Ask about this productRelated genes to: TIE2 antibody
- Gene:
- TEK NIH gene
- Name:
- TEK receptor tyrosine kinase
- Previous symbol:
- VMCM
- Synonyms:
- TIE2, TIE-2, VMCM1, CD202b
- Chromosome:
- 9p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-24
- Date modifiied:
- 2018-08-07
Related products to: TIE2 antibody
Related articles to: TIE2 antibody
- Venous malformations (VMs) are congenital vascular anomalies characterized by abnormal vascular proliferation, with limb VMs often leading to functional impairment and physical discomfort. However, the cellular heterogeneity and underlying molecular mechanisms driving pathological proliferation in limb VMs remain incompletely elucidated. - Source: PubMed
Publication date: 2026/08/07
Lin JunjieLiu TingtingFang BinFeng XiaojuanJiao WentingChen ChangkuanDing YaqingZhu GaozanWang WenqiuLiu WenboLi YuanqiHou ShoufuWei JiansheQiao Junbo - Quiet quitting has increasingly been examined among healthcare professionals, yet little is known about how it manifests before entry into professional practice. Although nursing students experience substantial academic and clinical pressures, the extent of quiet quitting among them and the meanings underlying pronounced quiet quitting scores remain insufficiently understood. - Source: PubMed
Publication date: 2026/07/31
Tek Sevindik SedaMansuroğlu SercanAzizoğlu Keleş DılşaOkanli Ayşe - To determine whether circulating soluble Flt-1 (sFlt-1) and soluble Tie-2 (sTie-2) are associated with intraplaque neovascularization (IPN) in human carotid atherosclerotic plaques. - Source: PubMed
Publication date: 2026/07/21
Zamani MahtabSkagen KarolinaLindberg BeateBjerkeli VigdisDahl Tuva BMichelsen Annika ElisabethUeland ThorAukrust PålHalvorsen BenteSkjelland Mona - Performance of International Medical Graduates (IMGs) compared to US Medical Graduates (USMGs) remains a key area of interest. This meta-analysis compared performance of IMGs and USMGs regarding surgical residency matching, research productivity, and postoperative outcomes. - Source: PubMed
Publication date: 2026/08/04
Horesh NirEmile Sameh HanyGaroufalia ZoeSetton Ilana GrosmanMenzo Emanuele LoWexner Steven DRosenthal Raul J - Organs and tissues develop in close association with the vasculature, which transports blood and nutrients and helps to remove waste. The vasculature is composed primarily of endothelial cells, which provide structure, form barriers, and are a source of developmental signals. We recently found that Mediator, a multiprotein complex that regulates transcription, was essential for proper vascular development. Here, we investigated the specific role of the Mediator tail subunit Med23 in endothelial cells. Endothelial cell-specific knockout of in mouse embryos using resulted in vascular anomalies, including edema, hemorrhage, and mispatterned vasculature, alongside craniofacial defects such as micrognathia and cleft palate. Spatial transcriptomics revealed the downregulated expression of key vascular and osteogenic genes in mutants, including and , with altered signaling dynamics between endothelial and osteoblast populations. Elevated hypoxia-inducible factor 1-alpha (HIF1α) expression and reduced vascular endothelial growth factor (VEGF) signaling were observed in mutants, suggesting a hypoxia-driven suppression of neural crest cell-derived osteoblast maturation. Consistent with this model, the pharmacologic inhibition of HIF1α, combined with VEGFA supplementation, rescued craniofacial ossification and extended embryonic viability. These findings reveal a critical role for Med23 in coordinating vascular patterning and intramembranous ossification and highlight distinct hypoxic and angiogenic requirements in craniofacial dermal bone versus axial and appendicular endochondral bone development. Thus, the cranial vasculature, and more specifically endothelial cells, plays an instructive role in neural crest cell and osteogenic differentiation during cranioskeletal development. - Source: PubMed
Publication date: 2026/08/04
Dash SRettig J RGogol MTrainor P A