Basal expression levels of IFNAR and Jak-STAT components are determinants of cell-type-specific differences in cardiac antiviral responses - Wikidata - wikimedia - TriplyDB

Basal expression levels of IFNAR and Jak-STAT components are determinants of cell-type-specific differences in cardiac antiviral responses

Basal expression levels of IFNAR and Jak-STAT components are determinants of cell-type-specific differences in cardiac antiviral responses

http://www.wikidata.org/entity/Q36315128

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Murine Coronavirus Mouse Hepatitis Virus Is Recognized by MDA5 and Induces Type I Interferon in Brain Macrophages/Microglia Apoptosis in animal models of virus-induced disease Keeping it in check: chronic viral infection and antiviral immunity in the brain Constitutive type I interferon modulates homeostatic balance through tonic signaling TYK2 kinase activity is required for functional type I interferon responses in vivo Influenza virus non-structural protein 1 (NS1) disrupts interferon signaling Molecular cloning and expression analysis of the STAT1 gene from olive flounder, Paralichthys olivaceus Proteomic analysis reveals virus-specific Hsp25 modulation in cardiac myocytes.A Conserved Residue, Tyrosine (Y) 84, in H5N1 Influenza A Virus NS1 Regulates IFN Signaling Responses to Enhance Viral Infection.Replication of many human viruses is refractory to inhibition by endogenous cellular microRNAs.Human neuronal cells possess functional cytoplasmic and TLR-mediated innate immune pathways influenced by phosphatidylinositol-3 kinase signaling.Transcription of mouse Sp2 yields alternatively spliced and sub-genomic mRNAs in a tissue- and cell-type-specific fashion Activation of the type I interferon pathway is enhanced in response to human neuronal differentiation.Transient oscillatory dynamics of interferon beta signaling in macrophages Homeostatic interferon expression in neurons is sufficient for early control of viral infection Critical role of interferon-α constitutively produced in human hepatocytes in response to RNA virus infection.A single-amino-acid polymorphism in reovirus protein μ2 determines repression of interferon signaling and modulates myocarditis Cross-presenting CD103+ dendritic cells are protected from influenza virus infection.Activation of RNase L by Murine Coronavirus in Myeloid Cells Is Dependent on Basal Oas Gene Expression and Independent of Virus-Induced Interferon Generating primary cultures of murine cardiac myocytes and cardiac fibroblasts to study viral myocarditis.IFN-alpha expression and antiviral effects are subtype and cell type specific in the cardiac response to viral infection Rotavirus and reovirus modulation of the interferon response.An ITAM in a nonenveloped virus regulates activation of NF-κB, induction of beta interferon, and viral spread.In vivo ablation of type I interferon receptor from cardiomyocytes delays coxsackieviral clearance and accelerates myocardial disease.Interferon signaling in Peromyscus leucopus confers a potent and specific restriction to vector-borne flaviviruses.NF-κB activation is cell type-specific in the heart.Enterovirus 71 disrupts interferon signaling by reducing the level of interferon receptor 1 Murine Coronavirus Cell Type Dependent Interaction with the Type I Interferon Response Spontaneous activation of a MAVS-dependent antiviral signaling pathway determines high basal interferon-β expression in cardiac myocytes.Antiviral effects of interferon-β are enhanced in the absence of the translational suppressor 4E-BP1 in myocarditis induced by Coxsackievirus B3.Interferon regulatory factor 3 attenuates reovirus myocarditis and contributes to viral clearance.Reovirus mu2 protein inhibits interferon signaling through a novel mechanism involving nuclear accumulation of interferon regulatory factor 9.Annexin A5 suppresses cyclooxygenase-2 expression by downregulating the protein kinase C-ζ-nuclear factor-κB signaling pathway in prostate cancer cells.Tumor Restrictions to Oncolytic Virus.Alpha/Beta Interferon (IFN-α/β) Signaling in Astrocytes Mediates Protection against Viral Encephalomyelitis and Regulates IFN-γ-Dependent Responses.

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P2860

Basal expression levels of IFNAR and Jak-STAT components are determinants of cell-type-specific differences in cardiac antiviral responses

http://www.wikidata.org/entity/Q36315128

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2007 nî lūn-bûn

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2007年の論文

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2007年学术文章

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2007年学术文章

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2007年學術文章

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2007年學術文章

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Journal of Virology

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Basal expression levels of IFN ...... in cardiac antiviral responses

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Barbara Sherry

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Jennifer Zurney

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Kristina E Howard

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P2860

Functional role of type I and type II interferons in antiviral defense

Subunit of an alpha-interferon-responsive transcription factor is related to interferon regulatory factor and Myb families of DNA-binding proteins

Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins

How cells respond to interferons

Characterization of the interferon regulatory factor-7 and its potential role in the transcription activation of interferon A genes

Identification of genes differentially regulated by interferon alpha, beta, or gamma using oligonucleotide arrays

STATs in oncogenesis

Distinct and essential roles of transcription factors IRF-3 and IRF-7 in response to viruses for IFN-alpha/beta gene induction

Transcriptional responses to polypeptide ligands: the JAK-STAT pathway

Essential role of GATA-4 in cell survival and drug-induced cardiotoxicity.

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13668-13680

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scholarly article

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10.1128/JVI.01172-07

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24

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81

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2007-10-17T00:00:00Z

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5902164

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17942530

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2168836

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