ArticleCancer biology & therapy2014
Mice lacking G0S2 are lean and cold-tolerant.
Article in Cancer biology & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 37 citations in OpenAlex.
- Human Intervention Study to Assess the Effects of Supplementation with Olive Leaf Extract on Peripheral Blood Mononuclear Cell Gene Expression.International journal of molecular sciences · 2016Trial
- Identification of differentially expressed lncRNAs in different daily weight gains of Jiangquan black pigs and functional analysis of LOC100518120.BMC genomics · 2026Article
- Novel Insights into G0S2 as a Central Regulator of Lipid Metabolism and Its Implications for Meat Quality.Animals : an open access journal from MDPI · 2026Review
- Recent advances on the role of G0S2.Discover oncology · 2025Review
- Absence of the intracellular lipolytic inhibitor G0S2 enhances intravascular triglyceride clearance and abolishes diet-induced hypertriglyceridemia.The Journal of clinical investigation · 2025Article
- G0S2 promotes antiestrogenic and pro-migratory responses in ER+ and ER- breast cancer cells.Translational oncology · 2023Article
- Prediction of cellular targets in diabetic kidney diseases with single-cell transcriptomic analysis of db/db mouse kidneys.Journal of cell communication and signaling · 2023Article
- Identification of motifs and mechanisms for lipid droplet targeting of the lipolytic inhibitors G0S2 and HIG2.Journal of cell science · 2022Article
- Loss of G0/G1 switch gene 2 (G0S2) promotes disease progression and drug resistance in chronic myeloid leukaemia (CML) by disrupting glycerophospholipid metabolism.Clinical and translational medicine · 2022Article
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- Adipose Triglyceride Lipase in Hepatic Physiology and Pathophysiology.Biomolecules · 2021Review
- Lipolysis: cellular mechanisms for lipid mobilization from fat stores.Nature metabolism · 2021Review
- Integrative ATAC-seq and RNA-seq Analysis of the Longissimus Muscle of Luchuan and Duroc Pigs.Frontiers in nutrition · 2021Article
- Hypoxia, hypoxia-inducible gene 2 (HIG2)/HILPDA, and intracellular lipolysis in cancer.Cancer letters · 2020Review
- Leptin: Is It Thermogenic?Endocrine reviews · 2020Review
- RNA-seq analysis identifies cytoskeletal structural genes and pathways for meat quality in beef.PloS one · 2020Article
- Identification of an intrinsic lysophosphatidic acid acyltransferase activity in the lipolytic inhibitor GFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Adipose Triglyceride Lipase Regulation: An Overview.Current protein & peptide science · 2018Review
- G0S2: A small giant controller of lipolysis and adipose-liver fatty acid flux.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
G 0/G 1 switch gene 2 (G0S2) is a protein that was first identified in a search for lymphocyte G 0/G 1 switch genes. A direct role for G0S2 in cell cycle regulation has proven elusive. Yet, there is prior evidence for G0S2 functioning in tumor suppression, immune regulation and lipolysis. To explore definitively G0S2 functions, mice lacking G0S2 were generated and characterized. G0S2(-/-) mice were born at a Mendelian ratio and were phenotypically normal, with the exception of a possible lactation defect. G0S2(-/-) female mice carried viable pups to term, but could not typically sustain them beyond 48 h. G0S2 is shown here to be most highly expressed in adipose tissue. It is also expressed in liver, skeletal muscle, lung, ventricles of the heart, and components of the kidney. G0S2 loss significantly decreased relative body weight gain as compared with wild-type (WT) (G0S2(+/+)) mice, with a significant decrease in gonadal fat pad weight and a significant increase in serum glycerol levels. This decreased relative body weight gain is not associated with a significant decrease in food intake or increase in activity of G0S2(-/-) mice. In fact, G0S2(-/-) mice were significantly less active at night than G0S2(+/+) mice. When fed with a high fat diet (45% fat diet), G0S2 loss did not prevent diet-induced obesity in mice. Intriguingly, G0S2 loss improved acute cold tolerance, augmenting expression of genes involved in thermogenesis. In summary, in vivo roles for G0S2 were found in lactation, energy balance, and thermogenesis. This study provides a basis for tumor suppressive effects of G0S2 by regulating lipolysis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.