Anti_Mouse, mab TREM_1 Source Rat
- Known as:
- Anti_Mouse, mab TREM_1 Source Rat
- Catalog number:
- 103-M279
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab TREM_1 Source Rat
Related genes to: Anti_Mouse, mab TREM_1 Source Rat
- 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: Anti_Mouse, mab TREM_1 Source Rat
Related articles to: Anti_Mouse, mab TREM_1 Source Rat
- Tumor-associated macrophages (TAMs) are a major immune component of the glioblastoma microenvironment, but macrophage-oriented transcriptomic stratification remains difficult to reproduce across datasets and to validate at the tissue level. - Source: PubMed
Publication date: 2026/06/17
Li GuanpengYan XiaohaoFang Shenying - Heart failure (HF) after myocardial infarction (MI) involves adverse cardiac remodeling. Trem1 may be a potential therapeutic target for MI, but its role in the HF process remains unclear. Our work aimed to investigate the effect of Trem1 on myocardial remodeling in MI-induced HF and the downstream molecular mechanism. The HF mouse model was established by left anterior descending (LAD) ligation, and cardiac function, hypertrophy markers, and fibrosis were measured. Additionally, Mouse cardiac fibroblasts (MCFs) were stimulated with angiotensin II (Ang II), and cell phenotypes, including proliferation and fibrosis, were detected. The regulation of Trem1 on the Rap1 pathway was evaluated using bioinformatics and western blot. We found that Trem1 was upregulated in HF mice (mean fold-change at RNA level was 4.68 and at protein level was 4.43) and AngII-treated MCFs (mean fold-change at RNA level was 6.28 and at protein level was 4.01). Trem1 knockdown improved cardiac function, as indicated by an increase in left ventricular ejection fraction (LVEF) from 36.45% to 58.62% and left ventricular fractional shortening (LVFS) from 18.78% to 30.19%, reduced hypertrophy (heart weight/body weight fold reduced from 6.40 to 4.85 and ANP and BNP mRNA expression was downregulated), and reduced collagen volume fraction from 30.47% to 14.33% in vivo. In AngII-stimulated MCFs, Trem1 silencing decreased cell viability by 48.76%, reduced EdU-positive cells by 46.92%, and downregulated fibrosis-related marker expression. Mechanistically, silencing of Trem1 promoted Rap1 pathway activation, manifested as an increase of 3.79 folds in Epac1, 1.90 folds in active Pap1, and 5.56 folds in Rac1 protein levels. Inhibition of Rap1 caused by GGTI298 partly reversed the effects of Trem1 knockdown both in vivo and in vitro. In conclusion, Trem1 promotes myocardial remodeling in post-MI HF by suppressing the Rap1 pathway, suggesting Trem1 is a potential therapeutic target. - Source: PubMed
Publication date: 2026/06/30
Liu JingKou ZhenCao PengChen TingtingZhang Wanlin - Early identification of sepsis-associated acute kidney injury (SA-AKI) is important to enable timely supportive management and reduce further renal injury. However, conventional diagnostic criteria for acute kidney injury (AKI), based on serum creatinine and urine output, may delay early detection. Soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) has emerged as a potential biomarker in septic conditions. To evaluate the diagnostic value of plasma and urinary soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) in children with sepsis-associated acute kidney injury. This prospective observational cohort study included 50 children with sepsis admitted to the Pediatric Intensive Care Unit, Children's Hospital, Ain Shams University, Cairo, Egypt, between October 2023 and March 2024. Plasma and urinary sTREM-1 levels were measured at the time of sepsis diagnosis according to pediatric Sequential Organ Failure Assessment (pSOFA) criteria. Patients were prospectively followed for the development of SA-AKI, and in those who developed AKI according to pediatric Risk, Injury, Failure, Loss, End-stage kidney disease (pRIFLE) criteria, sTREM-1 levels were reassessed at the time of AKI diagnosis. The median age of the study population was 8.5 months (range 3-24), with a slight female predominance (54%). Plasma sTREM-1 levels were significantly higher in children who developed SA-AKI than in septic children without AKI [222.7 (165.2-325.9) vs 130.3 (85.1-206.2) pg/mL, p = 0.006]. Receiver operating characteristic (ROC) analysis showed an area under the curve (AUC) of 0.729, with a cutoff value of 159.6 pg/mL, yielding 80% sensitivity and 60% specificity. Urinary sTREM-1 levels were also significantly higher in children who developed SA-AKI [116.3 (53.9-197.3) vs 68.5 (46.7-112.2) pg/mL, p = 0.045]. ROC analysis showed an AUC of 0.666, with a cutoff value of 62.2 pg/mL, yielding 72% sensitivity and 48% specificity. - Source: PubMed
Publication date: 2026/06/30
Magdy Sondos MEl-Gawaad Tarek AAbdHussein Fatma AEl-Farsy Mohamed S - Microglia accumulate in malignant gliomas and play a pivotal role in tumor progression. Using single‑cell RNA sequencing studies researchers have probed gene expression in the myeloid cells in experimental gliomas at relatively late stages of the tumor development. Therefore, the early changes in gene expression in microglia in response to glioma are not fully characterized. We have previously reported distinct profiles of gene expression in the rat primary microglia cultures treated for 6 hours with either rat C6 glioma‑conditioned medium (GCM) or lipopolysaccharide. In the current study, using RNA‑seq, we characterized the transcriptional response of rat primary microglia to GCM in vitro at different time‑points: 6 h, 24 h, and 48 h, as compared to the control treated for 6 h with its own medium. We observed that during the GCM treatment gene expression changes in a biphasic, swing‑like pattern. This includes the genes involved in innate immune response, which are mostly down‑regulated at 6 h by the GCM treatment, as compared to the time‑matched control, and subsequently up‑regulated at 48 h, as compared to the earlier time‑points of the GCM treatment. Conversely, the genes involved in the cell cycle are up‑regulated at 6 h and down‑regulated at 48 h, which coincides with the induction of Tgfb1. Notable exceptions to this biphasic pattern include key genes activating immune response, such as Tlr9 and Myd88, which are down‑regulated early and persistently, while genes inhibiting immune activation, such as Trem1, and genes involved in a metabolic switch, such as Pfkl, are persistently up‑regulated. Most notably, the up‑regulated genes include Ptgs1 (alias Cox1) and Tbxas1, which encode the enzymes catalyzing the synthesis of thromboxane A2, a known inducer of T cell suppression. Further studies are needed to test the functional consequences of their up‑regulation. - Source: PubMed
Publication date: 2026/04/27
Dąbrowski MichałKaza BeataGielniewski BartłomiejWojtaś BartoszKamińska BożenaMaleszewska Marta - This study was to investigate the role of exosomes derived from distal airway stem cells (DASC) in apoptosis of pulmonary vascular endothelial cells (PVEC) in chronic obstructive pulmonary disease (COPD) and to explore the potential mechanisms. - Source: PubMed
Publication date: 2026/06/25
Song QingLiu CongLin LingZhou AiyuanLi TaoZhang PingZeng YuqinChen Ping