CD74 (159-171) antibody Ab
- Known as:
- CD74 (159-171) (anti-) Antibody
- Catalog number:
- 1487988
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- CD74 (159-171) antibody
Ask about this productRelated genes to: CD74 (159-171) antibody Ab
- Gene:
- CD74 NIH gene
- Name:
- CD74 molecule
- Previous symbol:
- DHLAG
- Synonyms:
- -
- Chromosome:
- 5q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: CD74 (159-171) antibody Ab
Related articles to: CD74 (159-171) antibody Ab
- Endometriosis (EMS) is a common gynecological disease that seriously affects women's health and quality of life. However, the detailed dynamic cellular and molecular mechanisms underlying EMS pathogenesis remain largely unknown. This study establishes a novel diagnostic model to distinguish ectopic endometrium (EC) from eutopic endometrium (EU) samples. This study elucidated the critical role of low-density lipoprotein receptor-related protein 1 (LRP1) in EMS pathogenesis through integrated multi-omics analyses. Our comprehensive approach began with merging three GEO datasets (GSE7305, GSE11691, GSE25628), identifying 1,404 differentially expressed genes (DEGs) and 489 co-expressed genes with the brown module using weighted gene co-expression network analysis (WGCNA). A machine learning algorithm identified 30 hub genes, among which LRP1 exhibited the highest diagnostic performance. Immune profiling revealed a strong positive correlation between LRP1 and M2 macrophage infiltration (r=0.62, p<0.001), while Mendelian randomization analysis confirmed a causal relationship (OR = 1.35, 95%CI:1.13-1.61, p=0.001). Single-cell RNA sequencing demonstrated LRP1 is predominantly expressed in fibroblasts and monocytes, orchestrating cell-cell communication through the MIF signaling pathway, particularly through CD74/CXCR4 interactions. Experimental validation confirmed significantly elevated LRP1 expression in ectopic lesions at both mRNA (p<0.01) and protein levels. Mechanistically, LRP1 may promote the progression of EMS by enhancing cell migration, invasion, and proliferation through the MIF signaling pathway. Collectively, these findings identified LRP1 as a central regulator of EMS progression through immunomodulation and intercellular crosstalk, offering novel diagnostic and therapeutic potential. - Source: PubMed
Publication date: 2026/04/15
Xie ChengmaoLiu Yong - Multiple sclerosis (MS) and neuromyelitis optica (NMO) are distinct autoimmune demyelinating diseases of the central nervous system with overlapping clinical features, complicating early diagnosis. Accurate differentiation is essential to avoid inappropriate treatment and improve outcomes. We conducted a comprehensive proteomic analysis of cerebrospinal fluid (CSF) from MS and NMO patients using both conventional proteomics and a nanoparticle-based low-abundance protein enrichment strategy (LAPE). Deep CSF proteome coverage yielded 3,816 proteins. Proteomic profiling revealed shared and distinct molecular features of MS and NMO. The common downregulation of neuronal adhesion pathways and the activation of immune responses highlight convergent mechanisms of neurodegeneration and inflammation, whereas MS-specific alterations in glycosylation suggest divergent molecular processes. Differential proteomic analysis delineated disease-specific signatures, with MS characterized by enhanced macrophage signaling, chemokine production, and complement activation, while NMO was distinguished by hemostasis-related pathways, Toll-like receptor 4 signaling, and neuroinflammatory responses. LAPE uncovered MS-associated changes in focal adhesion, cognition, and learning, and NMO-associated enrichment of lysosomal and phagocytic processes. Validation in an independent cohort using enzyme-linked immunosorbent assay (ELISA) confirmed CD74 as an MS-specific and CD14 as an NMO-specific biomarker with ROC analyses (AUC 0.75 for CD74; 0.72 for CD14) supporting their robust utility as discriminating biomarkers in clinical practice. - Source: PubMed
Publication date: 2026/04/30
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