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Interferon regulatory factor 5

IRF5, interferon regulatory factor 5
This gene encodes a member of the interferon regulatory factor (IRF) family, a group of transcription factors with diverse roles, including virus-mediated activation of interferon, and modulation of cell growth, differentiation, apoptosis, and immune system activity. Members of the IRF family are characterized by a conserved N-terminal DNA-binding domain containing tryptophan (W) repeats. Multiple transcript variants encoding different isoforms have been found for this gene, and a 30-nt indel polymorphism (SNP rs60344245) can result in loss of a 10-aa segment. [provided by RefSeq, Mar 2010] (from NCBI)
Top mentioned proteins: IRF, STAT4, CAN, IRF-7, Interferon Regulatory Factor-3
Papers on IRF5
Positive Darwinian selection within interferon regulatory factor genes of Gymnocypris przewalskii (Cyprinidae) on the Tibetan Plateau.
Zhao et al., Xining, China. In Fish Shellfish Immunol, Feb 2016
Within this gene family, IRF3, IRF5, IRF7 and IRF8 contained positive selection sites.
Vigneri et al., Catania, Italy. In Curr Cancer Drug Targets, Feb 2016
Finally, we have recently demonstrated that IRF5 is a target of BCR-ABL kinase activity and reduces CML cell proliferation.
The pentacyclic triterpene Lupeol switches M1 macrophages to M2 and ameliorates experimental inflammatory bowel disease.
Fei et al., Tangshan, China. In Int Immunopharmacol, Jan 2016
IRF5, a transcription factor that is critically involved in M1 polarization, was down-regulated in M1 macrophages after being incubated with Lupeol, associated with a marked decrease in the phosphorylation of p38 mitogen activated protein kinase.
Interferon regulatory factor 5 in human autoimmunity and murine models of autoimmune disease.
Udalova et al., Oxford, United Kingdom. In Transl Res, Jan 2016
Interferon regulatory factor 5 (IRF5) has been demonstrated as a key transcription factor of the immune system, playing important roles in modulating inflammatory immune responses in numerous cell types including dendritic cells, macrophages, and B cells.
Polymorphisms in STAT4 and IRF5 increase the risk of systemic sclerosis: a meta-analysis.
Yang et al., Beijing, China. In Int J Dermatol, Jan 2016
The aim of this study was to investigate the association of signal transducer and activator of transcription 4 (STAT4) rs7574865 and interferon regulatory factor 5 (IRF5) rs2004640 polymorphisms with risk of SSc.
Low-grade inflammatory polarization of monocytes impairs wound healing.
Li et al., Denver, United States. In J Pathol, Jan 2016
Mechanistically, super-low dose endotoxin caused cellular stress, altered lysosome function and increased the transcription factor IRF5. TUDCA, a potent inhibitor of cellular stress, effectively blocked the monocyte polarization, and improved wound healing in mice injected with super-low dose endotoxin.
Identification of a systemic lupus erythematosus risk locus spanning ATG16L2, FCHSD2, and P2RY2 in Koreans.
Tsao et al., Oklahoma City, United States. In Arthritis Rheumatol, Jan 2016
We replicated ten previously established SLE risk loci: STAT1-STAT4, TNFSF4, TNFAIP3, IKZF1, HIP1, IRF5, BLK, WDFY4, ETS1 and IRAK1-MECP2.
Association of the IRF5 rs2070197 polymorphism with systemic lupus erythematosus: a meta-analysis.
Li et al., Beijing, China. In Clin Rheumatol, Sep 2015
The aim of this study was to explore whether the interferon regulatory factor 5 (IRF5) gene rs2070197 polymorphism was associated with systemic lupus erythematosus (SLE) in multiple ethic populations.
Irf5 deficiency in macrophages promotes beneficial adipose tissue expansion and insulin sensitivity during obesity.
Venteclef et al., Paris, France. In Nat Med, Jun 2015
Transcription factor interferon regulatory factor 5 (IRF5) has been implicated in polarizing macrophages towards an inflammatory phenotype.
[Mechanisms underlying the pathogenesis of neuropathic pain revealing by the role of glial cells].
Tsuda, In Nihon Shinkei Seishin Yakurigaku Zasshi, Feb 2015
Furthermore, interferon regulatory factor-8 (IRF8) and IRF5 are identified as microglial transcription factors whose expression is upregulated in spinal microglia after PNI, and the IRF8-IRF5 transcriptional cascade is the core process for shifting spinal microglia toward a state with high expression of P2X4 receptors.
Different pathways of macrophage activation and polarization.
Myśliwska et al., Gdańsk, Poland. In Postepy Hig Med Dosw (online), 2014
Mediators of M1 macrophage TLR-dependent polarization include transcription factors such as NF-κB, AP-1, PU.1, CCAAT/enhancer-binding protein α (C/EBP-α), STAT1 as well as interferon regulatory factor 5 (IRF5), while the transcription factors which promote M2 activation include IRF4, C/EBP-β, Krüppel-like factor 4 (KLF4), STAT6 and PPARγ receptor.
Variants at multiple loci implicated in both innate and adaptive immune responses are associated with Sjögren's syndrome.
Sivils et al., Oklahoma City, United States. In Nat Genet, 2013
In addition to strong association within the human leukocyte antigen (HLA) region at 6p21 (Pmeta = 7.65 × 10(-114)), we establish associations with IRF5-TNPO3 (Pmeta = 2.73 × 10(-19)), STAT4 (Pmeta = 6.80 × 10(-15)), IL12A (Pmeta = 1.17 × 10(-10)), FAM167A-BLK (Pmeta = 4.97 × 10(-10)), DDX6-CXCR5 (Pmeta = 1.10 × 10(-8)) and TNIP1 (Pmeta = 3.30 × 10(-8)).
Interferon-β production via Dectin-1-Syk-IRF5 signaling in dendritic cells is crucial for immunity to C. albicans.
Ardavín et al., Madrid, Spain. In Immunity, 2013
Dectin-1-induced IFN-β production required the tyrosine kinase Syk and the transcription factor IRF5. Type I IFN receptor-deficient mice had a lower survival after C. albicans infection, paralleled by defective renal neutrophil infiltration.
Intracellular antibody-bound pathogens stimulate immune signaling via the Fc receptor TRIM21.
James et al., Cambridge, United Kingdom. In Nat Immunol, 2013
TRIM21 catalyzed the formation of Lys63 (K63)-linked ubiquitin chains and stimulated the transcription factor pathways of NF-κB, AP-1, IRF3, IRF5 and IRF7.
IRF5 polymorphism predicts prognosis in patients with systemic sclerosis.
Assassi et al., Houston, United States. In Ann Rheum Dis, 2012
IRF5 polymorphism predicts prognosis in patients with systemic sclerosis.
Unique contribution of IRF-5-Ikaros axis to the B-cell IgG2a response.
Pitha et al., Baltimore, United States. In Genes Immun, 2012
these results identify the IRF-5-Ikaros axis as a critical modulator of IgG2a/c class switching.
Cross-interference of RLR and TLR signaling pathways modulates antibacterial T cell responses.
Taniguchi et al., Tokyo, Japan. In Nat Immunol, 2012
The RLR-activated transcription factor IRF3 bound dominantly, relative to IRF5, to the Il12b promoter, where it interfered with the TLR-induced assembly of a productive transcription-factor complex.
IRF5 risk polymorphisms contribute to interindividual variance in pattern recognition receptor-mediated cytokine secretion in human monocyte-derived cells.
Abraham et al., New Haven, United States. In J Immunol, 2012
IRF5 disease-associated polymorphisms to a wide spectrum of microbial triggers has broad implications for global immunological responses, host defenses against pathogens, and inflammatory/autoimmune disease susceptibility.
Irf5-deficient mice are protected from pristane-induced lupus via increased Th2 cytokines and altered IgG class switching.
Barnes et al., Newark, United States. In Eur J Immunol, 2012
overexpression of IRF5 in blood cells of systemic lupus erythematosus(SLE) patients may contribute to disease pathogenesis.
Effects of IRF5 lupus risk haplotype on pathways predicted to influence B cell functions.
Poole et al., Oklahoma City, United States. In J Biomed Biotechnol, 2011
One known genetic factor associated with lupus is a haplotype of the IRF5 gene. Gene expression microarray data identified multiple interferon- and inflammation-related gene sets significantly overrepresented in cells with the risk haplotype.
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