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TEK (基因名), Angiopoietin-1 receptor (蛋白名), tie2_human.
产品名称:

Human TEK/ Angiopoietin-1 receptor Recombinant Protein
血管生成素1受体

货号:

R0126h

商标:
EIAab®
监管等级:
别名:

Endothelial tyrosine kinase, Tunica interna endothelial cell kinase, Tyrosine kinase with Ig and EGF homology domains-2, Tyrosine-protein kinase receptor TEK, Tyrosine-protein kinase receptor TIE-2, p140 TEK, hTIE2, CD202b, TIE2, VMCM, VMCM1

序列号:
Q02763
来源:
E.coli
种属:
Human
标签:
His
纯度:
>90% by SDS-PAGE
浓度:
Reconstitution Dependent
形态:
Liquid
内毒素水平:
Please contact protein@eiaab.com The technician for more information.
应用:
存储缓冲液:
50mM NaH2PO4, 500mM NaCl Buffer with 500mM Imidazole, 10%glycerol(PH8.0)
存储:
Store at -20°C. (Avoid repeated freezing and thawing.)
研究领域:
-
Human TEK Protein
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Human TEK Protein
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产品说明书
说明书: 下载说明书
MSDS: MSDS
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R&D 技术数据
更多信息,请参阅手册,或联系我们的技术支持: tech@eiaab.com.
基因位点
Cytogenetic band: 9p21.2 by HGNC 9p21.2 by Entrez Gene 9p21.2 by Ensembl
TEK Gene in genomic location: bands according to Ensembl, locations according to GeneLoc (and/or Entrez Gene and/or Ensembl if different)
基因位点
通用注释


亚单元:
Homodimer. Heterodimer with TIE1. Interacts with ANGPT1, ANGPT2 and ANGPT4. At cell-cell contacts in quiescent cells, forms a signaling complex composed of ANGPT1 plus TEK molecules from two adjoining cells. In the absence of endothelial cell-cell contacts, interaction with ANGPT1 mediates contacts with the extracellular matrix. Interacts with PTPRB; this promotes endothelial cell-cell adhesion. Interacts with DOK2, GRB2, GRB7, GRB14, PIK3R1 and PTPN11/SHP2. Colocalizes with DOK2 at contacts with the extracellular matrix in migrating cells. Interacts (tyrosine phosphorylated) with TNIP2. Interacts (tyrosine phosphorylated) with SHC1 (via SH2 domain).


功能:
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.


亚细胞位置:
Cell membrane Single-pass type I membrane protein Cell junction Cell junction Focal adhesion Cytoplasm Cytoskeleton Secreted Recruited to cell-cell contacts in quiescent endothelial cells. Colocalizes with the actin cytoskeleton and at actin stress fibers during cell spreading. Recruited to the lower surface of migrating cells, especially the rear end of the cell. Proteolytic processing gives rise to a soluble extracellular domain that is secreted.


该产品尚未在任何出版物中被引用。

[1].
"Somatic mutations in angiopoietin receptor gene TEK cause solitary and multiple sporadic venous malformations."

[2].
"Tyrosine phosphatase beta regulates angiopoietin-Tie2 signaling in human endothelial cells."

[3].
"Angiopoietin 2 is a partial agonist/antagonist of Tie2 signaling in the endothelium."

[4].
"Tie2: a journey from normal angiogenesis to cancer and beyond."

[5].
"Angiopoietins assemble distinct Tie2 signalling complexes in endothelial cell-cell and cell-matrix contacts."

[6].
"Adaptor ShcA protein binds tyrosine kinase Tie2 receptor and regulates migration and sprouting but not survival of endothelial cells."

[7].
"The antiinflammatory endothelial tyrosine kinase Tie2 interacts with a novel nuclear factor-kappaB inhibitor ABIN-2."

[8].
"Mechanistic effects of autophosphorylation on receptor tyrosine kinase catalysis: enzymatic characterization of Tie2 and phospho-Tie2."

[9].
"Structure of the Tie2 RTK domain: self-inhibition by the nucleotide binding loop, activation loop, and C-terminal tail."

[10].
"Allelic and locus heterogeneity in inherited venous malformations."
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