F11R _ JAM_A
- Known as:
- F11R _ JAM_A
- Catalog number:
- Y214153
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- F11R _ JAM_A
Related genes to: F11R _ JAM_A
- 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 _ JAM_A
Anti-Human CD321 (F11R) Purified 100 ugAnti-Human CD321 (F11R) Purified 25 ugAnti-human JAM-B, Source: Monoclonal Murine, MABAnti-human JAM-C, Source: Monoclonal Murine, MABAnti-murine JAM-A, Source: Monoclonal Rat, MABAnti-murine JAM-B, Source: Monoclonal Rat, MABAntibodies: F11R _ JAM-A HOST: Goat Clonality: pAbAntibodies: JAM-1 Clone: BV12Antibodies: JAM-1 Clone: BV16Antibodies: JAM-1 Clone: M.Ab.F11Antigens F11R, 26-238aa, Human, His tag, E.coli, RecombinantBovine F11 receptor (F11R) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine Junctional adhesion molecule A(F11R) ELISA kitBovine Junctional adhesion molecule A(F11R) ELISA kit SpeciesBovineBV12 JAM-1 Related articles to: F11R _ JAM_A
- 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 - Dendritic cell-T cell (DC-T) co-signalling pathways are central switches directing immunity, tolerance, or evasion. Despite characterisation of known pathways, additional mediators that may contribute uniquely to regulating T-cell responses remain to be defined. - Source: PubMed
Publication date: 2026/01/28
Bonilha Caio Santos - Long-standing diabetes mellitus (long-DM) (≧3 years) is associated with worse clinical outcomes in patients with pancreatic ductal adenocarcinoma (PDAC). Emerging evidence suggests that epigenetic alterations may contribute to this association; however, the underlying mechanisms remain largely unclear. This study aimed to elucidate the role of the tumor-suppressive long noncoding RNA maternally expressed gene 3 (MEG3) and related molecules in the development of PDAC with long-DM. A total of 117 patients who underwent surgical resection for PDAC at Hirosaki University Hospital were retrospectively analyzed. Histopathological assessment followed World Health Organization criteria and the Union for International Cancer Control tumor-node-metastasis classification. Promoter methylation of MEG3 was assessed via methylation-specific PCR using formalin-fixed paraffin-embedded tissue. MEG3 expression levels were assessed by real-time quantitative PCR. Additionally, proteomic profiling was performed using liquid chromatography-tandem mass spectrometry on formalin-fixed paraffin-embedded tissue samples. Among the 117 cases with PDAC, patients with long-DM exhibited significantly poorer tumor differentiation and reduced cancer-specific survival. MEG3 promoter methylation was more prevalent in patients with long-DM. MEG3 methylation was correlated with reduced MEG3 expression, increased venous invasion, higher recurrence rates, and worse prognosis. Proteomic analysis and protein structure prediction tool revealed F11 receptor (F11R) as a potential downstream effector of MEG3. F11R protein expression levels were evaluated using semiquantitative immunohistochemistry. Higher F11R expression was observed in patients with long-DM, correlating with poor histologic differentiation and unfavorable outcomes. Patients with PDAC showing simultaneous MEG3 methylation and F11R high expression were more likely to have long-DM, with additive effects of these changes and tumor recurrence. Our results demonstrated that MEG3 and its potential downstream regulator, F11R, could be involved in PDAC progression, particularly in patients with long-DM. The findings underscore the clinical significance of epigenetic regulation in DM-related PDAC, suggesting novel targets, such as MEG3 and F11R, for potential therapeutic intervention. - Source: PubMed
Publication date: 2025/12/16
Yamazaki KeisukeMizukami HirokiYamada TakahiroHara YutaroTamba HiroakiTatara YotaWang ZhenchaoItaya AkikoKushibiki HanaeRyuzaki MasakiSasaki TakanoriRuike HidefumiOgasawara SaoriTu YiIshido KeinosukeItoh KenHakamada Kenichi - Extensive leukocyte diapedesis is a defining step in inflammation and contributes critically to myocardial ischemia/reperfusion injury (MI/RI). Infiltrating leukocytes amplify local inflammation and exacerbate myocardial damage. However, the upstream control of the trans-endothelial migration step remains incompletely understood. Peripheral blood myeloid cells were isolated from MI/RI patients and healthy donors to examine MAP3K3 expression and its correlation with cardiac markers. Mouse MI/RI models were established to investigate MAP3K3 expression of myeloid cells in the heart. Myeloid-specific deficiency mice were used to evaluate the impact of MAP3K3 depletion on MI/RI severity and on myeloid cell diapedesis from the bone marrow. RNA sequencing and various manipulations of the MAP3K3/TAL1/JAM-A axis were used to elucidate its role in diapedesis. Finally, the therapeutic potential of pazopanib, a MAP3K3 inhibitor, was evaluated in the mouse MI/RI model. MAP3K3 expression was upregulated in both monocytes and neutrophils from MI/RI patients and was positively correlated with the severity of MI/RI. In mice, MAP3K3 in cardiac myeloid cells peaked at day 3 post-MI/RI. Myeloid cell-specific depletion of MAP3K3 alleviated MI/RI by reducing the infiltration of myeloid cells into cardiac tissue. Functionally, MAP3K3 facilitated myeloid cell de-adhesion and transmigration across endothelial barriers. Further mechanistic studies identified the MAP3K3/TAL1/JAM-A signaling pathway as a key regulator of myeloid cell diapedesis. MAP3K3 phosphorylates TAL1 at Ser-122, leading to its ubiquitination and attenuating its transcriptional repression of (encoding JAM-A). Through JAM-A, MAP3K3 promotes integrin internalization, thereby enhancing de-adhesion and myeloid cell transmigration. Treatment with pazopanib, a MAP3K3 inhibitor, ameliorated MI/RI injury and reduced myeloid cell diapedesis into the heart by blocking MAP3K3 phosphorylation activity. MAP3K3 orchestrates myeloid cell diapedesis via a TAL1/JAM-A dependent program during MI/RI. Targeting MAP3K3, exemplified by pazopanib, may offer a therapeutic strategy for MI/RI and related inflammatory conditions. - Source: PubMed
Publication date: 2026/01/01
Hu ShiyuZhang JianWang JingpuLi ChenguangWang YiwenLiang JiayuHuang RongYang Ji'eGao YangQu YananYang HongboQian JuyingTang WenwenCao JiatianZhang FengGe Junbo