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 >  Protein>TIE2 >TI2-C5253

Cynomolgus TIE2 Protein, His Tag (MALS verified)

分子别名(Synonym)

TIE2,Tie-2,TEK,VMCM, VMCM1,CD202b,Angiopoietin-1 receptor

表达区间及表达系统(Source)

Cynomolgus TIE2, His Tag (TI2-C5253) is expressed from human 293 cells (HEK293). It contains AA Ala 23 - Lys 745 (Accession # A0A2K5VRI3-1).

Predicted N-terminus: Ala 23

Request for sequence

蛋白结构(Molecular Characterization)

Online(Ala 23 - Lys 745) A0A2K5VRI3-1

This protein carries a polyhistidine tag at the C-terminus.

The protein has a calculated MW of 82.5 kDa. The protein migrates as 90-100 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

内毒素(Endotoxin)

Less than 1.0 EU per μg by the LAL method.

纯度(Purity)

>95% as determined by SDS-PAGE.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in PBS, pH7.4. Normally sucrose is added as protectant before lyophilization.

Contact us for customized product form or formulation.

重构方法(Reconstitution)

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

存储(Storage)

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:

  1. -20°C to -70°C for 12 months in lyophilized state;
  2. -70°C for 3 months under sterile conditions after reconstitution.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
 

电泳(SDS-PAGE)

Cynomolgus TIE2, His Tag (Cat. No. TI2-C5253) SDS-PAGE gel

Cynomolgus TIE2, His Tag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 95%.

SEC-MALS

Cynomolgus TIE2, His Tag (Cat. No. TI2-C5253) MALS images

The purity of Cynomolgus TIE2, His Tag (Cat. No. TI2-C5253) is more than 85% and the molecular weight of this protein is around 93-113 kDa verified by SEC-MALS.

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背景(Background)

Tyrosine-protein kinase that acts as cell-surface receptor for ANGPT1, ANGPT2 and ANGPT4 and regulates angiogenesis, endothelial cell survival, proliferation, migration, adhesion and cell spreading, reorganization of the actin cytoskeleton, but also maintenance of vascular quiescence. Has anti-inflammatory effects by preventing the leakage of proinflammatory plasma proteins and leukocytes from blood vessels. Required for normal angiogenesis and heart development during embryogenesis. Required for post-natal hematopoiesis. After birth, activates or inhibits angiogenesis, depending on the context. Inhibits angiogenesis and promotes vascular stability in quiescent vessels, where endothelial cells have tight contacts. In quiescent vessels, ANGPT1 oligomers recruit TEK to cell-cell contacts, forming complexes with TEK molecules from adjoining cells, and this leads to preferential activation of phosphatidylinositol 3-kinase and the AKT1 signaling cascades. In migrating endothelial cells that lack cell-cell adhesions, ANGT1 recruits TEK to contacts with the extracellular matrix, leading to the formation of focal adhesion complexes, activation of PTK2/FAK and of the downstream kinases MAPK1/ERK2 and MAPK3/ERK1, and ultimately to the stimulation of sprouting angiogenesis. ANGPT1 signaling triggers receptor dimerization and autophosphorylation at specific tyrosine residues that then serve as binding sites for scaffold proteins and effectors. Signaling is modulated by ANGPT2 that has lower affinity for TEK, can promote TEK autophosphorylation in the absence of ANGPT1, but inhibits ANGPT1-mediated signaling by competing for the same binding site. Signaling is also modulated by formation of heterodimers with TIE1, and by proteolytic processing that gives rise to a soluble TEK extracellular domain. The soluble extracellular domain modulates signaling by functioning as decoy receptor for angiopoietins. TEK phosphorylates DOK2, GRB7, GRB14, PIK3R1; SHC1 and TIE1.

 

 

前沿进展

Regorafenib exerts an inhibitory effect on the proliferation of human lung fibroblasts by reducing the production of several cytokines in vitro study
Nakamura, Tabata, Tabata
Tissue Cell (2025) 95, 102876
Abstract: Pulmonary fibrosis is a disease that leads to respiratory failure and death. There has been little progress in therapeutic strategies for pulmonary fibrosis. There have been several reports on the cytokines associated with pulmonary fibrosis, including IL-6 and TGF-β1. Angiogenesis is one of the most important phenomena in the pathogenesis of pulmonary fibrosis. Previously, we reported the preventive effects of thalidomide against pulmonary fibrosis via the inhibition of neovascularization by angiogenic factors such as VEGF. Regorafenib is a multikinase inhibitor, which inhibits tyrosine kinase receptors such as VEGFR1-3 and TIE2. In the clinical setting, regorafenib has been widely used for anti-cancer therapy for metastatic colorectal cancer. In this study, we examined the preventive effects of regorafenib against pulmonary fibrosis.We investigated whether regorafenib had an inhibitory effect on the proliferation, viability, and production of several cytokines in lung fibroblasts.We demonstrated an inhibitory effect of regorafenib on the proliferation and viability of lung fibroblasts. Moreover, regorafenib reduced the production of several cytokines associated with the pathogenesis of pulmonary fibrosis, including IL-6, VEGF and TGF- β1, and collagen synthesis from lung fibroblasts.These data suggest that regorafenib may have potential clinical applications in the prevention of pulmonary fibrosis.Copyright © 2025 Elsevier Ltd. All rights reserved.
Endothelial but not systemic ferroptosis inhibition protects from antineutrophil cytoplasmic antibody-induced crescentic glomerulonephritis
Rousselle, Lodka, Sonnemann et al
Kidney Int (2025)
Abstract: Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV) are systemic autoimmune diseases featuring small blood vessel inflammation and organ damage, including necrotizing crescentic glomerulonephritis (NCGN). Persistent vascular inflammation leads to endothelial and kidney cell necrosis. Ferroptosis is a regulated cell death pathway executed by reactive oxygen species and iron-dependent lipid peroxidation culminating in cell membrane rupture. Here we show that ANCA-activated neutrophils induced endothelial cell (EC) death in vitro that was prevented by ferroptosis inhibition with Ferrostatin-1, Liproxstatin-1 and small inhibiting RNA against the enzyme AcylCoA Synthetase Long Chain Family Member 4 (ACSL4). In contrast, neither necroptosis nor apoptosis inhibition affected EC death. Moreover, both ferroptosis inhibitors alleviated lipid peroxide accumulation in EC. Increased lipid peroxidation was detected in kidney sections of AAV mice by immunohistochemistry. We generated MPO-/- ACSL4flox Tie2-Cre+ mice lacking ACSL4 specifically in EC (ACSL4ΔEC) to study the significance of endothelial ferroptosis in vivo. ACSL4ΔEC chimeric mice, but not control mice (ACSL4WT), were protected from NCGN in a MPO-AAV bone-marrow transplantation model. These data establish that EC ferroptosis contributes to ANCA-induced glomerulonephritis. However, systemic pharmacological ferroptosis inhibition with Ferrostatin-1 or Liproxstatin-1 did not protect from NCGN in a murine AAV model. Ferrostatin-1 treatment both directly activated T cell proliferation and indirectly myeloid-mediated T cell proliferation and polarization in vitro. Conceivably, both effects may cancel the beneficial effect of endothelial ferroptosis inhibition. Mechanistically, we describe the importance of EC ferroptosis for the development of AAV. However, the lack of protection with systemic pharmacological ferroptosis inhibition should discourage clinicians from evaluating this treatment strategy in clinical AAV studies.Copyright © 2025. Published by Elsevier Inc.
Human skeletal development and regeneration are shaped by functional diversity of stem cells across skeletal sites
Ambrosi, Taheri, Chen et al
Cell Stem Cell (2025)
Abstract: The skeleton is one of the most structurally and compositionally diverse organ systems in the human body, depending on unique cellular dynamisms. Here, we integrate prospective isolation of human skeletal stem cells (hSSCs; CD45-CD235a-TIE2-CD31-CD146-PDPN+CD73+CD164+) from ten skeletal sites with functional assays and single-cell RNA sequencing (scRNA-seq) analysis to identify chondrogenic, osteogenic, stromal, and fibrogenic subtypes of hSSCs during development and their linkage to skeletal phenotypes. We map the distinct composition of hSSC subtypes across multiple skeletal sites and demonstrate their unique in vivo clonal dynamics. We find that age-related changes in bone formation and regeneration disorders stem from a pathological fibroblastic shift in the hSSC pool. Utilizing a Boolean algorithm, we uncover gene regulatory networks that dictate differences in the ability of hSSCs to generate specific skeletal tissues. Importantly, hSSC lineage dynamics are pharmacologically malleable, providing a new strategy to treat aberrant hSSC diversity central to aging and skeletal maladies.Copyright © 2025 The Author(s). Published by Elsevier Inc. All rights reserved.
Inhibitor of DNA binding-1 is a key regulator of cancer cell vasculogenic mimicry
Thompson, Dorward, Jurrius et al
Mol Oncol (2025)
Abstract: Solid tumours routinely access the blood supply by promoting endothelium-dependent angiogenesis; but tumour vasculature can also be formed by cancer cells themselves via vasculogenic mimicry (VM). Investigation of the gene expression profile during the early stages of VM formation by MDA-MB-231-LM2 breast cancer cells identified the transcriptional regulator inhibitor of DNA binding 1 (ID1) to be elevated ~ 10-fold within the first 2 hours. This role for ID1 in promoting VM was supported by ID1 genetic knockdown or chemical inhibition interrupting VM formation by MDA-MB-231-LM2 (breast) and BxPC-3 (pancreatic) cancer cells. More specifically, reducing ID1 lowered cancer cell expression of endothelial cell genes (e.g. CDH5, TIE2) and production of pro-angiogenic proteins (e.g. VEGF, CD31, MMP9 and IL-8). In silico analysis of MDA-MB-231 cells engrafted into mice identified elevated ID1 expression in cancer cells that had metastasised to the lungs or liver, and an enrichment of pro-angiogenic genes. Additionally, Id1 knockdown in 4T1.13 murine breast cancer cells demonstrated reduced tumour growth and metastasis in vivo. Taken together, this study further implicates ID1 in a vascular program within cancer cells that supports disease progression.© 2025 The Author(s). Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.
Showing 1-4 of 3552 papers.
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TIE2靶点信息
英文全称:TEK receptor tyrosine kinase
中文全称:泰克酪氨酸激酶
种类:Homo sapiens
上市药物数量:4详情
临床药物数量:8详情
最高研发阶段:批准上市
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