F2R Gene coagulation factor II (thrombin) receptor
- Known as:
- F2R Gene coagulation factor II (thrombin) receptor
- Catalog number:
- F2RL2
- Category:
- -
- Supplier:
- Transposagen
- Gene target:
- F2R Gene coagulation factor (thrombin) receptor
Related genes to: F2R Gene coagulation factor II (thrombin) receptor
- Gene:
- FOXD3 NIH gene
- Name:
- forkhead box D3
- Previous symbol:
- -
- Synonyms:
- Genesis, HFH2
- Chromosome:
- 1p31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-22
- Date modifiied:
- 2015-08-25
Related products to: F2R Gene coagulation factor II (thrombin) receptor
Related articles to: F2R Gene coagulation factor II (thrombin) receptor
- SIX1 variants underlying Branchio-oto-renal syndrome occur in the SIX domain (SD) or homeodomain (HD). We tested whether different variants - V17E (SD), Y129C (HD) - cause distinct developmental phenotypes in embryos with reduced Six1 in comparison to wildtype Six1 (Six1WT). In Six1-morphants, Six1WT restored neural crest and preplacodal gene expression; V17E restored foxd3 and irx1 better than Y129C and Y129C restored sox11 better. In six1-null otic vesicles, Six1WT partially restored tbx1 and sobp, V17E was less effective and Y129C was least effective; all three restored dlx5. In six1-heterozygotes, Six1WT and Y129C had similar pleiotropic effects on tbx1, whereas V17E had no effect; Six1WT restored dlx5 expression, V17E was less effective and Y129C was most deficient. In six1-null tadpoles, reduced cranial cartilage volume and individual cartilage abnormalities were rescued by Six1WT, less so by V17E and not by Y129C. In heterozygotes and wildtypes, Y129C caused a higher frequency of abnormal cartilages compared to Six1WT or V17E. Thus, variants with different functional deficits have distinguishable effects in both nulls and heterozygotes on the formation of the tissues affected in Branchio-oto-renal syndrome. - Source: PubMed
Publication date: 2026/06/15
Coppenrath KelseyShaidani Nikko-IdeenNaert ThomasMajumdar Himani DHorb MarkoLienkamp Soeren SKlein Steven LMoody Sally A - BACKGROUND: Cancer stemness-related long non-coding RNAs (lncRNAs) play a crucial role in tumor initiation and progression. This study aimed to identify stemness-related lncRNAs in cervical cancer (CESC) and evaluate the prognostic significance, clinical relevance, and biological functions. MATERIALS & METHODS: Transcriptome data from the Cancer Genome Atlas were used to construct a co-expression network of cancer stemness-related genes and CESC-specific lncRNAs, focusing on cervical squamous cell carcinoma and endocervical adenocarcinoma. Identified stemness-related lncRNAs were used to develop a prognostic model through univariate, LASSO, and multivariate Cox regression analyses. Quantitative real-time PCR and in situ hybridization were performed to measure EMX2OS expression in normal and cancerous cervical tissues. Statistical tests were applied to analyze the association between EMX2OS expression and clinicopathological features. The effects of EMX2OS overexpression on cell proliferation, migration, and invasion were investigated using using the Cell Counting Kit-8 (CCK-8) assay, 5-ethynyl-2’-deoxyuridine (EdU) assay, plate cloning assay, wound healing assay, and transwell assays. RESULTS: A prognostic model comprising five lncRNAs (FOXD3-AS1, KCNMB2-AS1, EMX2OS, LINC02446, SOCS2-AS1) was developed, demonstrating robust prognostic performance. EMX2OS expression was significantly down-regulated in CESC tissues compared to normal tissues. In situ hybridization showed a marked association between EMX2OS expression and tumor size (P = 0.005), depth of stromal invasion (P = 0.009), and 5-year survival status (P = 0.003). The 5-year survival rate was significantly lower in the low expression group (P = 0.006). Overexpression of EMX2OS significantly suppressed cell proliferation, migration, and invasion. CONCLUSIONS: The prognostic model based on 5 lncRNAs reflecting the stemness of CESC stem cells can reliably predict the prognosis of patients with CESC. Additionally, EMX2OS serves as a significant tumor suppressor marker in CESC. - Source: PubMed
Publication date: 2026/04/20
Liu XiaochenLiao YuandongLiu YunyunHuang HuaZhang ChunyuHuang ShiyingQin ShuhangChen MingXia MengLiu TianyuLiang YanchunYao Shuzhong - Docetaxel (DTX) is a standard chemotherapy agent for castration-resistant prostate cancer (CRPC); however, DTX resistance remains a major clinical challenge, and the underlying molecular mechanisms are not fully understood. In our study, it was found that OTUB2 was highly expressed in DTX-resistant CRPC and could be served as a key driver of DTX resistance. Mechanistically, OTUB2 stabilizes the m5C reader ALYREF by removing its K48-linked polyubiquitin chains, leading to increased ALYREF protein levels. And then, ALYREF enhances the mRNA stability and expression of ABCG4, thereby promoting ATP-dependent efflux of DTX. Moreover, the expression of OTUB2 mRNA and protein could be regulated by FOXD3-AS1 derived from cancer-associated fibroblasts (CAFs). More importantly, treatment with OTUB2 inhibitor (OTUB2-IN-1) resensitized resistant CRPC to DTX. Together, our findings establish OTUB2 as a novel driver of DTX resistance in CRPC and highlight the role of CAFs-derived FOXD3-AS1 and OTUB2/ALYREF/ABCG4 axis in modulating DTX resistance of CRPC. - Source: PubMed
Publication date: 2026/03/17
Ke Zhi-BinChen Jia-YinLin BinChen Chao-RanXue Yu-TingSun Jiang-BoYan Zi-HengZhao Yu-XuanLiu Meng-XinWang ZhenXue Xue-YiZheng Qing-ShuiWei YongXu Ning - The neural crest is a vertebrate stem cell population with broad developmental potential. While a gene regulatory network describing establishment of these cells has been generated, much remains to be learned about the dynamics of this process. Here, we use fluorescent in situ hybridization chain reaction to quantify the spatiotemporal dynamics of neural crest formation in Xenopus. We find that the initial onset of neural crest genes is broad and partially overlapping, with distinct anterior-posterior and medio-lateral biases. A shared neural crest domain emerges, but some genes retain relative expression differences that persist into migratory stages, producing stream-specific gene expression patterns. These differences correlate with dynamic expression of the neural plate border factors pax3 and zic1. Correlating relative intensities of pax3 and zic1 with the presence or absence of nascent neural crest transcripts predicts that these factors can differentially regulate snai2 and sox8, which we confirm experimentally. Strikingly, later stages display an inverse correlation between neural crest and neural plate border factors, suggesting that pax3 and zic1 initially promote neural crest gene activation but are downregulated as neural crest identity emerges. - Source: PubMed
Publication date: 2026/02/20
Montequin AndrewLaBonne Carole - Motor Exit Point (MEP) glia are spinal cord-derived glial cells that myelinate peripheral motor axons, bridging the central and peripheral nervous systems. They have a hybrid profile, sharing features with oligodendrocytes and Schwann cells. Yet, significant gaps remain in our understanding of complex MEP glial lineage and identity. MEP glia express neural tube and canonical oligodendrocyte lineage markers and , as well as the neural crest marker . Here, we show that the oligodendrocyte markers and are not expressed in MEP glia. These findings refine the molecular signature of MEP glia, enhancing their peripheral identity. - Source: PubMed
Publication date: 2026/01/21
Dallo Tessa CFontenas Laura