Ask about this productRelated genes to: JAml antibody
- Gene:
- JAML NIH gene
- Name:
- junction adhesion molecule like
- Previous symbol:
- AMICA1
- Synonyms:
- Gm638, AMICA
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-12
- Date modifiied:
- 2016-11-16
Related products to: JAml antibody
Related articles to: JAml antibody
- - Source: PubMed
Publication date: 2026/04/23
Wu DiLiao XimingGao JingWang MuyunMeng LinlinXu WujianHe YananZhang QianLi QiangWang KunGao Wei - Atherosclerosis is a chronic inflammatory disease initiated by endothelial dysfunction. Junctional adhesion molecule-like protein (JAML) is known to regulate inflammatory responses; however, its function in vascular endothelial cells and atherosclerosis remains unclear. This study aimed to investigate the function of endothelial JAML in atherosclerosis and to uncover the molecular mechanisms involved. - Source: PubMed
Publication date: 2026/04/18
Han QingmeiXue FeiLi JingweiWu ZhenguoGuo ChenghuZhang YujieWu XiaoYan JieGuo DachuanZou XiaohanZhang WenchengZhang MengZhang ChengYang Jianmin - Immune checkpoint inhibitors (ICIs) can cause immune-related adverse events (irAEs), with acute interstitial nephritis (ICI-AIN) being the most common irAE. While the exact mechanism remains unclear, upregulation of IFN-γ and TNF-α pathways has been implicated. This study used a humanized chimeric PD-1/PD-L1 mouse model to assess renal effects of ICIs, alone or combined with proinflammatory cytokines, and to test if selective TNF-α blockade could prevent ICI-AIN. Mice were randomly divided into 4 experimental groups: Control, ICI-Only, ICI-Cytokines (ICI-Cyt), and ICI-Block (ICI-TNF-α blockade). Renal function and cytokine profiles were assessed, while kidney tissue was analyzed using microscopy and single-cell RNA-seq. Histology revealed increased renal infiltration of CD4+/CD8+ T cells in ICI-treated groups and decreased TNF-α expression following TNF-α blockade. Additionally, kidney tissue ELISA demonstrated reduced IFN-γ levels following TNF-α blockade. Plasma IL-6, MCP-1, and TNF-α were lower in ICI-Block mice. Single-cell RNA-seq revealed shifts in immune cell populations and genes of interest including Bcl2a1, Icos, Il18r1, Ccr2, and Jaml. This humanized model replicates ICI-AIN key features, revealing a synergistic role of ICIs and proinflammatory cytokines. TNF-α blockade demonstrated protective effects, supporting its potential role in mitigating the risk of ICI-AIN. - Source: PubMed
Publication date: 2026/03/05
Cuenca Narvaez Victor DNava Chavez CoraimaAl Refai OmarJacobs Johanna EjGutierrez Luis EZhang SongLi XiaoyanHirdler Jacob BRomero Michael FHerrmann JoergLi XiaogangDong HaidongEirin AlfonsoHerrmann Sandra M - Campylobacter jejuni is a foodborne bacterial infection that is of global concern and responsible for 90% of campylobacter-associated diarrheal diseases in humans. To date, there is no data on the prevalence of C. jejuni in poultry meat in Yemen. This study is the first one that aimed to molecularly detect and determine the antimicrobial susceptibility pattern of C. jejuni isolates from poultry meat in Sana’a, the capital of Yemen. Three hundred and thirty samples of poultry meat (180 local and 150 imported) were collected from various fresh poultry shops and slaughterhouses in the Yemeni capital, Sana’a, during the period from 2023 to 2024. C. jejuni isolates were identified using phenotypic methods and confirmed using molecular techniques, including polymerase chain reaction (PCR), sequence alignment, and phylogenetic analysis. The Kirby-Bauer method was used to determine the antimicrobial susceptibility profile of the isolates. The overall rate of C. jejuni was detected in 40/330 (12.12%) poultry meat samples, 38/180 (21.1%) local meat, and 2/150 (1.3%) imported meat (P = 0.003; Odds Ratio (OR) = 6.57). From local meat, 18 (10%) isolates were recovered from intestinal samples, and only two were recovered from skin samples (1.3%) of the imported meat. The prevalence of C. jejuni peaked in the autumn (12, 3.7%; OR = 1.92). All C. jejuni isolates were completely resistant to macrolide antibiotics and clindamycin and highly resistant to aminoglycosides. In addition, the sensitivity of C. jejuni isolates was reported to be 100% for ampicillin and chloramphenicol and 90.0% for ciprofloxacin. All C. jejuni isolates exhibited multidrug resistance, with the majority being resistant to five antibiotics (60%). These findings revealed that multi-antibiotic-resistant C. jejuni was recovered from poultry meat, particularly local meat. Consequently, it is imperative to establish policies that will mitigate the transmission of animal diseases, restrict the use of antibiotics in poultry farming, provide slaughterhouse employees with training on the proper handling of meat, and enforce strict standards for meat imports. - Source: PubMed
Publication date: 2026/03/04
Al-Bana Mohammed NajeebAlghalibi Saeed MunasserAbdullah Qais YusufEdrees Wadhah HassanAl-Shehari Wadee AbdullahAl-Arnoot SaadAl-Thobhani AssemJaml Nousiba LotfAl-Akhali Basem - Doxorubicin (DOX) is a chemotherapeutic agent used to treat solid tumors and hematologic malignancies, though DOX-induced cardiomyopathy poses a risk of severe cardiac impairment and poor prognosis. Immune cells have been increasingly implicated in cardiovascular inflammation, with overproduction of inflammatory cytokines and macrophage accumulation. However, its molecular mechanism remains unclear and needs to be further investigated. This study investigated the involvement of IKKα in regulating cardiac function in response to early-stage DOX stimulation. Results indicated that IKKα mice were more susceptible to DOX-induced cardiac injury than IKKα mice, showing reduced heart function, extensive cardiac fibrosis, and elevated inflammatory markers. Single-cell transcriptomic analysis revealed cellular heterogeneity in DOX-induced cardiomyopathy tissue between IKKα and IKKα mice, identifying 11 cell types, 8 of which were immune cells. Bar plots and cell density analysis showed a higher proportion of T cells in IKKαmice, while IKKα mice had increased monocytes and macrophages. Notably, IKKα deletion promoted a shift in macrophage polarization from Fcna M2 to Jaml M1 and impaired T cell activation and differentiation. Additionally, IKKα played a critical role in mediating macrophage-T cell interactions. Loss of macrophage IKKα activated T cells through Jaml M1 macrophage, and activated T cells subsequently enhanced M1 macrophage activation via IFN-γ and IL-6. These findings highlight the potential of targeting immune cell interactions as a therapeutic strategy. - Source: PubMed
Publication date: 2026/02/23
Chen GanyiYao YiweiJiang YunfeiQi HaoyuLiu YimingYin LiLi JianCao YideChen XinZhu YifanLiu ShengchenTao Zhonghao