ArticleJournal of neurovirology2007
Influenza A virus transactivates the mouse envelope gene encoding syncytin B and its regulator, glial cells missing 1.
Article in Journal of neurovirology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 14 citations in OpenAlex.
- Differential Expression of Endogenous Retroviruses and Inflammatory Mediators in Female and Male Offspring in a Mouse Model of Maternal Immune Activation.International journal of molecular sciences · 2022Article
- The Role of Syncytin in Placental Angiogenesis and Fetal Growth.Frontiers in cell and developmental biology · 2022Article
- Schizophrenia and Influenza at the Centenary of the 1918-1919 Spanish Influenza Pandemic: Mechanisms of Psychosis Risk.Frontiers in psychiatry · 2020Review
- Transcriptional derepression of the ERVWE1 locus following influenza A virus infection.Journal of virology · 2014Article
- Behavioral disturbances in adult mice following neonatal virus infection or kynurenine treatment--role of brain kynurenic acid.Brain, behavior, and immunity · 2014Article
- Neonatal infection with neurotropic influenza A virus induces the kynurenine pathway in early life and disrupts sensorimotor gating in adult Tap1-/- mice.The international journal of neuropsychopharmacology · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, two candidate analogs for human syncytin, denoted syncytins A and B, were identified in the murine genome. These were found to have expression patterns and functions similar to human syncytin. In addition, the identification of glial cells missing (GCM)-binding motifs in putative promoter regions of the mouse syncytins imply analogous regulation. Transcriptional modulation of syncytin by exogenous agents was recently suggested by studies reporting transactivation of syncytin in human cell lines following virus infections. The authors report that influenza A virus infection increased the levels of transcripts encoding Gcm1 and syncytin B, but not syncytin A, in NIH-3T3 cells as well as in mouse primary neurons or glia. Overexpression of human GCM1 in NIH-3T3 cells resulted in increased levels of transcripts encoding syncytin B but not syncytin A. Systemic administration of neurotropic influenza A virus resulted in a neuronal infection and increased levels of Gcm1-encoding transcripts in brains of young mice. The mouse may therefore be useful for studies on the expression and function of endogenous retroviral envelope genes and transcription factors regulating their expression in the placenta and brain during physiological or pathological conditions.
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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.