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
- TIE2 is an endothelial receptor tyrosine kinase (RTK) essential for vascular integrity, and constitutively active TIE2 mutants are involved in venous malformations (VMs). VMs are currently treated by surgery or sclerotherapy, but effective pharmacologic options remain limited, especially for surgically challenging Blue Rubber Bleb Nevus Syndrome (BRBNS). TIE2 activation has typically been assessed by immunoblotting of phosphoproteins, yet scalable assays applicable to pharmacological evaluation are still lacking. Here, we present a bioluminescence resonance energy transfer (BRET) biosensor that quantifies receptor-proximal TIE2 activation by monitoring recruitment of GRB2, a major adaptor in RTK signaling. This BRET sensor detects angiopoietin-1 (ANG-1) at physiological plasma concentrations and is compatible with a high-throughput format. Furthermore, it captures constitutive activity of TIE2 mutants associated with VMs and enables pharmacological evaluation of TIE2 variants. Notably, the T1105N-T1106P variant, frequently observed in BRBNS, exhibited relatively higher sensitivity to the clinical oncology drugs regorafenib and lenvatinib. To validate selected BRET-defined pharmacological profiles in an endothelial context, we used HUVEC-derived HUEhT-2 cells and established endothelial TIE2-GRB2 BRET measurements, followed by downstream AKT/ERK signaling analysis and tube formation assays. These endothelial assays largely supported the selected HEK293T BRET findings, particularly the pharmacological profile of T1105N-T1106P mutant, at receptor-proximal, downstream signaling, and functional levels. Together, this BRET-based biosensor establishes a two-step framework: HEK293T BRET enables efficient primary profiling, whereas endothelial assays provide orthogonal validation to support biological interpretation. This framework offers a practical strategy for prioritizing pharmacological candidates for further endothelial and in vivo validation toward therapeutic development. - Source: PubMed
Publication date: 2026/08/13
Matsutani HitomiOishi AtsuroIzumi-Tamura TakuyaHayashi YumikoKurita MasakazuMuto TomoyaYoshimi AkihideUeno HitoshiShiraishi TomohiroHarii KiyonoriTakushima AkihikoKidoya HiroyasuOzaki Mine - Gallstone ileus (GSI) is a rare surgical emergency. Its diagnosis is challenging and frequently delayed. Moreover, there is no consensus regarding the optimal surgical approach. The primary point of debate is whether cholecystectomy and fistula repair should be performed and, if so, when. Several studies have suggested that omitting cholecystectomy and fistula repair may increase the risk of cholangitis, gallbladder cancer, and recurrent gallstone ileus. However, most of these data originate from studies conducted in the previous century and have not been supported by contemporary evidence. This study aimed to present our clinical experience with gallstone ileus, discuss diagnostic and therapeutic strategies, and review the relevant literature. - Source: PubMed
Feratoğlu FatihHacıalioğlu CemalYılmaz Tarık EmreKaya Selçuk - Vascular endothelial cells play a crucial role in maintaining the structural integrity and microcirculatory function of the coronary microvasculature. Endothelial dysfunction, a critical pathological process in various cardiovascular diseases including myocardial infarction (MI), leads to reduced myocardial blood flow due to a lack of nitric oxide gas inside blood vessel walls that ultimately causes inflammation, thrombosis and coronary artery obstruction. Therefore, the identification of molecular mechanisms that protect against endothelial cell injury is necessary for effective MI treatment. In this study, we identified a novel interaction between TEK receptor tyrosine kinase (TEK) and signal transducer and activator of transcription 3 (STAT3), promoting the phosphorylation and nuclear translocation of STAT3. In particular, the upregulation of STAT3 and p-STAT3 could be prevented by inhibiting the binding of STAT3 to TEK using specific STAT3 domain inhibitors. Additionally, chromatin immunoprecipitation (ChIP) analysis revealed that STAT3 acts as a transcription factor, binding to the promoter region of lysyl oxidase (LOX) and LOX propeptide (LOX-PP) and inhibiting their transcription. Notably, excessive LOX-PP has been shown to induce endothelial cell injury, leading to reduced nitric oxide synthesis, increased permeability, and impaired functionality in terms of proliferation, migration, and tube formation. These novel findings reveal a new mechanism of endothelial cell injury after myocardial ischemia and may offer new insights for developing future therapeutic approaches. - Source: PubMed
Publication date: 2026/08/12
Li ChaoZhang MuxinLu MengkaiHao JiaqiLin LinZhang LeiHu YuanlongZhang ZhiyuanHuang XueyingLi Yunlun - 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
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