Ask about this productRelated genes to: LMAN2 antibody
- Gene:
- LMAN2 NIH gene
- Name:
- lectin, mannose binding 2
- Previous symbol:
- C5orf8
- Synonyms:
- GP36B, VIP36
- Chromosome:
- 5q35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-18
- Date modifiied:
- 2016-10-05
Related products to: LMAN2 antibody
Related articles to: LMAN2 antibody
- Earlier research observed the effects of plasma proteins on ischemic stroke (IS). This Mendelian randomization (MR), in vivo study additionally assesses the associations of localized populations of plasma proteins with IS to further confirm the causality and explore drug targets. - Source: PubMed
Publication date: 2026/03/17
Ren HaoxuDing YingyueWang RuonanLi JinjianYang ChenganWang XuZhao Dexi - Gout is a prevalent inflammatory arthropathy driven by monosodium urate crystal deposition, yet the causal relationships between circulating biomarkers and disease susceptibility remain incompletely characterized. Establishing robust causal associations and mapping them to specific effector genes and tissues is essential for identifying mechanistically informed therapeutic targets. - Source: PubMed
Publication date: 2026/02/24
Huang LiangLiu JianiZheng XiaohuiZhang KaiChen YixinChen XiaolingZhang SiqiCai ShanshanCai LiGuo YanyanZhu PengLi Meng - Heart failure (HF) and its main subtypes, heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF), impose an enormous health burden on elders. Assessment of the circulating proteome to illuminate pathogenesis could open new opportunities for treatment. - Source: PubMed
Publication date: 2026/02/04
Njoroge Joyce NSanders van Wijk SandraAustin Thomas RBrody Jennifer ASitlani Colleen MHamerton EmilyBis Joshua CHenry AlbertLumbers R Thomas Seshaiah TaliaShojaie AliYang YiminLamberson VictoriaYu BingShah Amil MBansal NishaShah Sanjiv JTracy Russell PGerszten Robert EJennings Lori LGudmundsdottir ValborgGudnason VilmundurEmilsson ValurPsaty Bruce MKizer Jorge R - Recent advances in proteomics have enabled the identification of early protein biomarkers and metabolic disturbances associated with type 2 diabetes (T2D), a major global health challenge. This systematic review and meta-analysis synthesize evidence from 27 studies comparing proteomic profiles of individuals with T2D and normoglycemic controls, selected from 2,422 initial records. The QUADOMICS assessment showed good methodological reporting for sample handling and proteomic analysis (>70% of studies), but over 60% lacked information on confounding clinical factors and biomarker validation. A qualitative synthesis focused on 85 recurrently reported proteins (≥8 studies), which showed strong interconnectivity and were involved in immune response, lipid-protein organization, detoxification, proteolysis, and coagulation, key pathways implicated in T2D. An omics-based meta-analysis identified seven promising protein biomarkers for T2D related to lipid/glucose metabolism (Q12907_LMAN2, P02652_POA2, P07602_PSPA, P09622_DLD); cell binding/adhesion (P12109_COL6A1, P12830_CDH1); and translational regulation and mitochondrial function (P35232_PHB). Random-effects meta-analysis revealed variation in effect sizes across studies for previously highlighted biomarkers, but three of them (P02763_ORM1, P00738_HP, P25311_AZGP1) exhibited considerable consistency. To enhance accessibility and further exploration of findings, we provide the interactive web tool : https://jgcurras.shinyapps.io/metaMarkersT2D/. - Source: PubMed
Publication date: 2025/11/30
García-Currás JuliaPérez-Lois RaquelL Taboada GuillermoP Pata María - As the pediatric COVID-19 landscape evolves, it is essential to evaluate whether SARS-CoV-2 infection predisposes children to allergic disorders. This narrative review synthesizes current epidemiological and immunological evidence linking pediatric COVID-19 with new-onset atopy. Epidemiological data remain heterogeneous: large Korean and multinational cohorts report increased risks of asthma and allergic rhinitis following COVID-19, whereas U.S. cohorts show neutral or protective associations, highlighting geographic and methodological variability. Mechanistic insights provide biological plausibility: epithelial injury and the release of alarmin cytokines (IL-33, IL-25, TSLP) promote Th2 polarization and ILC2 expansion, while epigenetic "scars" (e.g., LMAN2 methylation changes) and hematopoietic stem cell reprogramming may sustain long-term Th2 bias. Cytokine memory involving IL-7 and IL-15 contributes to altered T- and B-cell homeostasis, whereas disrupted regulatory T-cell function may reduce tolerance thresholds. Paradoxical trade-offs exist, such as ACE2 downregulation in allergic airways, which may lower viral entry but simultaneously amplify type-2 inflammation. Together, these processes suggest that SARS-CoV-2 infection could foster a pro-allergic milieu in susceptible children. Although current evidence is inconclusive, integrating epidemiological surveillance with mechanistic studies is crucial for predicting and alleviating post-COVID allergic outcomes. Longitudinal pediatric cohorts and interventions targeting epithelial alarmins or microbiome restoration may hold promise for prevention. - Source: PubMed
Publication date: 2025/09/28
Filippatos FilipposMatara Dimitra-IfigeneiaMichos AthanasiosKakleas Konstantinos