TREM2
- Known as:
- TREM2
- Catalog number:
- Y213704
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- TREM2
Related genes to: TREM2
- 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
Related articles to: TREM2
- Large-artery (LAA-stroke) is a leading cause of cardiovascular morbidity and mortality worldwide. Recent evidence indicates that lysosomal dysfunction plays a critical role in its pathogenesis, yet the underlying molecular mechanisms remain incompletely understood. Identifying characteristic lysosome-related genes (LRGs) offers new perspectives for deciphering disease mechanisms and developing novel therapeutic strategies. - Source: PubMed
Publication date: 2026/04/24
Bai FanghuiHu YuanzhengWang ZongqingGuo YueBie PengkunShi ZhanwangLi XiangxinLi DanDanZhao ChengpengXu Qian - Heart failure (HF) and cognitive impairment (CI) frequently coexist. The objective of this meta-analysis was to synthesize evidence on the association between circulating biomarkers of neurodegenerative diseases and (1) the incidence of HF; (2) cognitive dysfunction in patients with HF; and (3) adverse HF outcomes. - Source: PubMed
Shokravi ArveenLuo YuchenRabkin Simon W - White adipose tissue (WAT) expands through adipocyte hypertrophy or hyperplasia-associated differentiation of progenitor adipose stem cells (ASC). The triggering receptor expressed on myeloid cells 2 (TREM2) reportedly promotes adipocyte differentiation and whole body TREM2 deletion in mice leads to adipose hypertrophy and worsened metabolic health. However, whether TREM2 expression in ASC is involved is unknown. Here, we find TREM2 is expressed on platelet derived growth factor receptor-α (PDGFR-α) positive ASC in obesity. While global deletion of TREM2 strongly attenuated adipocyte differentiation in three different cell culture models, conditional TREM2 deletion within PDGFR-α ASC impacted early adipocyte differentiation. Obese animals where TREM2 was specifically deleted in PDGFR-α expressing cells exhibited moderately increased ASC, but WAT morphology, macrophage amounts as well as glucose and insulin tolerance were comparable to littermate controls. Thus, although TREM2 is important for adipocyte differentiation in cell culture, its expression in ASC is dispensable for WAT remodeling and metabolic health during obesity. - Source: PubMed
Publication date: 2026/04/23
Dobrijevic AnjaKorosec AnaBrunner Julia StefanieMatejovicova LenkaGemza AnnaLakovits KarinLam Hon ShingAgirre-Lizaso AloñaSchabbauer GernotKnapp SylviaSharif Omar - Niemann-Pick disease, type C1 (NPC1), is a rare, fatal, neurodegenerative lysosomal disorder caused by pathological variants in NPC1. Defects in lysosomal cholesterol transport result in the accumulation of unesterified cholesterol within the endo-lysosomal compartments. Delayed diagnosis, limited treatment options, and phenotypic heterogeneity characterized by a broad range of signs/symptoms underscore the urgent need for effective biomarkers to facilitate diagnosis, monitor disease progression and assess therapeutic response. The goal of this study was to identify serum protein biomarkers for NPC1. - Source: PubMed
Publication date: 2026/05/09
Singhal KhushbooMenold Matthew TCawley Niamh XCampbell KierstenFarhat Nicole YAlexander DerekDale Ryan KPorter Forbes D - Glioblastoma (GBM), the most aggressive primary brain tumor, develops within a tumor microenvironment (TME) dominated by tumor-associated macrophages (TAMs) that critically influence disease progression. Through single-cell RNA sequencing (scRNA-seq) and bioinformatic analysis, we delineated macrophage heterogeneity within the GBM TME and identified a distinct VCAN⁺ macrophage subpopulation. Pseudotime trajectory analysis revealed these cells at the terminal stage of macrophage differentiation, where they exhibit enhanced granulocyte migration and chemotaxis pathways and exhibit a pro-tumorigenic phenotype that diverges from classical M1/M2 polarization. These VCAN⁺ macrophages displayed a distinct polarization state driven by tumor necrosis factor-α (TNF-α), contributing to both a pro-inflammatory and an immunosuppressive TME. CellChat analysis demonstrated their pivotal role in intercellular communication-predominantly mediating crosstalk with GBM tumor cells, endothelial cells, and CD8⁺ T cells via SPP1 signaling: SPP1 binding to CD44 on tumor cells enhances their invasiveness, while its interaction with CD47 on CD8⁺ T cells inhibits anti-tumor immunity. Transcriptional regulatory network analysis identified that CDX2 and MXI1 serve as key transcription factors modulating VCAN⁺ macrophage function and maintaining their specific polarization and homeostasis. Through machine learning, we identified seven hub genes-C1QA, C1QC, C3, CCL4, CD44, SERPINE1, and TREM2 (all highly expressed in VCAN⁺ macrophages and involved in their polarization or intercellular communication)-and constructed an effective GBM prognostic model (AUC = 0.83 in validation cohort), underscoring their roles in immune regulation, extracellular matrix remodeling, and VCAN⁺ macrophage-mediated tumor progression. Further studies with larger cohorts and functional validation will clarify this subpopulation's therapeutic potential and spatial distribution patterns. - Source: PubMed
Publication date: 2026/05/09
Guo JiaxinZhu ZhanshengTong NanyangXu DingdingZhang HuanLin ChenshiWan GuipingWang YameiZhou QingqingXia Liang