Isoleucine deprivation of cellular monolayers prior to infection has been reported to result in partial complementation of a herpes simplex virus type 1 (HSV-1) ICP0 null (ICP0(-)) mutant. We now report that glutamine deprivation alone is able to enhance the plating efficiency of an ICP0(-) virus and that isoleucine deprivation has little or no effect. Because a low glutamine level is associated with stress and because stress is known to induce reactivation, low levels of glutamine may be relevant to the reactivation of HSV-1 from latency. Additionally, we demonstrate that arginine and methionine deprivation result in partial complementation of the ICP0(-) virus.
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http://dx.doi.org/10.1128/JVI.01086-08 | DOI Listing |
Nutrients
January 2025
Department of Gastrointestinal Surgery, Graduate School of Medicine, Kyoto University, Kyoto 606-8507, Japan.
Reprogramming of energy metabolism to support cellular growth is a "hallmark" of cancer, allowing cancer cells to balance the catabolic demands with the anabolic needs of producing the nucleotides, amino acids, and lipids necessary for tumor growth. Metabolic alterations, or "addiction", are promising therapeutic targets and the focus of many drug discovery programs. Asparagine metabolism has gained much attention in recent years as a novel target for cancer therapy.
View Article and Find Full Text PDFNat Commun
January 2025
Center of Growth, Metabolism and Aging, Key Laboratory of Bio-Resource and Eco-Environment, Ministry of Education, College of Life Sciences, Sichuan University, Chengdu, China.
Glucose deprivation, a hallmark of the tumor microenvironment, compels tumor cells to seek alternative energy sources for survival and growth. Here, we show that glucose deprivation upregulates the expression of mitochondrial-cytochrome c oxidase II (MT-CO2), a subunit essential for the respiratory chain complex IV, in facilitating glutaminolysis and sustaining tumor cell survival. Mechanistically, glucose deprivation activates Ras signaling to enhance MT-CO2 transcription and inhibits IGF2BP3, an RNA-binding protein, to stabilize MT-CO2 mRNA.
View Article and Find Full Text PDFBiochim Biophys Acta Rev Cancer
December 2024
Key Laboratory of Cell Biology, Department of Cell Biology, Ministry of Public Health and Key Laboratory of Medical Cell Biology, Ministry of Education, School of Life Sciences, China Medical University, Shenyang, Liaoning 110122, China. Electronic address:
Glutamine, akin to glucose, is a fundamental nutrient for human physiology. Tumor progression is often accompanied by elevated glutamine consumption, resulting in a disrupted nutritional balance and metabolic reprogramming within the tumor microenvironment. Furthermore, immune cells, which depend on glutamine for metabolic support, may experience functional impairments and dysregulation.
View Article and Find Full Text PDFJ Invest Dermatol
December 2024
Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Electronic address:
T9 cells are implicated in allergic skin inflammation and depend on the transcription factor PPAR-γ for full effector function. In this study, we uncovered a role for PPAR-γ in the amino acid metabolism of human T9 cells. In in-vitro-primed T9 cells, PPAR-γ expression positively correlated with the expression of SLC7A8, which encodes LAT2, a transporter of large neutral amino acids, including cystine.
View Article and Find Full Text PDFCell Death Differ
December 2024
Division of Hematology and Oncology, Department of Pediatrics, Penn State College of Medicine, Hershey, PA, USA.
Disulfidptosis is a recently identified form of cell death characterized by the aberrant accumulation of cellular disulfides. This process primarily occurs in glucose-starved cells expressing higher levels of SLC7A11 and has been proposed as a therapeutic strategy for cancers with hyperactive SCL7A11. However, the potential for inducing disulfidptosis through other mechanisms in cancers remains unclear.
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