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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.


IFNAR2, type I interferon receptor, IFN-r
The protein encoded by this gene is a type I membrane protein that forms one of the two chains of a receptor for interferons alpha and beta. Binding and activation of the receptor stimulates Janus protein kinases, which in turn phosphorylate several proteins, including STAT1 and STAT2. Multiple transcript variants encoding at least two different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, HAD, V1a, Interferon-beta, STAT1
Papers using IFNAR2 antibodies
A type I interferon autocrine–paracrine loop is involved in Toll-like receptor-induced interleukin-12p70 secretion by dendritic cells
Garrone Pierre et al., In The Journal of Experimental Medicine, 2002
... Mouse anti–human IFNAR2 antibodies (CD118; PBL Biomedical Laboratories) and mouse anti–human ...
Papers on IFNAR2
Sumoylation coordinates the repression of inflammatory and anti-viral gene-expression programs during innate sensing.
Dejean et al., Paris, France. In Nat Immunol, Feb 2016
Overproduction of several NF-κB-dependent inflammatory cytokines required expression of the type I interferon receptor, which identified type I interferon as a central sumoylation-controlled hub for inflammation.
Type I interferon restricts type 2 immunopathology through the regulation of group 2 innate lymphoid cells.
Fritz et al., Montréal, Canada. In Nat Immunol, Jan 2016
Here we found that deficiency in signaling via type I interferon receptor led to deregulated activation of group 2 innate lymphoid cells (ILC2 cells) and infection-associated type 2 immunopathology.
Renal microRNA- and RNA-profiles in progressive chronic kidney disease.
Mayer et al., Innsbruck, Austria. In Eur J Clin Invest, Jan 2016
In particular miR-206 and miR-532-3p were associated with distinct biological processes via the expression of their target mRNAs: Reduced expression of miR-206 in progressive disease correlated with the upregulation of target mRNAs participating in inflammatory pathways (CCL19, CXCL1, IFNAR2, NCK2, PTK2B, PTPRC, RASGRP1, and TNFRSF25).
Small Molecule Agonists for the Type I Interferon Receptor: An In Silico Approach.
Fish et al., Toronto, Canada. In J Interferon Cytokine Res, Jan 2016
Cognizant that the biological potency of an IFN-α subtype is determined by its binding affinity to the type I IFN receptor, IFNAR, we identified a panel of small molecule nonpeptide compounds using an in silico screening strategy that incorporated specific structural features of amino acids in the receptor-binding domains of the most potent IFN-α, IFN alfacon-1.
Type I interferon signaling is decoupled from specific receptor orientation through lenient requirements of the transmembrane domain.
Schreiber et al., Israel. In J Biol Chem, Jan 2016
Binding of IFNs to its receptors, IFNAR1 and IFNAR2, is leading to activation of the IFN response.
Emodin potentiates the antiproliferative effect of interferon `/β by activation of JAK/STAT pathway signaling through inhibition of the 26S proteasome.
Wang et al., Chengdu, China. In Oncotarget, Jan 2016
Emodin inhibited IFN-α-stimulated ubiquitination and degradation of type I interferon receptor 1 (IFNAR1).
Signaling through RIG-I and type I interferon receptor: Immune activation by Newcastle disease virus in man versus immune evasion by Ebola virus (Review).
Schirrmacher, Köln, Germany. In Int J Mol Med, Jul 2015
In this review, two types of RNA viruses are compared with regard to the type I interferon (IFN) response in order to obtain a better understanding of the molecular mechanisms of immune activation or evasion.
Bioactivity of umbilical cord blood dendritic cells and anti-leukemia effect.
Wang et al., Xi'an, China. In Int J Clin Exp Med, 2014
The levels of interferon-r (IFN-r), tumor necrosis factor-a (TNF-α) and interleukin-12 (IL-12) were determined by ELISA.
Interferons in the central nervous system: a few instruments play many tunes.
Asgari et al., In Glia, 2014
We will review evidence that differential signaling by IFN-α versus IFN-β through the common heterodimeric receptor IFNAR is the basis for CNS-selective Type I IFN response, and the capacity of CNS glial cells to produce and respond to Type I IFN.
microRNA control of interferons and interferon induced anti-viral activity.
Sedger, Port Macquarie, Australia. In Mol Immunol, 2013
They act by binding to IFN-receptors (IFN-R), which trigger JAK/STAT cell signalling and the subsequent induction of hundreds of IFN-inducible genes, including both protein-coding and microRNA genes.
Structural basis of a unique interferon-β signaling axis mediated via the receptor IFNAR1.
Hertzog et al., Australia. In Nat Immunol, 2013
All interferons are considered to signal via the heterodimeric IFNAR1-IFNAR2 complex, yet some subtypes such as interferon-β (IFN-β) can exhibit distinct functional properties, although the molecular basis of this is unclear.
Type I interferons: ancient peptides with still under-discovered anti-cancer properties.
Vitale et al., Napoli, Italy. In Protein Pept Lett, 2013
Type I interferons (IFNs) represent a group of cytokines that act through a common receptor composed by two chains (IFNAR-1 and IFNAR-2).
Structural and dynamic determinants of type I interferon receptor assembly and their functional interpretation.
Schreiber et al., Osnabrück, Germany. In Immunol Rev, 2012
Type I interferons (IFNs) form a network of homologous cytokines that bind to a shared, heterodimeric cell surface receptor and engage signaling pathways that activate innate and adaptive immune responses.
Interferon (alpha, beta and omega) receptor 2 is a prognostic biomarker for lung cancer.
Kohno et al., Hiroshima, Japan. In Pathobiology, 2011
IFNAR2 overexpression was observed in various histological types of lung cancer, and appears to be associated with lung cancers that behave aggressively.
Structural linkage between ligand discrimination and receptor activation by type I interferons.
Garcia et al., Stanford, United States. In Cell, 2011
Sixteen human type I IFN variants signal through the same cell-surface receptors, IFNAR1 and IFNAR2, yet they can evoke markedly different physiological effects.
Stochastic receptor expression determines cell fate upon interferon treatment.
Schreiber et al., Israel. In Mol Cell Biol, 2011
A low number of receptors suffices for antiviral response and is thus a robust feature common to all cells. Conversely, a high number of receptors is required for antiproliferative activity, which allows for fine-tuning on a single-cell level.
Indirect inhibition of Toll-like receptor and type I interferon responses by ITAM-coupled receptors and integrins.
Ivashkiv et al., New York City, United States. In Immunity, 2010
We show that high-avidity ligation of ITAM-coupled beta2 integrins and FcgammaRs in macrophages inhibited type I interferon receptor and Toll-like receptor (TLR) signaling and induced expression of interleukin-10 (IL-10); signaling inhibitors SOCS3, ABIN-3, and A20; and repressors of cytokine gene transcription STAT3 and Hes1.
Interferons direct an effective innate response to Legionella pneumophila infection.
Schindler et al., New York City, United States. In J Biol Chem, 2009
ability of L. pneumophila to induce IFN-I expression was found to be dependent on IRF-3, but not NF-kappaB. Secreted IFN-Is then in turn suppress the intracellular replication of L. pneumophila
Association study of IFNAR2 and IL10RB genes with the susceptibility and interferon response in HBV infection.
Zhang et al., Shanghai, China. In J Viral Hepat, 2009
The IFNAR2-8SS genotype was associated with HBeAg negative patients; IFNAR2-8F allele was associated with the risk to high viral loads; the IFNAR2-8FF genotype predisposed to higher MxA gene induction and correlated with sustained IFN response.
IFNAR1 and IFNAR2 polymorphisms in patients with Behçet's disease.
Dinc et al., In Clin Exp Rheumatol, 2009
IFNAR1 (interferon-alpha receptor 1) (G/C in SNP18417) and IFNAR1 (interferon-alpha receptor 2) (G/T in SNP 11876) polymorphisms jointly, but not individually, may confer susceptibility to Behcets disease in a Turkish population
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