ERAP2
- Known as:
- ERAP2
- Catalog number:
- Y213992
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ERAP2
Related genes to: ERAP2
- Gene:
- ERAP2 NIH gene
- Name:
- endoplasmic reticulum aminopeptidase 2
- Previous symbol:
- -
- Synonyms:
- L-RAP, LRAP
- Chromosome:
- 5q15
- Locus Type:
- gene with protein product
- Date approved:
- 2007-11-21
- Date modifiied:
- 2014-11-19
Related products to: ERAP2
anti-ERAP2anti-ERAP2Antibodies: ERAP2 HOST: Goat Clonality: pAbBos taurus,Bovine,Endoplasmic reticulum aminopeptidase 2,ERAP2Bovine endoplasmic reticulum aminopeptidase 2 (ERAP2) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine Endoplasmic reticulum aminopeptidase 2(ERAP2) ELISA kitBovine Endoplasmic reticulum aminopeptidase 2(ERAP2) ELISA kit SpeciesBovineELISA Kit for Endoplasmic Reticulum Aminopeptidase 2 (ERAP2)ELISA Kit for Endoplasmic Reticulum Aminopeptidase 2 (ERAP2) Homo sapiens (Human)ELISA Kit for Endoplasmic Reticulum Aminopeptidase 2 (ERAP2) Organism: Homo sapiens (Human)Endoplasmic reticulum aminopeptidase 2,ERAP2,Homo sapiens,Human,Leukocyte-derived arginine aminopeptidase,LRAP,L-RAPERAL1 Gene Era G-protein-like 1 (E. coli)ERAP2 LRAP antibody Ab host: GoatERAP2 AntibodyERAP2 Peptide Related articles to: ERAP2
- - Source: PubMed
Mpakali Anastasia - Genome-wide association studies (GWASs) have identified multiple genetic regions that confer risk for juvenile idiopathic arthritis (JIA). However, identifying the single-nucleotide polymorphisms (SNPs) that drive disease risk has been impeded by the fact that the SNPs used to identify risk loci are in linkage disequilibrium (LD) with hundreds of other SNPs. Since the causal SNPs remain unknown, it is difficult to identify target genes and thus use genetic information to elucidate disease biology and inform patient care. We next used existing genotyping data from 3,939 children with JIA and 14,412 healthy controls to identify SNPs on JIA-risk haplotypes that present within open chromatin in multiple immune cell types and are more common in children with JIA than the controls (p < 0.05) in the genotyping datasets. We identified SNPs within cis-regulatory regions (cis-regulatory elements [CREs]) using precision run-on sequencing data and identified likely target genes using MicroC in both resting and activated CD4+ T cells. We identified 138 SNPs within the PROseq-identified CREs and n = 41 genes with which these CREs physically interacted. Data from Genotype-Tissue Expression (GTEx) and the Database of Immune Cell Expression Quantitative Trait Loci (DICE) corroborated these analyses by showing allelic effects for SNPs within the CREs in the ERAP2/LNPEP and locus. We further corroborated IRF1 allelic effects using a luciferase reporter assay. Our findings significantly reduce the genomic search space for risk-driving variants and target genes and support the roles of IRF1, ERAP2, and LNPEP in driving risk for JIA. - Source: PubMed
Publication date: 2026/04/28
Jiang KaiyuHaley Emma KBarshad GiladHe AdamRogic AnitaRice EdwardSudman MarcThompson Susan DMurphy David AFu YaoPonder LoriMunoz Maurice DavenportKolachala PrashantPrahalad SampathGaffney Patrick MDanko Charles GJarvis James N - The aim of this review is to examine the contribution of genomic variation to preeclampsia susceptibility in Africans. PubMed/Medline, Scopus, African Index Medicus and Sabinet African Journals databases were used to access studies conducted in populations of African descent focussing on the genomics of preeclampsia. Studies were selected according to PRISMA guidelines and assessed for quality and risk of bias using the Critical Appraisal Skills Programme (CASP) and Joanna Briggs Institute (JBI) checklists. Meta-analysis was conducted using a random effects model, and publication bias was evaluated using the Eggers test and funnel plots. Grading of Recommendations, Assessment, Development and Evaluation (GRADE) was applied to evaluate the certainty of evidence outcomes. Sixty-six (66) studies reporting on genomics of preeclampsia were retrieved. Forty-four (44) studies had a quality assessment score ≥75%. Vascular pathway genes (, , and ; OR (95% CI): 1.61 (1.38-1.88); : 0.0%, = 0.87; GRADE: low certainty), immune/inflammatory pathway genes (, , , , and ; OR (95% CI): 2.07 (1.68-2.54); : 42.2%, = 0.04; GRADE: low certainty) and cellular homeostasis genes (, , and ; OR (95% CI): 1.65 (1.43-1.91); : 0.0%, = 0.99; GRADE: low certainty) showed pooled effect estimates suggestive of moderate to increased preeclampsia risk. G1 or G2 risk alleles seemed to contribute 1.70-fold (95% CI: 1.39-2.07; : 0.0%; = 0.51; GRADE: low certainty), respectively, to overall preeclampsia risk. Vascular, immune/inflammatory and cellular homeostasis genes may be ideal starting points for future research, and further validation of the role of G1 or G2 risk alleles in preeclampsia may be essential. - Source: PubMed
Publication date: 2026/03/12
Katsukunya Jonathan NDavidson BiancaMnika KhuthalaSoko Nyarai DOsman AyeshaMatjila MushiJones ErikaDandara Collet - Many viruses have adapted to persist in infected humans for life. Variable host control of their ongoing abundance (viral load) can lead to clearance or disease. Here we analysed the viral DNA load of 31 common viruses in human blood and saliva using whole-genome sequencing data from UK Biobank (n = 490,401), All of Us (n = 414,817) and Simons Foundation Powering Autism Research for Knowledge (SPARK; n = 12,519). Viral DNA load varied markedly with age, time of day and season; most viruses were also present at greater abundance in men than in women. Human genetic variation at dozens of loci associated with DNA load of seven viruses: Epstein-Barr virus (EBV, 45 loci), human herpesvirus (HHV)-7 (37 loci), HHV-6B, Merkel cell polyomavirus and three anelloviruses. Variation at the major histocompatibility complex (MHC) locus generated the strongest associations (P = 5.8 × 10 to 2.5 × 10), which were specific to each virus. The HLA-B*08:01 allele also exhibited a host-virus genetic interaction with EBV subtype (P = 7.4 × 10). Other human genetic effects implicated genes encoding proteins that process peptides for antigen presentation, such as ERAP1 (HHV-7, P = 2.7 × 10) and ERAP2 (EBV, P = 4.6 × 10). Mendelian randomization analyses supported a strong causal effect of EBV DNA load on increased risk of Hodgkin's lymphoma (P = 1.8 × 10), but not multiple sclerosis (P = 0.52). This suggests that higher chronic EBV load increases lymphoma risk, whereas associations of EBV infection with autoimmune conditions reflect host immune responses to particular viral epitopes. - Source: PubMed
Publication date: 2026/03/25
Kamitaki NolanTang DavidMcCarroll Steven ALoh Po-Ru - Sepsis, involving systemic inflammation and organ failure, presents significant challenges due to its complex and heterogeneous immunological reactions. T-helper 17 (Th17) cells contribute significantly to immune regulation, and their dysregulation is implicated in sepsis pathogenesis. Understanding how Th17 cell differentiation-related genes contribute to sepsis heterogeneity and prognosis is crucial for improving patient prognosis. - Source: PubMed
Publication date: 2026/02/27
Li XiuhuaTan LifeiDing YingweiZhang Bingwen