M.Ab.F11 JAM-1
- Known as:
- M.Antibody.F11 JAM-1
- Catalog number:
- mc-199
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- ..F11 JAM-1
Related genes to: M.Ab.F11 JAM-1
- Gene:
- AGAP14P NIH gene
- Name:
- ArfGAP with GTPase domain, ankyrin repeat and PH domain 14, pseudogene
- Previous symbol:
- CTGLF11P, AGAP14
- Synonyms:
- bA145E20.1
- Chromosome:
- 10q11.22
- Locus Type:
- pseudogene
- Date approved:
- 2004-05-27
- Date modifiied:
- 2017-08-14
- Gene:
- BTF3P11 NIH gene
- Name:
- basic transcription factor 3 pseudogene 11
- Previous symbol:
- BTF3L1
- Synonyms:
- HUMBTFB, TNFRSF11B, OPG, OCIF
- Chromosome:
- 13q22.3
- Locus Type:
- pseudogene
- Date approved:
- 1997-12-12
- Date modifiied:
- 2016-10-05
- Gene:
- C1QL4 NIH gene
- Name:
- complement C1q like 4
- Previous symbol:
- -
- Synonyms:
- C1QTNF11, CTRP11
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-22
- Date modifiied:
- 2016-07-04
- Gene:
- C6orf99 NIH gene
- Name:
- chromosome 6 open reading frame 99
- Previous symbol:
- -
- Synonyms:
- yR211F11.1
- Chromosome:
- 6q25.3
- Locus Type:
- unknown
- Date approved:
- 2003-11-26
- Date modifiied:
- 2019-03-01
- Gene:
- C18orf25 NIH gene
- Name:
- chromosome 18 open reading frame 25
- Previous symbol:
- -
- Synonyms:
- MGC12909, ARKL1, RNF111L1, Ark2N
- Chromosome:
- 18q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-19
- Date modifiied:
- 2018-05-15
Related products to: M.Ab.F11 JAM-1
Related articles to: M.Ab.F11 JAM-1
- 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 - Salivary gland carcinomas are rare, heterogeneous, and often resistant to conventional treatments, highlighting the need for new therapeutic strategies. This retrospective study evaluated the expression of three immunologically relevant biomarkers-PRAME, FOLR1, and CLDN18.2-as potential therapeutic targets in salivary gland carcinomas. Tumor samples from 54 patients with seven histological subtypes treated at Saarland University Medical Center between 2013 and 2023 were analyzed using immunohistochemistry and scored with the Immunoreactive Score. PRAME was strongly expressed in 89% of cases, while FOLR1 and CLDN18.2 showed markedly lower expression at 41% and 6%, respectively. High PRAME expression was significantly associated with the presence of distant metastases, regardless of histological subtype. Patients with low PRAME expression tended to have improved overall survival, as indicated by Kaplan-Meier analysis and Log-Rank testing. These findings suggest PRAME as a promising immunotherapeutic and diagnostic target for salivary gland carcinomas, particularly through T-cell-based therapies already under investigation in other malignancies such as acute myeloid leukemia. Further preclinical studies are needed to validate the functional and therapeutic significance of PRAME, FOLR1, and CLDN18.2 in this context. - Source: PubMed
Brust Lukas AKühn Jan PhilippKörner SandrinaKnebel MoritzBraun Felix LZeidan PhilippeWemmert SilkeSchick BernhardSmola SigrunWagner MathiasErtz MartinLinxweiler Maximilian - Preterm birth remains a leading cause of neonatal morbidity and mortality. It is classified as spontaneous, characterized by the unexpected onset of labor, or medically indicated, resulting from obstetric intervention due to pregnancy complications. The mechanisms underlying each subtype are incompletely understood, and obesity further modulates preterm birth risk through unclear biological pathways. This study aims to identify second trimester maternal plasma proteomic signatures distinguishing spontaneous and medically-indicated preterm birth and to determine how body mass index modifies these profiles. - Source: PubMed
Publication date: 2026/02/12
Lopez Zapana Paola ADeBolt Chelsea AKarginov LukaRiis ValerieNcube LiqhwaEdlow Andrea GElovitz Michal ALauffenburger Douglas A