Ask about this productRelated genes to: CD138 antibody
- Gene:
- SDC1 NIH gene
- Name:
- syndecan 1
- Previous symbol:
- SDC
- Synonyms:
- CD138, syndecan, SYND1
- Chromosome:
- 2p24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-03-18
- Date modifiied:
- 2014-11-19
Related products to: CD138 antibody
Related articles to: CD138 antibody
- Proteases are promiscuous enzymes acting on multiple substrates. Inhibiting pathogenic proteolysis while sparing physiological ones is essential for the development of effective and safe inhibitors. By engineering β-lactamase and levansucrase as selection and counterselection markers in E. coli periplasm, this study established functional positive and negative selections for the facile discovery of protease inhibitory mAbs rendering substrate specificity. Isolated anti-matrix metalloproteinase (MMP)-14 inhibitory mAbs exhibited nanomolar binding affinities and inhibitory potencies, exclusive selectivity, high proteolysis stability, and substrate-specific (SS) inhibition, that is, blocking MMP-14 mediated proteolysis of pro-tumorigenic syndecan-1 (Sdc-1) while allowing cleavage of anti-inflammatory macrophage chemoattractant protein 3 (MCP-3). Mechanistic studies suggested that the isolated Fabs were active-site competitive inhibitors and their substrate specificity was achieved by recognizing the protease's prime subsites shared with Sdc-1 but distinct to that of MCP-3. Given the pharmaceutical significance of SS inhibition, we envision the dual functional selection can be widely applicable to important protease targets. - Source: PubMed
Lee Ki BaekLee SangcheonReddi BharatiKrishnan SushmaWang ZeningGe Xin - Damage to the endothelial glycocalyx plays a key role in the pathogenesis of sepsis. Syndecan-1 is a widely used biomarker of glycocalyx degradation. The objectives of this study were (1) to determine whether the pathogen type is correlated with differences in glycocalyx disruption in critically ill patients with bacterial bloodstream infection (BSI) and (2) to assess the association of plasma syndecan-1 levels with host response changes implicated in the pathogenesis of sepsis. - Source: PubMed
Publication date: 2026/06/02
Wang HuiButler Joe MMichels Erik H AReijnders Tom D Yvan Engelen Tjitske S Rde Vos Alex FCremer Olaf LPeters-Sengers Hesselvan der Poll Tom - Oral mucosa exhibits region-specific keratinization, essential for periodontal health, yet the spatial and molecular mechanisms driving these differences remain poorly understood. This study aimed to generate a high-resolution spatial transcriptomic atlas of the human oral mucosa around the mucogingival junction, to reveal stromal-epithelial interactions, that distinguish keratinized from non-keratinized programs. Formalin-fixed paraffin-embedded specimens from the mucogingival junction area of two healthy donors were analyzed with the 10 × Genomics Visium HD platform, yielding two keratinized and two non-keratinized regions. Spatial clustering, pseudotime trajectory inference, cell-type integration with a single-cell reference, and ligand-receptor network analysis were applied to delineate epithelial and stromal compartments. Sixteen reproducible clusters, recapitulating tissue architecture, were identified and revealed distinct transcriptional signatures, distinguishing gingiva from lining mucosa. Pseudotime analysis revealed bifurcating epithelial lineages, originating from a shared basal progenitor layer into keratinized and non-keratinized programs. Gingival keratinization was driven by stromal collagen ligands (COL1A1, COL1A2, COL6A1, COL6A2) engaging epithelial receptors (CD44, SDC1), further reinforced within the epithelium by desmosomal adhesion via DSG1-DSC2/3. Gingival keratinization emerges from integrated stromal collagen signaling and epithelial adhesion. This spatially resolved framework advances understanding of oral mucosal specialization and provides a foundation for biologically guided regenerative therapies. - Source: PubMed
Publication date: 2026/06/15
Rosental Vazani NoyLusthaus MichalCaetano AnaKhosravi RamiSarusi Portuguez AvitalNemcovsky Carlos EBender OmerBar Daniel ZWeinreb MironWeinberg Evgeny - Inflammatory bowel disease (IBD) is a chronic and recurrent gastrointestinal disease, the pathogenesis of which has not been fully elucidated. Increasing evidence suggests that the disorder of mitochondrial metabolism is closely related to the pathogenesis of IBD, but its specific regulatory network and key genes remain to be further investigated. IBD-related transcriptome datasets (GSE3365 and GSE75214) and single-cell sequencing dataset (GSE134809) were obtained from the Gene Expression Omnibus database. Differentially expressed genes and hub genes were identified through differential expression analysis and weighted gene co-expression network analysis, and candidate genes were obtained by intersecting these with mitochondrial metabolism-related genes, followed by functional enrichment analysis. Machine learning algorithms were used to screen key genes and construct risk prediction models. Additionally, analysis of GSE134809 single-cell data identified characteristic cell types and expression distribution of key genes in IBD and explored communication between different cell types. Furthermore, immune cell infiltration, competitive endogenous RNA (ceRNA) network, and transcription factor prediction were performed. Finally, the diagnostic performance of key genes was validated in GSE75214 and reverse transcription-quantitative polymerase chain reaction. Two key genes, mitochondrial ribosomal protein L35 () and , were identified, which were downregulated in IBD, and had good diagnostic potential. Single-cell analysis revealed that key genes were predominantly highly expressed in mononuclear phagocyte (MNP) cells. MNP cells communicated with other cells through receptor ligands including MIF-(CD74 + CXCR4), MDK-SDC1, and ITGB2-ICAM2, which are complexly related to mitochondrial metabolism. With the progression of IBD, infiltration levels of resting natural killer cells, naive B cells, M2 macrophages, and naive CD4 T cells decreased, and correlations between different cells continuously changed. A ceRNA network centered on XIST, hsa-miR-103a-3p, and was constructed. Additionally, therapeutic drugs targeting key genes were predicted, including cimetidine, eugenol, chlortetracycline, vincristine, irinotecan, bisacodyl, and sulpiride, with molecular docking validating high affinity between these drugs and key targets. This study constructed a multiomics integrated analysis strategy and identified and as potential markers and therapeutic targets, providing new insights for the diagnosis and treatment of IBD. - Source: PubMed
Publication date: 2026/06/15
Li HaoWu XichuanWu QingpingWang Jian - Obstructive sleep apnea (OSA) is associated with cardiovascular disease. The endothelial glycocalyx (eGCX) is a shear-sensitive intravascular barrier. The relevance of OSA and intermittent hypoxia (IH) for eGCX perturbation and cardiovascular disease in humans remains unclear. - Source: PubMed
Publication date: 2026/06/12
Müller Martin BernhardKammerer TobiasKhan HumayunSchmid AnnikaHirschberger SimonHübner MaxBarth Teresa KMitsigiorgi ReaStihl ClemensHolzer MartinJira DanielPatscheider MartinWeiss Bernhard GReichel Christoph AndreasUhl Bernd