ArticleThe Journal of nutrition2009
Glycerol-3-phosphate acyltransferase 1 is essential for the immune response to infection with coxsackievirus B3 in mice.
Article in The Journal of nutrition, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Transcriptomic Changes ofFrontiers in microbiology · 2022Article
- Update on glycerol-3-phosphate acyltransferases: the roles in the development of insulin resistance.Nutrition & diabetes · 2018Review
- Association between theInternational journal of clinical and experimental pathology · 2018Article
- Pathogenicity-associated protein domains: The fiercely-conserved evolutionary signatures.Gene reports · 2017Review
- Diet-induced obesity prolongs neuroinflammation and recruits CCR2(+) monocytes to the brain following herpes simplex virus (HSV)-1 latency in mice.Brain, behavior, and immunity · 2016Article
- Article
- Mitochondrial glycerol-3-phosphate acyltransferase-1 is essential for murine CD4(+) T cell metabolic activation.Biochimica et biophysica acta · 2014Article
- Chemical modulation of glycerolipid signaling and metabolic pathways.Biochimica et biophysica acta · 2014Review
- Eicosanoids in metabolic syndrome.Advances in pharmacology (San Diego, Calif.) · 2013Review
- Article
- Mammalian triacylglycerol metabolism: synthesis, lipolysis, and signaling.Chemical reviews · 2011Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Livers and hearts from mice deficient in glycerol-3-phosphate acyltransferase 1 (GPAT1; Gpat1(-/-)) have a decreased content of glycerolipid intermediates and triacylglycerol, an altered composition of liver phospholipids, and elevated markers of oxidative stress. Compared with control C57BL/6 mice, infection of Gpat1(-/-) mice with coxsackievirus B3 (CVB3) resulted in higher mortality, an approximately 50% increase in heart pathology, a significant increase in liver viral titers, and a 100-fold increase in heart viral titers. Moreover, heart mRNA levels for proinflammatory cytokines tumor necrosis factor-alpha, interleukin (IL)-6, and IL-1B were increased in the Gpat1(-/-) mice. Loss of Gpat1 also resulted in dysregulation of specific immune cells. Splenic dendritic cells from Gpat1(-/-) mice were fully capable of stimulating T cells from control mice; however, splenic T cells from Gpat1(-/-) mice were defective in their response to CVB3 antigen. Our data indicate that a lack of GPAT1 activity affects both innate and adaptive immune mechanisms. Innate mechanisms may be affected by altered membrane composition or host redox status, whereas the adaptive response may require GPAT1 activity itself.
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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.