Mouse TREM-1 PicoKine ELISA Kit
- Known as:
- Mouse TREM-1 PicoKine Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- EK0845
- Product Quantity:
- 1x96 well plate
- Category:
- -
- Supplier:
- boster immunoleader
- Gene target:
- Mouse TREM-1 PicoKine ELISA Kit
Related genes to: Mouse TREM-1 PicoKine ELISA Kit
- Gene:
- TREM1 NIH gene
- Name:
- triggering receptor expressed on myeloid cells 1
- Previous symbol:
- -
- Synonyms:
- TREM-1, CD354
- Chromosome:
- 6p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-09
- Date modifiied:
- 2014-11-19
Related products to: Mouse TREM-1 PicoKine ELISA Kit
Related articles to: Mouse TREM-1 PicoKine ELISA Kit
- Cerebral amyloid angiopathy (CAA) is a common age-associated cerebrovascular disease marked by amyloid-β (Aβ) accumulation in cerebral vessel walls, and it is tightly linked to Alzheimer's disease (AD) and cognitive impairment. However, the specific mechanism in CAA progression remains poorly elucidated. - Source: PubMed
Publication date: 2026/08/18
Zhang YizhouYe MengyaoMi ShixiongZhou YiYu QihanLiang JiayiWang ShiyiYang QianSu YuhongCui HuixianMa XiaoweiDu Juan - Ulcerative colitis (UC) is a chronic immune-mediated inflammatory disease characterized by dysregulated mucosal immunity in genetically susceptible individuals exposed to environmental and microbial triggers. Tumor necrosis factor-alpha (TNF-α) antagonists have transformed the management of moderately-to-severely active UC and remain a cornerstone of therapy, although approximately one third of patients demonstrate primary non-response and up to half experience secondary loss of response over time. Historically, treatment failure has been attributed to pharmacokinetic factors such as inadequate drug exposure or immunogenicity. Increasing evidence suggests that TNF-α resistance is frequently mediated by pharmacodynamic factors, including cytokine redundancy and non-TNF inflammatory circuits. Among the most prominent mechanisms are activation of the IL-6 signaling axis, stromal cytokines such as oncostatin M, IL-23-driven Th17 inflammation, and IL-1-mediated innate immune responses. More exploratory mechanisms include perturbations in B-cell and plasmablast biology, transcriptional signatures associated with myeloid activation, genetic susceptibility pathways such as TREM-1 signaling, and microbiome-driven metabolic dysfunction. Emerging data also suggest a role for neutrophil extracellular traps. Although biologically plausible, the clinical relevance and therapeutic implications of several of these emerging mechanisms remain to be established. Advances in transcriptomics, single-cell sequencing, and systems biology approaches have further highlighted the heterogeneity of inflammatory pathotypes in UC and the importance of precision medicine strategies. Understanding the molecular determinants of TNF-α resistance could inform more rational therapeutic sequencing, guide optimization of existing therapies, and identify novel targets for combination or next-generation treatments aimed at improving outcomes in patients with difficult-to-treat UC. In this review, we highlight key mechanisms of TNF-α non-response, identify potentially druggable therapeutic targets within this framework, and define future directions for advancing care in patients with UC who experience TNF-α non-response. - Source: PubMed
Publication date: 2026/08/26
Fairweather MorganFaggiani IlariaMa Christopher - Chronic obstructive pulmonary disease (COPD) and lung cancer (LC) frequently co-occur and share environmental and biological determinants, yet their cross-scale associations remain incompletely understood. Artificial intelligence and machine learning-based integration of exposome and multi-omics data provide new opportunities for dissecting this complex comorbidity. - Source: PubMed
Publication date: 2026/08/07
Fei YiranChai YinyingTong ShiyuanSun BohaoChen ZiqiangChen ShiliangZhang ZhezhongHe YiboQiu Shengliang - Animal immune cells express a range of surface receptors that promote the detection of diverse host and pathogen-derived molecules. The triggering receptors expressed on myeloid cells (TREMs) encompass a family of cell surface receptors involved in the modulation of immune signaling cascades. Mammalian TREM-1 has emerged as a critical mediator of antibacterial immune defense and inflammatory disease, yet much remains unknown regarding its evolution and relevant molecular interactions. Here we applied a comparative phylogenetic approach to investigate patterns of divergence and natural selection among mammalian TREM-1 orthologs. We identify evidence of repeated positive selection acting within the extracellular ligand binding domain of TREM-1 among primates, rodents, and particularly bats. Structural simulations further suggest that genetic variation in TREM-1 impacts recognition of putative host and microbial ligands, with implications for downstream signaling functions. Together our findings identify patterns of rapid divergence in mammalian TREM-1, suggesting a history of evolutionary conflict in response to pathogen antagonism. - Source: PubMed
Publication date: 2026/08/10
Aleru OmosholaBunn Kaitlyn EBarber Matthew F - Intestinal fibrosis is a major complication of Crohn's disease (CD), a subtype of inflammatory bowel disease (IBD) driven by chronic inflammation and resulting in irreversible structural damage requiring surgery. However, the molecular differences between inflammatory and fibrotic CD remain poorly defined. - Source: PubMed
Publication date: 2026/08/04
Philip DaryllSantos DanielaMondal SudipAlomar HaneenGkoutos GeorgiosAcharjee Animesh