Mouse Anti-Human CD58, Biotinylated
- Known as:
- Mouse Antibody toHuman CD58, Biotinylated
- Catalog number:
- 128-10046-2
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Mouse Anti-Human CD58 Biotinylated
Related genes to: Mouse Anti-Human CD58, Biotinylated
- Gene:
- CD58 NIH gene
- Name:
- CD58 molecule
- Previous symbol:
- LFA3
- Synonyms:
- -
- Chromosome:
- 1p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-06
- Date modifiied:
- 2016-10-05
Related products to: Mouse Anti-Human CD58, Biotinylated
Related articles to: Mouse Anti-Human CD58, Biotinylated
- Bulky disease represents a clinically aggressive subset of diffuse large B-cell lymphoma (DLBCL) associated with adverse clinical outcomes. The aim of this study was to investigate the influence of oncogenic mutations and tumor microenvironment alterations on bulky disease in DLBCL. - Source: PubMed
Wang Yu-QingWang YueDu Zhi-ShanHuang Xin-YunDong YanTian ShuangFu DiCheng ShuWang LiXu Peng-PengFan Sheng-JinWang Shu-Ye - In this study, we describe the design of peptide aptamers to modulate interactions between CD2 and CD58 (co-stimulatory molecules) in the immune response. We designed peptide aptamers based on the sunflower trypsin inhibitor-1 (SFTI-1) template, incorporating functional groups that confer conformational stability and aqueous solubility. To address the challenges posed by conformational isomerism in the sunflower trypsin inhibitor template due to proline-proline sequences in peptide design, we developed two aptamer peptides, SFTI-FGUA and SFTI-DMY, incorporating specific functional groups. SFTI-FGUA features a side-chain guanidine group on phenylalanine, while SFTI-DMY features a dimethyl group at the meta position relative to tyrosine's hydroxyl group. These bulky substitutions on the phenyl ring effectively restrict conformational flexibility and enhance solubility. Evaluation of these peptides using cell adhesion inhibition assays revealed that both aptamer peptides not only exhibited significant inhibition of cell adhesion but also exhibited a predominant conformation in solution. Furthermore, these peptides exhibited stability against enzymatic degradation. - Source: PubMed
Publication date: 2026/09/02
Chowdhury ArpanShrestha PrajeshSubramanian VivekanandanMayandi VenkateshMahajan MukeshJois Seetharama D - Primary Sjögren's syndrome (pSS) is a chronic autoimmune disorder. Dysregulated interferon-gamma (IFN-γ) signalling is implicated in pSS pathogenesis, yet the underlying mechanisms remain elusive. This study aimed to identify key IFN-γ-associated diagnostic genes and delineate their roles in immune dysregulation using peripheral blood transcriptomic and single-cell RNA sequencing (scRNA-seq) data. Publicly available Gene Expression Omnibus (GEO) datasets were used, and the bioinformatics findings were further supported by reverse transcription-quantitative PCR (RT-qPCR) validation. Peripheral blood transcriptomic data from training and validation cohorts were analysed, and key genes were screened using machine learning algorithms, receiver operating characteristic (ROC) curve analysis, and differential expression analysis. A diagnostic model and nomogram were subsequently constructed. Immune infiltration, pathway enrichment, and gene regulatory networks were also investigated, while scRNA-seq analysis was performed to characterize cellular heterogeneity, pseudotime trajectories, and cell-cell communication. Four key genes, HERC6, IL15, CD58 and PTGS2, were identified, and the resulting diagnostic model and nomogram demonstrated high diagnostic accuracy. Immune profiling revealed marked dysregulation of the immune microenvironment in pSS, accompanied by extensive alterations in metabolic and signalling pathways. Pathway enrichment analysis further demonstrated both distinct and shared functional roles of the four key genes. Single-cell analysis suggested that macrophages may act as central regulators in pSS pathogenesis, as evidenced by altered pseudotime trajectories, enrichment in early differentiation states, and intensified cell-cell communication networks. RT-qPCR further confirmed the significant upregulation of HERC6, IL15, and PTGS2 in patients with pSS. Collectively, this study established an IFN-γ-associated diagnostic model for pSS and implicated macrophages as potential key contributors to immune dysregulation through altered differentiation, enhanced intercellular communication, and IFN-γ-associated gene expression. These findings provide new insights into the pathogenesis of pSS and identify potential diagnostic biomarkers and therapeutic targets. - Source: PubMed
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