ArticleJournal of virology2012
Xpr1 is an atypical G-protein-coupled receptor that mediates xenotropic and polytropic murine retrovirus neurotoxicity.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 29 citations in OpenAlex.
- RBM15-mediated m6A modification of XPR1 promotes the malignant progression of lung adenocarcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Comparative Gut Proteome ofMicroorganisms · 2025Article
- Structure and function of human XPR1 in phosphate export.Nature communications · 2025Article
- Inorganic phosphate exporter heterozygosity in mice leads to brain vascular calcification, microangiopathy, and microgliosis.Brain pathology (Zurich, Switzerland) · 2023Article
- PHOSPHATE exporter XPR1/SLC53A1 is required for the tumorigenicity of epithelial ovarian cancer.Cancer science · 2022Article
- Clinical implication of xenotropic and polytropic retrovirus receptor 1 in papillary thyroid carcinoma.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021Article
- Interplay between primary familial brain calcification-associated SLC20A2 and XPR1 phosphate transporters requires inositol polyphosphates for control of cellular phosphate homeostasis.The Journal of biological chemistry · 2020Article
- Identification of the Genetic Requirements for Zinc Tolerance and Toxicity inG3 (Bethesda, Md.) · 2020Article
- Xenotropic and polytropic retrovirus receptor 1 (XPR1) promotes progression of tongue squamous cell carcinoma (TSCC) via activation of NF-κB signaling.Journal of experimental & clinical cancer research : CR · 2019Article
- Vtc5, a Novel Subunit of the Vacuolar Transporter Chaperone Complex, Regulates Polyphosphate Synthesis and Phosphate Homeostasis in Yeast.The Journal of biological chemistry · 2016Article
- XPR1 mutations are a rare cause of primary familial brain calcification.Journal of neurology · 2016Article
- Neuropeptide Y Negatively Influences Monocyte Recruitment to the Central Nervous System during Retrovirus Infection.Journal of virology · 2015Article
- XPR1: a Gene Linked to Primary Familial Brain Calcification Might Help Explain a Spectrum of Neuropsychiatric Disorders.Journal of molecular neuroscience : MN · 2015Article
- Mutations in XPR1 cause primary familial brain calcification associated with altered phosphate export.Nature genetics · 2015Article
- Frequent infection of human cancer xenografts with murine endogenous retroviruses in vivo.Viruses · 2015Article
- Review
- Retroviral vectors: from cancer viruses to therapeutic tools.Human gene therapy · 2014Review
- Escape variants of the XPR1 gammaretrovirus receptor are rare due to reliance on a splice donor site and a short hypervariable loop.Virology · 2014Article
- The phosphate exporter xpr1b is required for differentiation of tissue-resident macrophages.Cell reports · 2014Article
- Xenotropic MLV envelope proteins induce tumor cells to secrete factors that promote the formation of immature blood vessels.Retrovirology · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Xenotropic murine leukemia virus-related virus (XMRV) was first identified in human prostate cancer tissue and was later found in a high percentage of humans with chronic fatigue syndrome (CFS). While exploring potential disease mechanisms, we found that XMRV infection induced apoptosis in SY5Y human neuroblastoma cells, suggesting a mechanism for the neuromuscular pathology seen in CFS. Several lines of evidence show that the cell entry receptor for XMRV, Xpr1, mediates this effect, and chemical cross-linking studies show that Xpr1 is associated with the Gβ subunit of the G-protein heterotrimer. The activation of adenylate cyclase rescued the cells from XMRV toxicity, indicating that toxicity resulted from reduced G-protein-mediated cyclic AMP (cAMP) signaling. Some proteins with similarity to Xpr1 are involved in phosphate uptake into cells, but we found no role of Xpr1 in phosphate uptake or its regulation. Our results indicate that Xpr1 is a novel, atypical G-protein-coupled receptor (GPCR) and that xenotropic or polytropic retrovirus binding can disrupt the cAMP-mediated signaling function of Xpr1, leading to the apoptosis of infected cells. We show that this pathway is also responsible for the classic toxicity of the polytropic mink cell focus-forming (MCF) retrovirus in mink cells. Although it now seems clear that the detection of XMRV in humans was the result of sample contamination with a recombinant mouse virus, our findings may have relevance to neurologic disease induced by MCF retroviruses in mice.
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