ArticleJournal of neuroimmunology2012
Extended JAK activation and delayed STAT1 dephosphorylation contribute to the distinct signaling profile of CNS neurons exposed to interferon-gamma.
Article in Journal of neuroimmunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Getting on your last nerve: IFNs and resistance to infection.Journal of immunology (Baltimore, Md. : 1950) · 2026Review
- Prolonged STAT1 activation in neurons drives a pathological transcriptional response.Journal of neuroimmunology · 2023Article
- Unique aspects of IFN-γ/STAT1 signaling in neurons.Immunological reviews · 2022Review
- Type II interferon signaling in the brain during a viral infection with age-dependent pathogenesis.Developmental neurobiology · 2020Article
- Covalently Immobilizing Interferon-γ Drives Filopodia Production through Specific Receptor-Ligand Interactions Independently of Canonical Downstream Signaling.Bioconjugate chemistry · 2020Article
- The antiviral cytokine interferon-gamma restricts neural stem/progenitor cell proliferation through activation of STAT1 and modulation of retinoblastoma protein phosphorylation.Journal of neuroscience research · 2017Article
- Glutamate‑mediated effects of caffeine and interferon‑γ on mercury-induced toxicity.International journal of molecular medicine · 2017Article
- Keeping it in check: chronic viral infection and antiviral immunity in the brain.Nature reviews. Neuroscience · 2016Review
- CD4Virology · 2016Article
- Interferon Gamma: Influence on Neural Stem Cell Function in Neurodegenerative and Neuroinflammatory Disease.Clinical medicine insights. Pathology · 2016Review
- Bst2/Tetherin Is Induced in Neurons by Type I Interferon and Viral Infection but Is Dispensable for Protection against Neurotropic Viral Challenge.Journal of virology · 2015Article
- Interferon gamma induces protective non-canonical signaling pathways in primary neurons.Journal of neurochemistry · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Although interferon-gamma (IFN-γ) plays a critical role in the noncytolytic elimination of many neurotropic viral infections, the signaling response to this cytokine has not been extensively characterized in primary CNS neurons. We previously demonstrated that the IFN-γ response at the signaling and gene expression levels is temporally extended in primary mouse hippocampal neurons, as compared to the transient response of primary mouse embryonic fibroblasts (MEF). We hypothesize that the protracted kinetics of STAT1 phosphorylation in IFN-γ-treated neurons are due to extended receptor activation and/or delayed STAT1 dephosphorylation in the nucleus. Here, we show that in response to IFN-γ, the Janus kinases (JAK1/JAK2) associated with the neuronal IFN-γ receptor complex remain active for an extended period as compared to MEF. Experimental inactivation of JAK1/JAK2 in neurons after IFN-γ treatment did not reverse the extended STAT1 phosphorylation phenotype. These results suggest that the extended kinetics of neuronal IFN-γ signaling are a product of distinct negative feedback mechanisms operating at both the receptor and within the nucleus.
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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.