glycolysis, strongly supporting the key role of PLZF in NKT cell metabolism and homeostasis. We are currently investigating the underlying mechanisms by which PLZF controls metabolism in NKT cells using several approaches including metabolomics.

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Lukey, Michael J., and Richard A. Cerione. "The regulation of cancer cell glutamine metabolism." Translational Cancer Research 5, S6 (November 2016): S1297—S1298. http://dx.doi.org/10.21037/tcr.2016.11.39.

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Kořánová, Tereza, Lukáš Dvořáček, Dana Grebeňová, Pavla Röselová, Adam Obr, and Kateřina Kuželová. "PAK1 and PAK2 in cell metabolism regulation." Journal of Cellular Biochemistry 123, no. 2 (November 8, 2021): 375–89. http://dx.doi.org/10.1002/jcb.30175.

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Vüqar qızı Mehdiyeva, Günel. "Regulation of cell metabolism of Chlorella vulgaris." NATURE AND SCIENCE 18, no. 3 (March 19, 2022): 25–28. http://dx.doi.org/10.36719/2707-1146/18/25-28.

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Mikroyosunların inkişaf prosesini məhdudlaşdıran şəraitdə (üzvi və mineral maddələrin çatışmazlığı, müxtəlif stress faktorları - işıq, temperatur və s.) ehtiyat maddə və metabolit toplama qabiliyyəti elmə yaxşı məlumdur. Bu baxımdan son illərdə Chlorella vulgaris hüceyrəsində bu və ya digər məhsulun toplanması istiqamətində metabolizmin məqsədyönlü idarə olunması texnologiyası araşdırılır. Təqdim edilən məqalədə fiziki və kimyəvi faktorlarının yaratdığı müxtəlif stress şəraitində C.vulgaris hüceyrəsində toplanan lipid, karbohidrat, antioksidant molekulları haqqında ümumi məlumat öz əksini tapır. Bundan əlavə son dövrlər dünyada aktual olan “algae-refinery concept” əsasında mikroyosun hüceyrəsindən əldə olunan birləşmələrin müxtəlif sahələrdə istifadəsi haqqında məlumat verilir. Açar sözlər: Chlorella vulgaris, mikroyosunlar, antioksidant, hüceyrə metabolizmi, inkişaf faktorları Gunel Vugar Mehdiyeva Regulation of cell metabolism of Chlorella vulgaris Abstract The ability to accumulate nutrients and metabolites under conditions that limit the development of microalgae (deficiency of organic and mineral substances, various stress factors - light, temperature, etc.) is well known to science. In recent years, the technology of purposeful control of metabolism in order to collect any product in the cell of Chlorella vulgaris is being studied. The presented article provides general information about lipid, carbohydrate and antioxidant molecules accumulated in C. vulgaris cell under various stress conditions caused by physical and chemical factors. In addition, information is provided on the use of compounds derived from microalgae cells in various fields on the basis of the “algae-refinery concept”, which has recently become an actual issue in the world. Key words: Chlorella vulgaris, microalgae, antioxidants, cell metabolism, growth factors

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Ghaffari, Saghi. "Regulation of Hematopoietic Stem Cell Mitochondrial Metabolism." Blood 128, no. 22 (December 2, 2016): SCI—33—SCI—33. http://dx.doi.org/10.1182/blood.v128.22.sci-33.sci-33.

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Abstract Hematopoietic stem cells (HSCs) like most, if not all, adult stem cells are primarily quiescent but have the potential to become highly active on demand. HSC quiescence is maintained by glycolytic metabolism and low levels of reactive oxygen species (ROS), which indicate that mitochondria are relatively inactive in quiescent HSC. However, HSC cycling - and exit of quiescence state - require a swift metabolic switch from glycolysis to mitochondrial oxidative phosphorylation. To improve our understanding of mechanisms that integrate energy metabolism with HSC homeostasis, my laboratory has been focused on the transcription factor FOXO3, which is critical for the maintenance of HSC quiescence and redox state and is implicated in HSC aging. We showed recently that FOXO3 is key to HSC mitochondrial metabolism, independent of its inhibition of ROS or mTOR signaling. Mitochondria divide and fuse constantly in part to segregate and dispose of their damaged counterparts. These processes are influenced by and highly linked to mitochondrial metabolism. We have recently developed imaging approaches to study HSC mitochondrial divisions. Mechanisms by which FOXO3 regulates HSC mitochondria and the impact of impaired FOXO3 on the HSC health and activity, and mitochondrial network will be discussed. Detailed understanding of the mitochondrial metabolism and divisions in HSC and their relationship to nuclear transcription are likely to have broad implications for the state of HSC fitness, regenerative capacity and aging. Disclosures No relevant conflicts of interest to declare.

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19

Jackowski, Suzanne. "Cell Cycle Regulation of Membrane Phospholipid Metabolism." Journal of Biological Chemistry 271, no. 34 (August 23, 1996): 20219–22. http://dx.doi.org/10.1074/jbc.271.34.20219.

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Gibart, Laetitia, Rajeev Khoodeeram, Gilles Bernot, Jean-Paul Comet, and Jean-Yves Trosset. "Regulation of Eukaryote Metabolism: An Abstract Model Explaining the Warburg/Crabtree Effect." Processes 9, no. 9 (August 25, 2021): 1496. http://dx.doi.org/10.3390/pr9091496.

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Adaptation of metabolism is a response of many eukaryotic cells to nutrient heterogeneity in the cell microenvironment. One of these adaptations is the shift from respiratory to fermentative metabolism, also called the Warburg/Crabtree effect. It is a response to a very high nutrient increase in the cell microenvironment, even in the presence of oxygen. Understanding whether this metabolic transition can result from basic regulation signals between components of the central carbon metabolism are the the core question of this work. We use an extension of the René Thomas modeling framework for representing the regulations between the main catabolic and anabolic pathways of eukaryotic cells, and formal methods for confronting models with known biological properties in different microenvironments. The formal model of the regulation of eukaryote metabolism defined and validated here reveals the conditions under which this metabolic phenotype switch occurs. It clearly proves that currently known regulating signals within the main components of central carbon metabolism can be sufficient to bring out the Warburg/Crabtree effect. Moreover, this model offers a general perspective of the regulation of the central carbon metabolism that can be used to study other biological questions.

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Steinert, Elizabeth M., Karthik Vasan, and Navdeep S. Chandel. "Mitochondrial Metabolism Regulation of T Cell–Mediated Immunity." Annual Review of Immunology 39, no. 1 (April 26, 2021): 395–416. http://dx.doi.org/10.1146/annurev-immunol-101819-082015.

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Recent evidence supports the notion that mitochondrial metabolism is necessary for T cell activation, proliferation, and function. Mitochondrial metabolism supports T cell anabolism by providing key metabolites for macromolecule synthesis and generating metabolites for T cell function. In this review, we focus on how mitochondrial metabolism controls conventional and regulatory T cell fates and function.

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Alptekin, Ahmet, Bingwei Ye, and Han-Fei Ding. "Transcriptional Regulation of Stem Cell and Cancer Stem Cell Metabolism." Current Stem Cell Reports 3, no. 1 (January 21, 2017): 19–27. http://dx.doi.org/10.1007/s40778-017-0071-y.

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Madi, Alaa, and Guoliang Cui. "Regulation of immune cell metabolism by cancer cell oncogenic mutations." International Journal of Cancer 147, no. 2 (February 25, 2020): 307–16. http://dx.doi.org/10.1002/ijc.32888.

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Wang, Jian, and Kostas Pantopoulos. "Regulation of cellular iron metabolism." Biochemical Journal 434, no. 3 (February 24, 2011): 365–81. http://dx.doi.org/10.1042/bj20101825.

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Iron is an essential but potentially hazardous biometal. Mammalian cells require sufficient amounts of iron to satisfy metabolic needs or to accomplish specialized functions. Iron is delivered to tissues by circulating transferrin, a transporter that captures iron released into the plasma mainly from intestinal enterocytes or reticuloendothelial macrophages. The binding of iron-laden transferrin to the cell-surface transferrin receptor 1 results in endocytosis and uptake of the metal cargo. Internalized iron is transported to mitochondria for the synthesis of haem or iron–sulfur clusters, which are integral parts of several metalloproteins, and excess iron is stored and detoxified in cytosolic ferritin. Iron metabolism is controlled at different levels and by diverse mechanisms. The present review summarizes basic concepts of iron transport, use and storage and focuses on the IRE (iron-responsive element)/IRP (iron-regulatory protein) system, a well known post-transcriptional regulatory circuit that not only maintains iron homoeostasis in various cell types, but also contributes to systemic iron balance.

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Hoffmann, Lars, Gernot Brauers, Thor Gehrmann, Dieter Häussinger, Ertan Mayatepek, Freimut Schliess, and Bernd C. Schwahn. "Osmotic regulation of hepatic betaine metabolism." American Journal of Physiology-Gastrointestinal and Liver Physiology 304, no. 9 (May 1, 2013): G835—G846. http://dx.doi.org/10.1152/ajpgi.00332.2012.

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Betaine critically contributes to the control of hepatocellular hydration and provides protection of the liver from different kinds of stress. To investigate how the hepatocellular hydration state affects gene expression of enzymes involved in the metabolism of betaine and related organic osmolytes, we used quantitative RT-PCR gene expression studies in rat hepatoma cells as well as metabolic and gene expression profiling in primary hepatocytes of both wild-type and 5,10-methylenetetrahydrofolate reductase (MTHFR)-deficient mice. Anisotonic incubation caused coordinated adaptive changes in the expression of various genes involved in betaine metabolism, in particular of betaine homocysteine methyltransferase, dimethylglycine dehydrogenase, and sarcosine dehydrogenase. The expression of betaine-degrading enzymes was downregulated by cell shrinking and strongly induced by an increase in cell volume under hypotonic conditions. Metabolite concentrations in the culture system changed accordingly. Expression changes were mediated through tyrosine kinases, cyclic nucleotide-dependent protein kinases, and JNK-dependent signaling. Assessment of hepatic gene expression using a customized microarray chip showed that hepatic betaine depletion in MTHFR −/− mice was associated with alterations that were comparable to those induced by cell swelling in hepatocytes. In conclusion, the adaptation of hepatocytes to changes in cell volume involves the coordinated regulation of betaine synthesis and degradation and concomitant changes in intracellular osmolyte concentrations. The existence of such a well-orchestrated response underlines the importance of cell volume homeostasis for liver function and of methylamine osmolytes such as betaine as hepatic osmolytes.

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Daddaoua, Abdelali, Tino Krell, and Juan-Luis Ramos. "Regulation of Glucose Metabolism inPseudomonas." Journal of Biological Chemistry 284, no. 32 (June 8, 2009): 21360–68. http://dx.doi.org/10.1074/jbc.m109.014555.

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Young, Andrew A. "Amylin regulation of fuel metabolism." Journal of Cellular Biochemistry 55, S1994A (1994): 12–18. http://dx.doi.org/10.1002/jcb.240550003.

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Wang, Fang, Dahai Zhang, Andrea Wan, and Brian Rodrigues. "Endothelial Cell Regulation of Cardiac Metabolism Following Diabetes." Cardiovascular & Hematological Disorders-Drug Targets 14, no. 2 (August 31, 2014): 121–25. http://dx.doi.org/10.2174/1871529x14666140505123221.

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McHugh, Jessica. "T cell metabolism connects complement and autoimmune regulation." Nature Reviews Rheumatology 14, no. 7 (May 30, 2018): 383. http://dx.doi.org/10.1038/s41584-018-0027-3.

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Brahimi-Horn, M. Christiane, and Jacques Pouysségur. "Hypoxia in cancer cell metabolism and pH regulation." Essays in Biochemistry 43 (August 10, 2007): 165–78. http://dx.doi.org/10.1042/bse0430165.

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At a molecular level, hypoxia induces the stabilization and activation of the α-subunit of an α/β heterodimeric transcription factor, appropriately termed HIF (hypoxia-inducible factor). Hypoxia is encountered, in particular, in tumour tissues, as a result of an insufficient and defective vasculature present in a highly proliferative tumour mass. In this context the active HIF heterodimer binds to and induces a panel of genes that lead to modification in a vast range of cellular functions that allow cancer cells to not only survive but to continue to proliferate and metastasize. Therefore HIF plays a key role in tumorigenesis, tumour development and metastasis, and its expression in solid tumours is associated with a poor patient outcome. Among the many genes induced by HIF are genes responsible for glucose transport and glucose metabolism. The products of these genes allow cells to adapt to cycles of hypoxic stress by maintaining a level of ATP sufficient for survival and proliferation. Whereas normal cells metabolize glucose through a cytoplasmic- and mitochondrial-dependent pathway, cancer cells preferentially use a cytoplasmic, glycolytic pathway that leads to an increased acid load due, in part, to the high level of production of lactic acid. This metabolic predilection of cancer cells is primarily dependent directly on the HIF activity but also indirectly through changes in the activity of tumour suppressors and oncogenes. A better understanding of HIF-dependent metabolism and pH regulation in cancer cells should lead to further development of diagnostic tools and novel therapeutics that will bring benefit to cancer patients.

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Friedman, Susan J., Heidi Bokesch, and Philip Skehan. "The regulation of sterol metabolism by cell interactions." Experimental Cell Research 172, no. 2 (October 1987): 463–73. http://dx.doi.org/10.1016/0014-4827(87)90404-6.

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Hu, Zhilin, Qiang Zou, and Bing Su. "Regulation of T cell immunity by cellular metabolism." Frontiers of Medicine 12, no. 4 (August 2018): 463–72. http://dx.doi.org/10.1007/s11684-018-0668-2.

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Eelen, Guy, Pauline de Zeeuw, Lucas Treps, Ulrike Harjes, Brian W. Wong, and Peter Carmeliet. "Endothelial Cell Metabolism." Physiological Reviews 98, no. 1 (January 1, 2018): 3–58. http://dx.doi.org/10.1152/physrev.00001.2017.

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Endothelial cells (ECs) are more than inert blood vessel lining material. Instead, they are active players in the formation of new blood vessels (angiogenesis) both in health and (life-threatening) diseases. Recently, a new concept arose by which EC metabolism drives angiogenesis in parallel to well-established angiogenic growth factors (e.g., vascular endothelial growth factor). 6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3-driven glycolysis generates energy to sustain competitive behavior of the ECs at the tip of a growing vessel sprout, whereas carnitine palmitoyltransferase 1a-controlled fatty acid oxidation regulates nucleotide synthesis and proliferation of ECs in the stalk of the sprout. To maintain vascular homeostasis, ECs rely on an intricate metabolic wiring characterized by intracellular compartmentalization, use metabolites for epigenetic regulation of EC subtype differentiation, crosstalk through metabolite release with other cell types, and exhibit EC subtype-specific metabolic traits. Importantly, maladaptation of EC metabolism contributes to vascular disorders, through EC dysfunction or excess angiogenesis, and presents new opportunities for anti-angiogenic strategies. Here we provide a comprehensive overview of established as well as newly uncovered aspects of EC metabolism.

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Soboll, Sibylle. "Regulation of energy metabolism in liver." Journal of Bioenergetics and Biomembranes 27, no. 6 (December 1995): 571–82. http://dx.doi.org/10.1007/bf02111655.

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Ma, Qing, Jing Wang, Yaoyao Ren, Fanlu Meng, and Lili Zeng. "Pathological Mechanistic Studies of Osimertinib Resistance in Non-Small-Cell Lung Cancer Cells Using an Integrative Metabolomics-Proteomics Analysis." Journal of Oncology 2020 (March 17, 2020): 1–12. http://dx.doi.org/10.1155/2020/6249829.

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Background. Osimertinib is the first-line therapeutic option for the T790M-mutant non-small-cell lung cancer and the acquired resistance obstructs its application. It is an urgent challenge to identify the potential mechanisms of osimertinib resistance for uncovering some novel therapeutic approaches. Methods. In the current study, the cell metabolomics based on ultra-high-performance liquid chromatography coupled with linear ion trap-Orbitrap mass spectrometry and the qualitative and tandem mass tags quantitative proteomics were performed. Results. 54 differential metabolites and 195 differentially expressed proteins were, respectively, identified. The amino acids metabolisms were significantly altered. HIF-1 signaling pathway modulating P-glycoproteins expression, PI3K-Akt pathway regulating survivin expression, and oxidative phosphorylation were upregulated, while arginine and proline metabolism regulating NO production and glycolysis/gluconeogenesis were downregulated during osimertinib resistance. Conclusion. The regulation of HIF-1 and PI3K-Akt signaling pathway, energy supply process, and amino acids metabolism are the promising therapeutic tactics for osimertinib resistance.

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Yan, Jiawei, and Tiffany Horng. "Lipid Metabolism in Regulation of Macrophage Functions." Trends in Cell Biology 30, no. 12 (December 2020): 979–89. http://dx.doi.org/10.1016/j.tcb.2020.09.006.

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Kardassis, Dimitris, Efstathia Thymiakou, and Angeliki Chroni. "Genetics and regulation of HDL metabolism." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1867, no. 1 (January 2022): 159060. http://dx.doi.org/10.1016/j.bbalip.2021.159060.

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Goedeke, Leigh, Alexandre Wagschal, Carlos Fernández-Hernando, and Anders M. Näär. "miRNA regulation of LDL-cholesterol metabolism." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1861, no. 12 (December 2016): 2047–52. http://dx.doi.org/10.1016/j.bbalip.2016.03.007.

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Caldez, Matias J., Mikael Bjorklund, and Philipp Kaldis. "Cell cycle regulation in NAFLD: when imbalanced metabolism limits cell division." Hepatology International 14, no. 4 (June 22, 2020): 463–74. http://dx.doi.org/10.1007/s12072-020-10066-6.

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Nunnari, Jodi, and Johan Auwerx. "Editorial overview: Cell regulation: Cell biology, fueling a renaissance in metabolism." Current Opinion in Cell Biology 33 (April 2015): vii—viii. http://dx.doi.org/10.1016/j.ceb.2015.02.005.

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Armbruster, Ute, and Deserah D. Strand. "Regulation of chloroplast primary metabolism." Photosynthesis Research 145, no. 1 (June 14, 2020): 1–3. http://dx.doi.org/10.1007/s11120-020-00765-4.

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Mullur, Rashmi, Yan-Yun Liu, and Gregory A. Brent. "Thyroid Hormone Regulation of Metabolism." Physiological Reviews 94, no. 2 (April 2014): 355–82. http://dx.doi.org/10.1152/physrev.00030.2013.

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Thyroid hormone (TH) is required for normal development as well as regulating metabolism in the adult. The thyroid hormone receptor (TR) isoforms, α and β, are differentially expressed in tissues and have distinct roles in TH signaling. Local activation of thyroxine (T4), to the active form, triiodothyronine (T3), by 5′-deiodinase type 2 (D2) is a key mechanism of TH regulation of metabolism. D2 is expressed in the hypothalamus, white fat, brown adipose tissue (BAT), and skeletal muscle and is required for adaptive thermogenesis. The thyroid gland is regulated by thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH). In addition to TRH/TSH regulation by TH feedback, there is central modulation by nutritional signals, such as leptin, as well as peptides regulating appetite. The nutrient status of the cell provides feedback on TH signaling pathways through epigentic modification of histones. Integration of TH signaling with the adrenergic nervous system occurs peripherally, in liver, white fat, and BAT, but also centrally, in the hypothalamus. TR regulates cholesterol and carbohydrate metabolism through direct actions on gene expression as well as cross-talk with other nuclear receptors, including peroxisome proliferator-activated receptor (PPAR), liver X receptor (LXR), and bile acid signaling pathways. TH modulates hepatic insulin sensitivity, especially important for the suppression of hepatic gluconeogenesis. The role of TH in regulating metabolic pathways has led to several new therapeutic targets for metabolic disorders. Understanding the mechanisms and interactions of the various TH signaling pathways in metabolism will improve our likelihood of identifying effective and selective targets.

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Lane, Andrew N., and Teresa W.-M. Fan. "Regulation of mammalian nucleotide metabolism and biosynthesis." Nucleic Acids Research 43, no. 4 (January 27, 2015): 2466–85. http://dx.doi.org/10.1093/nar/gkv047.

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Abstract Nucleotides are required for a wide variety of biological processes and are constantly synthesized denovo in all cells. When cells proliferate, increased nucleotide synthesis is necessary for DNA replication and for RNA production to support protein synthesis at different stages of the cell cycle, during which these events are regulated at multiple levels. Therefore the synthesis of the precursor nucleotides is also strongly regulated at multiple levels. Nucleotide synthesis is an energy intensive process that uses multiple metabolic pathways across different cell compartments and several sources of carbon and nitrogen. The processes are regulated at the transcription level by a set of master transcription factors but also at the enzyme level by allosteric regulation and feedback inhibition. Here we review the cellular demands of nucleotide biosynthesis, their metabolic pathways and mechanisms of regulation during the cell cycle. The use of stable isotope tracers for delineating the biosynthetic routes of the multiple intersecting pathways and how these are quantitatively controlled under different conditions is also highlighted. Moreover, the importance of nucleotide synthesis for cell viability is discussed and how this may lead to potential new approaches to drug development in diseases such as cancer.

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Tiburcio, Antonio F., Teresa Altabella, Antoni Borrell, and Carles Masgrau. "Polyamine metabolism and its regulation." Physiologia Plantarum 100, no. 3 (July 1997): 664–74. http://dx.doi.org/10.1111/j.1399-3054.1997.tb03073.x.

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Arfin, Saniya, Niraj Kumar Jha, Saurabh Kumar Jha, Kavindra Kumar Kesari, Janne Ruokolainen, Shubhadeep Roychoudhury, Brijesh Rathi, and Dhruv Kumar. "Oxidative Stress in Cancer Cell Metabolism." Antioxidants 10, no. 5 (April 22, 2021): 642. http://dx.doi.org/10.3390/antiox10050642.

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Abstract:

Reactive oxygen species (ROS) are important in regulating normal cellular processes whereas deregulated ROS leads to the development of a diseased state in humans including cancers. Several studies have been found to be marked with increased ROS production which activates pro-tumorigenic signaling, enhances cell survival and proliferation and drives DNA damage and genetic instability. However, higher ROS levels have been found to promote anti-tumorigenic signaling by initiating oxidative stress-induced tumor cell death. Tumor cells develop a mechanism where they adjust to the high ROS by expressing elevated levels of antioxidant proteins to detoxify them while maintaining pro-tumorigenic signaling and resistance to apoptosis. Therefore, ROS manipulation can be a potential target for cancer therapies as cancer cells present an altered redox balance in comparison to their normal counterparts. In this review, we aim to provide an overview of the generation and sources of ROS within tumor cells, ROS-associated signaling pathways, their regulation by antioxidant defense systems, as well as the effect of elevated ROS production in tumor progression. It will provide an insight into how pro- and anti-tumorigenic ROS signaling pathways could be manipulated during the treatment of cancer.

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Thurnher, Martin, and Georg Gruenbacher. "T lymphocyte regulation by mevalonate metabolism." Science Signaling 8, no. 370 (March 31, 2015): re4. http://dx.doi.org/10.1126/scisignal.2005970.

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van Echten, G., and K. Sandhoff. "Ganglioside metabolism. Enzymology, Topology, and regulation." Journal of Biological Chemistry 268, no. 8 (March 1993): 5341–44. http://dx.doi.org/10.1016/s0021-9258(18)53324-x.

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McClay, Joseph L. "Epigenetic regulation of drug metabolism in aging." Aging 13, no. 13 (July 11, 2021): 16898–99. http://dx.doi.org/10.18632/aging.203312.

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Stouthamer, A. H. "Metabolic regulation including anaerobic metabolism inParacoccus denitrificans." Journal of Bioenergetics and Biomembranes 23, no. 2 (April 1991): 163–85. http://dx.doi.org/10.1007/bf00762216.

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Yamaguchi, Shinjiro. "Gibberellin Metabolism and its Regulation." Annual Review of Plant Biology 59, no. 1 (June 2008): 225–51. http://dx.doi.org/10.1146/annurev.arplant.59.032607.092804.

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Journal articles on the topic 'Cell metabolism Regulation'

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