F11R (Human) Matched Antibody Pair
- Known as:
- F11R (Human) Matched Antibody Pair
- Catalog number:
- H00050848-AP61
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- F11R (Human) Matched Antibody Pair
Related genes to: F11R (Human) Matched Antibody Pair
- Gene:
- F11R NIH gene
- Name:
- F11 receptor
- Previous symbol:
- JAM1
- Synonyms:
- PAM-1, JCAM, JAM-1, JAM-A, JAMA, CD321
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-10
- Date modifiied:
- 2016-10-05
Related products to: F11R (Human) Matched Antibody Pair
Related articles to: F11R (Human) Matched Antibody Pair
- Tight junctions are sites of cell-cell contacts at the apical region of epithelial junctions that are involved in barrier formation, cellular signaling, and cell-cell adhesion. Tight junctions are formed by integral membrane proteins associated with cytoplasmic scaffolding and adapter proteins through which they are linked to the underlying actomyosin and microtubule cytoskeletons. Here, we have addressed the interaction of the Junctional Adhesion Molecule (JAM)-C with the zonula adherens (ZO) protein ZO-2. Using a combination of cell-based recruitment assays and biochemical in vitro experiments, we find that JAM-C and ZO-2 directly interact in a PDZ domain-dependent manner. Notably, the interaction requires PDZ domain 3 as well as the SH3 domain of ZO-2, indicating that ZO-2 forms a functional supramodule to interact with JAM-C. We also found that JAM-C is specifically localized to tight junctions in polarized epithelial cells and that JAM-A suppresses JAM-C mRNA expression in these cells. Our findings have implications for important aspects of tight junction biology, including mechanosensing and liquid-liquid phase separation. - Source: PubMed
Publication date: 2026/06/10
Schulte AnnikaSchwietzer Mariel FBrinkmann FraukeTeuber ValentinCiti SandraFuruse MikioAurrand-Lions MichelEbnet Klaus - Furosemide (FSD) is a widely prescribed loop diuretic; however, its potential reproductive toxicity and its underlying mechanism have not been explored yet. The current study assessed the dose-dependent effects of FSD on testicular function in Sprague Dawley rats. Thirty-two male Sprague Dawley rats were apportioned into four groups i.e., control, FSD (10 mg/kg), FSD (20 mg/kg), and FSD (30 mg/kg) treated group. FSD exposure significantly downregulated the expression of blood-testis barrier genes (CLDN11, OCLN, TJP1, F11R, CDH2, GJA1), as well as upregulated pro-inflammatory mediators (NF-κB, TNF-α, IL-1β, IL-6, COX-2) in a dose-dependent manner, which indicates disruption of intercellular junctions and testicular inflammation. Oxidative stress was significantly increased, as revealed by increased ROS and MDA concentrations and decreased antioxidant enzymes (CAT, SOD, GPx, GSR, HO-1) after FSD exposure. Moreover, FSD intoxication suppressed the levels of reproductive hormones (LH and FSH, testosterone), indicating the impairment of the hypothalamic-gonadal axis. Apoptotic indices showed increased Bax, Caspase-3, Caspase-9 and decreased Bcl-2 after FSD administration, confirming activation of mitochondrial-mediated germ cell death. Similarly, semen analysis showed FSD exposure reduced the number, motility, sperm membrane integrity, and viability while increasing sperm abnormalities. Steroidogenic enzymes (StAR, 3β-HSD, 17β-HSD) were suppressed, which may indicate impaired biosynthesis of testosterone and spermatogenesis. Histopathological evaluations revealed severe degree of seminiferous tubule degeneration, reduction of germ cell population, and structure change of testicular architecture following the administration of FSD. Collectively, these findings demonstrate the multifaceted testicular toxicity of FSD, via disruption of BTB, oxidative stress, hormonal dysregulation, apoptosis and structural degeneration, leading to eventual consequences on male reproductive health. These results distinguish the potential reproductive risk caused by FSD exposure, warranting clinical trials for validation in humans. - Source: PubMed
Publication date: 2026/06/01
Aloraini Ghfren SAlissa MohammedAlghamdi Abdullah - BackgroundIntegrated bioinformatics approaches were used to identify stage-specific candidate genes and potential drug targets in triple-negative breast cancer (TNBC).MethodsMicroarray (164 early-stage, 33 advanced-stage, and 53 normal samples) and RNA-seq (113 normal, 163 early-stage, and 30 advanced-stage TNBC samples) datasets were analyzed. Differentially expressed genes (DEGs) were identified, followed by co-expression analysis using Weighted Gene Co-expression Network Analysis (WGCNA) and protein-protein interaction analysis using the STRING database. miRNA co-regulation was evaluated using multiMiR and TCGA correlation analyses. Candidate genes were validated using UALCAN and immunohistochemistry data. Molecular docking assessed potential therapeutic agents.ResultsNovel stage-specific candidate biomarkers were identified, including , , , and in early-stage TNBC, and , , , and in advanced-stage TNBC. UALCAN analysis confirmed the dysregulation of these genes across 23 additional malignancies. STRING-based network analysis revealed stage-specific protein-protein interactions, including SKP2-SKP1 in early-stage and F11R-TJP1 in advanced-stage TNBC. miRNA co-regulation distinguished early-stage TNBC through PI3K-AKT-related pathways and advanced-stage TNBC through tumor progression-associated pathways. Docking-based drug repurposing highlighted conventional agents (e.g., doxorubicin) and potential novel candidates (e.g., sunitinib).ConclusionThis study identifies novel stage-specific gene candidates and suggests repurposable drugs for TNBC, supporting progression-specific targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/05/28
Shahraki FaezeMeshkini AzadehNazari Elham - Hepatocellular carcinoma ranks among the most prevalent malignancies worldwide. While stress can modulate tumor initiation, progression, metastasis, and therapeutic response through diverse mechanisms, its specific role in hepatocellular carcinoma pathobiology remains elusive. This study aimed to elucidate the role of the gut microbiota in stress-promoted hepatocellular carcinoma progression and to uncover the pathways associated with disease progression. - Source: PubMed
Publication date: 2026/05/12
Hu ZheYue PengfeiYuan MinlanZhang ZhenjieLi QiaoqiYang TingLi YiDing Bi-SenFan ZhenxinYang BiaoCao Zhongwei - Multiple myeloma (MM) is an incurable malignancy of terminally-differentiated plasma cells that represents a major clinical challenge despite unprecedented therapeutic advances, particularly for patients with cytogenetically-defined high-risk MM (HR-MM). Updated in 2025, the evolving cytogenetic classification of HR-MM includes gains or amplifications in chromosome 1q. One gene of emerging interest on chromosome 1q is F11R, which codes for a protein called Junctional Adhesion Molecule-A (JAM-A). Upregulation of JAM-A has been linked with the development of several aggressive malignancies, most recently MM. In the current study, F11R gene expression was found to be significantly higher in gain/amp(1q) MM patients from the CoMMpass database, and to correlate with poorer overall survival in MM patients. Furthermore, elevated F11R expression was accompanied by an increased burden of circulating CD138 cells, potentially an early hallmark of extramedullary disease (EMD). As JAM-A signalling putatively promotes tumorigenic behaviour through cis-dimerization-dependent adhesion signalling, structure-based rational design principles were utilised to design novel peptide inhibitors that selectively disrupt JAM-A cis-dimerization. In vitro testing of novel peptides across a panel of MM cell lines and primary CD138+ cells from MM patients demonstrated anti-proliferative and pro-senescence properties of the novel peptides. Moreover, candidate peptide P4 significantly inhibited the growth of CD138+ plasmacytoma-like tumours in an in vivo xenograft model involving implantation onto the chick chorioallantoic membrane. Collectively, these findings support the validity of JAM-A as an emerging druggable target and provide a strong rationale for further preclinical investigations of JAM-A inhibitors in MM. - Source: PubMed
Publication date: 2026/05/27
McAuley NiamhMcAvera RoisinBong DimitriDonnelly LaraCymer IzabelaBrennan MarianFay JoannaHudson LanceQuinn JohnGlavey Siobhan VHopkins Ann M