IL4I1 antibody
- Known as:
- IL4I1 (anti-)
- Catalog number:
- orb100203
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- IL4I1 antibody
Ask about this productRelated genes to: IL4I1 antibody
- Gene:
- IL4I1 NIH gene
- Name:
- interleukin 4 induced 1
- Previous symbol:
- -
- Synonyms:
- FIG1
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-20
- Date modifiied:
- 2016-01-15
Related products to: IL4I1 antibody
Related articles to: IL4I1 antibody
- The increasing availability of large chemical libraries and bioactivity datasets has created a growing need for cheminformatics tools capable of extracting interpretable structure-activity relationship (SAR) information across structurally diverse chemical series. However, many existing approaches rely on rigid scaffold definitions, descriptor-based clustering, or manually curated groupings, often limiting the identification of SAR trends spanning partially overlapping chemotypes. Here, we present SARgate, an open-source cheminformatics platform designed to organize chemical libraries into structurally coherent subsets and facilitate multi-level SAR exploration within a unified graphical environment. Starting from Bemis-Murcko scaffolds, SARgate applies automated aggregation procedures to derive generalized cores based on minimal shared substructures, enabling flexible R-group decomposition and improved recognition of chemically related series. Developed in Python using RDKit as the core cheminformatics engine, SARgate integrates dataset curation, scaffold organization, R-group analysis, matched molecular pair analysis (MMPA), stereochemical evaluation, similarity assessment, and structure-activity landscape visualization into a single interactive workflow accessible to users with different levels of computational expertise. The utility of SARgate is demonstrated through representative case studies involving AKT1 and IL4I1 inhibitor datasets derived from public repositories, externally curated collections, and manually assembled patent-derived libraries. These applications show that SARgate can recover known SAR determinants, identify activity-driving substituents and stereochemical constraints, reveal context-dependent effects, and support mechanistically interpretable medicinal chemistry insights directly from large-scale bioactivity data. - Source: PubMed
Publication date: 2026/06/24
Labrano LucioPrimavera ErikaRocchi MarcoMassuoli MicheleRagni Maria GraziaPoletta LaraGargaro MarcoFallarino FrancescaManfroni GiuseppeBarreca Maria LetiziaAstolfi Andrea - Necroptosis, a form of programmed cell death, promotes inflammation in immune-mediated diseases, but its role in alopecia areata (AA) remains unclear. In this study, we investigated necroptosis-related signatures in AA using integrated transcriptomic and histological analyses. Four bulk RNA-seq datasets from the GEO database, comprising 191 scalp samples from AA patients and healthy controls, were analysed by ssGSEA and GSEA to assess necroptosis-related signatures. To address the cellular heterogeneity inherent in bulk RNA data, we further performed single-cell RNA-sequencing (scRNA-seq) to investigate cell-specific mechanisms, and immunofluorescence staining of scalp biopsies was conducted to validate the expression and cellular localisation of key necroptosis-related markers. Necroptosis-related scores were significantly higher in AA than in controls, correlated with disease severity and decreased after JAK/TYK2 inhibitor therapy. At single-cell resolution, a macrophage subset (IL4I1 macrophages_1) showed the strongest necroptosis-related signal and was associated with enhanced macrophage-fibroblast communication involving TGFβ, ITGB2 and GAS6 signalling, suggesting perifollicular microenvironmental remodelling. Immunofluorescence further supported increased necroptosis-associated signalling and macrophage enrichment in AA lesions. Together, these findings suggest that macrophage-associated necroptosis-related programmes may represent a disease-associated inflammatory component in AA and support further mechanistic investigation of necroptosis-associated pathways in this disease. - Source: PubMed
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