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Validated All-in-One™ qPCR Primer for IRF5(NM_032643.5) Search again
Product ID:
HQP155785
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
SLEB10
Gene Description:
interferon regulatory factor 5
Target Gene Accession:
NM_032643.5(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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. Alternative splice variants encoding different isoforms exist. [provided by RefSeq].
Gene References into function
- this study defines the regulatory phosphorylation sites that control the activity of IRF-5 in Newcastle disease virus-infected cells and provides further insight into its structure and function
- IRF-5 can act as both an activator and a repressor of interferon gene induction dependent on the IRF-interacting partner, and IRF-5 may be a part of the regulatory network that ensures timely expression of the immediate early inflammatory genes
- IRF-5 is a downstream target of p53and its growth inhibitory and proapoptotic effects are independent of p53.
- IRF-5-and IRF-7-induced innate antiviral response results in a broad alteration of the transcriptional profile of cellular genes
- CRM1-dependent nuclear export pathway is involved in the regulation of IRF-5 subcellular localization
- identified IRF5 SNPs that displayed strong signals in joint analysis of linkage and association (unadjusted P<10(-7)) with SLE
- IRF5 and IRF7 are critical mediators of TLR7 signaling
- there are multiple IRF5 isoforms with distinct cell type-specific expression, localization, regulation, and function
- a common IRF5 haplotype driving elevated expression of multiple unique isoforms of IRF5 is an important genetic risk factor for SLE, establishing a causal role for type I IFN pathway genes in human autoimmunity
- Our results suggest that the IRF5 functional polymorphisms analyzed do not seem to be implicated in genetic susceptibility to rheumatoid arthritis.
- results exclude the IRF5 rs2004640-T allele as a major genetic factor for rheumatoid arthritis in this French Caucasian population
- results in an independent case-control sample confirm the robust association of the IRF5/rs2004640 T allele with SLE risk, and further support the relevance of the type I interferon system in the pathogenesis of SLE and autoimmunity
- we show an association of systemic lupus erythematosus with 2 SNPs in the first intron; data support new mechanism by which an IRF5 polymorphism controls expression of alternate transcript variants which may have different effects on interferon signallin
- the genetic effect on the risk of systemic lupus erythematosus mediated by IRF5 variants can be generally accepted in both white and Asian populations
- A structural insertion/deletion in the IRF5 gene leads to expression of specific isoforms in the risk haplotype associated with system lupus erythematosus.
- Assessment of three functional IRF5 alleles in patients with systemic lupus erythematosus illustrates how multiple common variants of the same gene can together influence the levels of risk of a common disease.
- IRF5 could be involved in the more active disease and organ involvement known to occur among Mexican SLE patients.
- functional IRF5 variations do not confer an obvious risk for type 1 diabetes
- results help to understand the role of the IRF5 locus in SLE (systemic lupus erythematosus)susceptibility by clearly separating protection from susceptibility as caused by independent polymorphisms
- Genetic variants of IRF5 contribute to a unique disease etiology and pathogenesis in rheumatoid arthritis patients/
- Epstein-Barr virus initially uses TLR7 signaling to enhance B-cell proliferation and subsequently modifies the pathway to regulate IRF-5 activity.
- An insertion-deletion polymorphism in the interferon regulatory Factor 5 (IRF5) gene confers risk of inflammatory bowel diseases.
- Primary Sjogren's syndrome and systemic lupus erythematosus share IRF gene polymorphisms as a common genetic susceptibility factor.
- IRF5 allele confers risk for inflammatory bowel diseases and multiple sclerosis, suggesting a general role for IRF5 in autoimmune diseases
- Polymorphisms at IRF5 did not associate with psoriasis per se; however, an interaction with class I major histocompatibility complex (MHC) genes was found.
- a haplotype of IRF5 (interferon regulatory factor 5) gene has ssociation with systemic lupus erythematosus in Chinese
- These findings add IRF5 to the short list of genes shown to be associated with multiple sclerosis in more than one population.
- Genetic variants of IRF5 associate with systemic lupus erythematosus (SLE) in multiple populations, providing evidence that IRF5 is likely to be a crucial component in SLE pathogenesis among multiple ethnic groups.
- IRF5 was found to be associated with systemic lupus erythematosus in Asian populations. Intron 1 single-nucleotide polymorphisms, rather than exon 6 and 3'-untranslated region polymorphisms, appeared to play a crucial role.
- IRF5 mRNA is expressed in cells in atherosclerotic tissue and its expression is modified by single nucleotide polymorphisms in the IRF5 gene.
- reveal the cell type-specific importance of IRF-5 in MyD88-mediated antiviral pathways and the widespread role of IRF-5 in the regulation of inflammatory cytokines
- findings indicate that the promoter polymorphism of IRF5 is a genetic factor conferring predisposition to RA, and that it contributes considerably to disease pathogenesis in patients that were SE negative.
- IRF5 polymorphisms seem to influence RA susceptibility
- epigenetic inactivation of the IFN pathway plays a critical role in cellular immortalization, and the reactivation of IFN-regulated genes by transcription factors IRF5 and/or IRF7 is sufficient to induce cellular senescence
- The SNP rs7582694 in STAT4 displayed a increased risk of systemic lupus erythematosus with two independent risk alleles of the IRF5.
- The IRF5 systemic lupus erythematosus (SLE) risk haplotype is associated with higher serum IFNalpha activity in SLE patients.
- TT genotype of the rs2004640 dimorphism associated with rheumatoid arthritis in a Tunisian population
- Data show that IRF-5, which is activated via the MyD88 pathway, is subjected to TRAF6-mediated K63-linked ubiquitination, which is important for IRF-5 nuclear translocation and target gene regulation.
- genetic effects of IRF5 polymorphisms on the risk of systemic lupus erythematosus according to ethnicity
- IRF5 polymorphism is associated with genetic susceptibility to rheumatoid arthritis at least in a Korean population
- Additive effects of the major risk alleles of IRF5 and STAT4 in primary Sjogren's syndrome are reported.
- The IRF5 rs2004640 GT substitution is associated with susceptibility to systemic sclerosis providing clues to the mechanisms leading to fibrosing alveolitis