Trem2 (mouse)
- Known as:
- Trem2 (mouse)
- Catalog number:
- Y214279
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Trem2 (mouse)
Related genes to: Trem2 (mouse)
- Gene:
- TREM2 NIH gene
- Name:
- triggering receptor expressed on myeloid cells 2
- Previous symbol:
- -
- Synonyms:
- TREM-2, Trem2a, Trem2b, Trem2c
- Chromosome:
- 6p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-08-09
- Date modifiied:
- 2019-04-23
Related products to: Trem2 (mouse)
Related articles to: Trem2 (mouse)
- DNAX-activated protein 12 (DAP12) is a key transmembrane adaptor protein containing an immunoreceptor tyrosine-based activation motif. DAP12 associates with a broad spectrum of cell surface receptors, including triggering receptors expressed on myeloid cells (TREM1 and TREM2), myeloid DAP12-associating lectin-1 (MDL-1), sialic acid-binding immunoglobulin-like lectin 15 (Siglec15), killer cell immunoglobulin-like receptor (KIR), NKG2C/CD94, and NKp44. They form a sophisticated signaling network that precisely regulates cellular activation, differentiation, and the balance between pro-inflammatory and anti-inflammatory responses. DAP12 is predominantly expressed in innate immune cells, including monocytes/macrophages, microglia, osteoclasts, and natural killer (NK) cells, where it governs key processes like cytokine production, cytoskeletal remodeling, and cytotoxic activity. Dysregulation of DAP12 signaling has been implicated in the pathogenesis of multiple immune-related inflammatory diseases, such as multiple sclerosis, Alzheimer's disease, rheumatoid arthritis, inflammatory bowel disease, and systemic lupus erythematosus. In these conditions, DAP12 contributes to either protective or pathological outcomes depending on the receptor complex and microenvironment. This review provides a comprehensive overview of the structural characteristics of DAP12, its interaction with relevant receptors, and its specific functions in various cell types and immune-mediated inflammation. - Source: PubMed
Publication date: 2026/05/06
Lu JiaqiShi LihaoJin GuiyuanYang YonghongZhu FengqinZhou Guangxi - Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease, ranging from simple steatosis (MASL) to metabolic dysfunction-associated steatohepatitis (MASH). However, reliable noninvasive strategies for accurately distinguishing MASL from MASH at an early stage remain limited. We therefore aimed to develop a robust molecular model to improve early identification of disease progression and subtype discrimination. - Source: PubMed
Publication date: 2026/04/20
Lin Guo WuLin Zhi YuanSu Qi YuanYe LiXu Wei NingNong Shun QiangWu Ru KaiZhou Wei JieHuang Qian Fang - Alzheimer's disease (AD) pathology is increasingly understood to be driven by complex neuroinflammatory processes, with microglia-the resident immune cells of the brain playing a pivotal role. The PI3K/Akt signaling pathway serves as a critical intracellular hub, orchestrating the diverse and often opposing functions of microglia. This review synthesizes current insights into the multifaceted role of Akt signaling in modulating microglial activity in the context of AD. We explore the dualistic nature of Akt, which can promote pro-inflammatory neurotoxicity through pathways such as NF-κB while simultaneously mediating neuroprotective functions, including anti-inflammatory resolution, amyloid-β (Aβ) phagocytosis, and regulation of key clearance receptors like triggering receptor expressed on myeloid cells 2 (TREM2). Additionally, we examine how the Akt/mTOR axis governs microglial immunometabolism, facilitating the transition between glycolytic, pro-inflammatory states and oxidative phosphorylation-driven, phagocytic phenotypes. Emerging therapeutic strategies are discussed, including natural compounds, pharmacological agents, indirect modulation via the gut-brain axis and physical brain stimulation, as well as advanced nanotechnology platforms designed to target this pathway in microglia with precision. Finally, we address key challenges such as isoform specificity, therapeutic timing, and translational relevance, and outline future perspectives aimed at achieving "precision immunomodulation" of the Akt pathway. Such fine-tuning of microglial function represents a promising yet complex avenue for developing effective therapies to combat AD. - Source: PubMed
Publication date: 2026/05/04
Xu YongxingLiang WeidongTang ZhikangLu FengXia LingyiXie HaiyuZhong MaolinLi Shihong - Alzheimer disease (AD) is the most common cause of dementia in the world with the prevalence expected to increase threefold to 152.8 million people by 2050. The current medications provide a short-term ameliorative effect, and this requires development of disease-modifying treatments, which address the biological pathogenesis. - Source: PubMed
Publication date: 2026/05/05
Hafez Mohamed MAbbas Haidy AShoman Nabil ASoubh Ayman AAly OmniaSallam Mohamed FSeliem MahmoudMalaak Fady A - Age-related macular degeneration (AMD) is a leading cause of irreversible central vision loss in older adults. Advanced AMD comprises an atrophic ("dry") form characterized by retinal pigment epithelium (RPE) and photoreceptor degeneration and a neovascular ("wet") form driven by choroidal neovascularization (CNV). Beyond genetic predisposition and environmental stressors, chronic dysregulation of innate immunity is increasingly recognized as a convergent mechanism linking drusen/Bruch's membrane alterations to outer retinal cell death and pathological angiogenesis. Retinal myeloid cells-including resident microglia and, in specific disease contexts, recruited monocyte-derived macrophages-can support homeostasis by clearing lipids and cellular debris, yet may also exacerbate inflammation, matrix remodeling, and neovascularization. Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune receptor expressed by microglia and other myeloid cells that regulates phagocytosis, lipid handling, migration, survival, immunometabolism, and inflammatory tone. Recent retinal studies suggest that TREM2-associated programs can restrain lesion expansion in outer retinal degeneration models and modulate CNV severity in experimental neovascularization; however, interpretation remains limited by disease stage, anatomical niche, and the difficulty of cleanly separating microglia from infiltrating macrophages . Here, we synthesize current evidence on retinal myeloid contributions to dry and neovascular AMD, provide an updated mechanistic framework for TREM2 signaling, and discuss therapeutic strategies and translational challenges for targeting TREM2 in AMD. - Source: PubMed
Publication date: 2026/04/17
Zhu ShengyuYang TaoshuoSheng LimeiShi Lei