F2RL2 Antibody
- Known as:
- F2RL2 Antibody
- Catalog number:
- 37795
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- F2RL2 Antibody
Related genes to: F2RL2 Antibody
- Gene:
- F2RL2 NIH gene
- Name:
- coagulation factor II thrombin receptor like 2
- Previous symbol:
- -
- Synonyms:
- PAR3
- Chromosome:
- 5q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-10-27
- Date modifiied:
- 2016-10-05
Related products to: F2RL2 Antibody
Related articles to: F2RL2 Antibody
- Neutrophil extracellular traps (NETs) play crucial roles in cancer progression, but their regulatory mechanisms in breast cancer remain poorly understood. We developed a NETs-related prognostic risk model using TCGA breast cancer data and identified key biomarkers through bioinformatics analysis. AZU1 expression was validated in clinical samples using qRT-PCR and immunohistochemistry. In vitro experiments investigated AZU1's effects on neutrophil activation and NET formation using recombinant protein treatment, co-culture assays, and flow cytometry. Mechanistic studies employed phospholipase C (PLC) inhibition and PAD4 knockdown approaches. An orthotopic mouse model validated in vivo findings. Four NETs-related genes (F2RL2, AZU1, IL33, ELANE) constituted a robust prognostic model with good predictive performance. AZU1 showed significant upregulation in breast cancer tissues and correlated with advanced tumor stages. AZU1 overexpression in breast cancer cells enhanced neutrophil recruitment and NET formation through PLC signaling activation. Recombinant AZU1 dose-dependently activated neutrophils, promoted NET formation, and enhanced cancer cell invasion via epithelial-mesenchymal transition induction. PLC inhibition and PAD4 knockdown effectively blocked AZU1-induced neutrophil activation. In vivo experiments confirmed that AZU1 overexpression accelerated tumor growth and metastasis, while PAD4 inhibition reversed these effects. AZU1 promotes breast cancer progression through PAD4-dependent NET formation, representing a potential therapeutic target for breast cancer treatment. - Source: PubMed
Publication date: 2026/08/01
Huang ZhenWu ZheZhu GuiyueQiu FangyuLi LihuiXie YujieWei ChunyuPan YinhuaZou QuanqingTang Yuntian - Coronary heart disease (CHD) has a high global disease burden. According to traditional Chinese medicine theory, the main syndrome type of CHD is the syndrome of intermingled phlegm and blood stasis (SI-GPBS). Tanyu Tongzhi Decoction (TYTZD) exerts clear cardioprotective effects on CHD patients with SI-GPBS, while its specific regulatory mechanism remains unclear. Clinical serum proteomics and network pharmacology were used to screen key targets and pathways for CHD with SI-GPBS. An APOE mouse model of CHD complicated with SI-GPBS was established and treated with TYTZD. Transcriptomics, proteomics and WGCNA were combined to screen core genes, with Western blotting, immunofluorescence, co-localization analysis and Carstairs staining for target verification and observation of coronary microthrombosis and endothelial injury. A total of 754 differentially expressed proteins were identified in CHD patients with SI-GPBS, significantly enriched in the platelet activation pathway, with ITGA2B as the upregulated core hub protein. Network pharmacology found 94 active ingredients and 144 therapeutic targets of TYTZD for CHD with SI-GPBS, and key components bound well with ITGA2B. In APOE mice with SI-GPBS, TYTZD improved cardiac function, reduced blood lipids, myocardial enzymes, aortic lipid deposition and myocardial damage, downregulated ITGA2B, F2RL2, FGA and FGB, inhibited integrin αIIbβ3 signaling, restrained endothelial activation and reduced coronary microthrombosis. TYTZD treats CHD with SI-GPBS mainly by inhibiting platelet activation, improving endothelial dysfunction, and reducing coronary microthrombosis. This study provides experimental basis for TYTZD's clinical application in CHD with SI-GPBS and new ideas for TCM syndrome-disease combination research. - Source: PubMed
Publication date: 2026/05/24
Yang YingLi XiangTang DanliLi ChengzeWu SijiaLi YingyingLei TongZong WenjingZhang Huamin - Breast cancer (BC) incidence continues to rise, and recurrence and metastasis remain major contributors to mortality. The epithelial-mesenchymal transition (EMT), associated with the acquisition of invasive functions by epithelial cells, also promotes resistance to anticancer therapies. Here, an EMT-based prognostic model was developed to enhance BC outcome prediction. - Source: PubMed
Publication date: 2026/03/15
Wu ZizhengZheng JieMen ShuaiSui ShuangruiYan WeitaoLiu YinfengHan Meng - Dysregulation of Ca-signaling genes has been shown in some types of cancer; however, it is virtually unknown in hepatitis B-derived hepatocellular carcinoma (HBV-HCC). Here, we evaluate the transcriptional and epigenetic regulation of Ca-signaling genes in HBV-HCC and whether their expression is associated with cancer hallmarks, and prognostic potential. - Source: PubMed
Publication date: 2026/01/27
Hernández-Martínez GuadalupeHernández-Oliveras AndrésZarain-Herzberg ÁngelSantiago-García Juan - Pancreatic ductal adenocarcinoma (PDAC) genetic susceptibility is partially identified. The complement system (CS) influences carcinogenesis and participates in immunological defense and homeostasis; however, its role in PDAC genetic susceptibility and prognosis is underexplored. The association of SNPs within 111 CS-related genes with PDAC risk is assessed in the PanGenEU study and validated in the UKBiobank. We investigate the association between the CS-related gene variation and PDAC risk, followed by an in-depth functional in silico study using TCGA and ICGC data. We assess whether CS-related genes are associated with prognosis at the germline and somatic levels. We investigate the immune infiltration of PDAC tumors according to their transcriptomic profile. Genetic variation in FCN1 and PLAT is significantly associated with PDAC risk. PDAC patients with elevated expression of IGHG3, IGKC, IGHM, F2R, F2RL2, CFI, A2M, or C4A display improved survival and higher infiltration of CD8, B cells, and Th1 cells. Individuals with high expression levels of either FGA, SERPINE1, FGG, or F3 exhibit poorer survival, higher infiltration of Tregs, and lower infiltration of CD8 cells. Results from this study suggest that CS-related genes play a role in PDAC genetic susceptibility and survival through specific immune cell infiltration. - Source: PubMed
Publication date: 2025/11/28
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