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Human IRF5 Protein expressed in HEK-293 Cells - ABIN2723539
Griesbeck, Ziegler, Laffont, Smith, Chauveau, Tomezsko, Sharei, Kourjian, Porichis, Hart, Palmer, Sirignano, Beisel, Hildebrandt, Cénac, Villani, Diefenbach, Le Gall, Schwartz, Herbeuval, Autran et al.: Sex Differences in Plasmacytoid Dendritic Cell Levels of IRF5 Drive Higher IFN-α Production in Women. ... in Journal of immunology (Baltimore, Md. : 1950) 2015
we demonstrated for the first time an association between IRF5 rs 2004640 G/T alleles and predisposing to juvenile idiopathic arthritis. Understanding the role of IRF5 in rheumatic arthritis might help identify biological pathways of importance in the pathogenesis of this disease.
A possible cross-reaction between IRF5/EBV homologous antigens and shifts in T cell balance disrupted by anti-IL-2 Abs.
study suggests a novel role for interferon regulatory factor 5 (IRF5) in the regulation of the inflammatory response in human myometrium
In IAV-infected patients, miR-302a expression was down-regulated, whereas IRF-5 expression was up-regulated. Taken together, this work uncovers and defines a signaling pathway implicated in an IAV-induced cytokine storm.
Analysis of clinical HCC specimens supports a pathologic role for IRF5 in HCV-induced HCC, as IRF5 expression was down-regulated in livers from HCV-positive versus HCV-negative HCC patients or healthy donor livers. These results identify IRF5 as an important suppressor of HCV replication and HCC pathogenesis.
Results indicated that IFR5 variants rs77571059 and rs2004640 and haplotype GTAA were associated with the susceptibility to CAP and rs77571059 was related to the severity of the disease, suggesting that IFR5 variants may contribute to the pathogenesis of community-acquired pneumonia (CAP), and may serve as prognostic markers of CAP susceptibility and outcome.
IRF5 and its related inflammatory cytokines are associated with the severity, prognosis, and causative pathogen of CAP patients.
this study shows that interferon regulatory factor 5 regulates the expression of matrix metalloproteinase-3 in human chondrocytes
IFR5 variants may contribute as a host factor in determining the pathogenesis in chronic HBV infections.
The presence of the interferon regulatory factor 5 rs2004640 T allele increases the risk of nephritis development in Egyptian children with systemic lupus erythematosus.
IRF5 was an adverse independent prognostic factor for both overall survival and recurrence free survival in patients with non-metastatic ccRCC.
Data suggest that IRAK4 activity regulates activation of IRF5, TAK1, and IKKB in monocytes; IRAK4 activation of TAK1-IKKB-IRF5 axis leads to induction of cytokines and interferons following TLR7/TLR8 stimulation. (IRAK4 = interleukin-1 receptor-associated kinase 4; IRF5 = interferon regulatory factor-5; TAK1 = MAPK kinase kinase 7; IKKB = I-kappa B kinase; TLR = toll-like receptor)
IRF5 and IRF5 disease-risk variants increase glycolysis and human m1 macrophage polarization by regulating proximal signaling and Akt2 activation.
the genomic pattern according to MATH demonstrated that mutation rates of TP53, IRF5 and KRAS were independently associated with MATH, and the latter two were only significant in male patients. As MATH increased, the fraction of somatic copy number alteration (SCNA) elevated. Moreover, more SCNA events was independently associated with MATH in male than in female
IRF-5 targeted the expression of vascular cell adhesion molecule 1 (VCAM-1) at the transcriptional level by binding to its promoter.
oncogenic IRF5 overexpression in HL is the result of a specific LTR transcriptional activation
the primary activating regulatory region of human IRF5 was located in its minimal promoter region between nucleotides -179 and +62. In addition, it was shown that Sp1 was able to bind to the multiple sites in IRF5 promoter region, and was involved in the transcriptional regulation of IRF5 at the basal level.
This study demonstrates the association of IRF5 with an increased susceptibility for systemic lupus erythematosus (SLE) in the population of Crete and emphasizes the association of the Neanderthal-derived IRF5 haplotype with SLE susceptibility. Patients carrying allele the Neanderthal allele C had greater type I IFN, supporting a functional consequence of this polymorphism.
this study shows that IRF5 polymorphisms are associated with unexplained recurrent pregnancy loss among Iranian women
The results demonstrated that STAT4 rs7574865 and IRF5 rs2004640G/T substitution are associated with a susceptibility to systemic sclerosis.
Scavenger receptor class A is regulated by pathogens and suppresses IRF5 nuclear translocation by direct interaction. Reduced abundance of nuclear IRF5 shifts macrophage polarization from M1 towards M2, which subsequently switches T-helper responses from type 1 to type 2.
Aged mice expressed higher IRF5 levels in the ischemic brains, suggesting that aging has a significant influence on stroke outcomes in mice, which is probably mediated by age-specific inflammatory responses.
this study shows a critical role for IRF5 in regulating allergic airway inflammation
BCG increased membrane expression of TRIM59 through the TLR2/ TLR4/IRF5 pathway in RAW264.7 macrophage cell line.
these results reveal a role for Lyn as a specific suppressor of the TLR-MyD88-IRF5 pathway and illustrate the importance of fine-tuning IRF5 activity for the maintenance of immune homeostasis
IRF5 siRNA reverses pancreatitis-induced activation of lung macrophages from M1 phenotype to M2 phenotype in severe acute pancreatitis associated with acute lung injury.
Our data show that miR-146b targets IRF5, resulting in the regulation of macrophage activation. Furthermore, miR-146b deficient mice developed intestinal inflammation with enhanced M1 macrophage polarization.
data suggest that IRF5 plays a causal role in inflammation, fibrosis and impaired vascular EC function in Tsk/+ mice
study sheds light on the TLR4-IRF5 pathway in the pathology of SSc with clinical implications of targeting the IRF5 pathways in the suppression of disease development
Collectively, these results indicate a key role for IRF-5 in modulating the host antiviral response in peripheral organs that controls bunyavirus neuroinvasion in mice.
studies extend prior ones suggesting that inhibiting IRF5 might be useful for chronic macrophage-induced inflammation and suggest that IRF5 blockade would ameliorate more acute forms of inflammation, including lung injury
IRF5 plays an important role in the development of disease in the MRL/lpr mouse model of lupus in the absence of the DOCK2 mutation and that IRF5 is required for the transition from mature B cells to plasma cells.
IRF5 expression in microglia is regulated by IRF8. IRF5 directly upregulates P2RX4 expression on microglia in peripheral nerve injury, and may play a role in neuropathic pain.
PAR1 suppression of IRF5 and IL-12/23 secretion by macrophages provides a novel mechanism by which the host suppresses the mucosal Th1 and Th17 response to H. pylori infection.
This study uncovers a new function for IRF5 in controlling the relative mass of different adipose tissue depots and thus insulin sensitivity in obesity.
IKKbeta is an IRF5 kinase that instigates inflammation
our results reveal a protective role for IRF5 in lupus-associated atherosclerosis that is mediated through the effects of IRF5 in both immune and nonimmune cells.
IRF5 has a critical role in shaping the early innate immune response towards West Nile virus in the draining lymph node, which impacts the spread of virus infection, optimal B cell immunity, and disease pathogenesis.
The IRF5 deficiency reduces IFN-alpha, IFN-beta and IL-6 production by Toll-like receptor 9 (TLR9)- and TLR7-stimulated DCs and reduces TLR7- and TLR9-induced IL-6 production by B cells
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.
interferon regulatory factor 5
, Interferon regulatory factor 5
, interferon regulatory factor 5-like
, interferon regulatory factor 5 bone marrow