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Protein-coding gene in the species Homo sapiens

Angiopoietin-1 receptor

Angiopoietin-1 receptor
All data from the card 19
Aliases
TEK, CD202B, TIE-2, TIE2, VMCM, VMCM1, TEK tyrosine kinase, TEK receptor tyrosine kinase, GLC3E
External IDs
OMIM: 600221; MGI: 98664; GeneCards: TEK
PDB
Ortholog search: PDBe RCSB
2.7.10.1
↗
Chr.
Chromosome 9 (human)
Band
9p21.2
End
27,230,174 bp
Chr.
Chromosome 4 (mouse)
Band
4 C5|4 43.34 cM
End
94,763,213 bp
BioGPS
More reference expression data
Databases
NCBI: entry; OMA: entry
Species
Human
Entrez
7010
Ensembl
ENSG00000120156
UniProt
Q02763
RefSeq (mRNA)
NM_000459NM_001290077NM_001290078NM_001375475NM_001375476
RefSeq (protein)
NP_000450NP_001277006NP_001277007NP_001362404NP_001362405
Location (UCSC)
Chr 9: 27.11 – 27.23 Mb

Angiopoietin-1 receptor is an angiopoietin receptor protein that in humans is encoded by the TEK gene. TEK is also known as TEK tyrosine kinase, TIE2 and CD202B (cluster of differentiation 202B).

Function

The TEK receptor tyrosine kinase is expressed almost exclusively in endothelial cells in mice, rats, and humans. (TEK is closely related to the TIE receptor tyrosine kinase.)

This receptor possesses a unique extracellular domain containing 2 immunoglobulin-like loops separated by 3 epidermal growth factor-like repeats that are connected to 3 fibronectin type III-like repeats. The ligand for the receptor is angiopoietin-1. TEK has also been suggested as a marker for nucleus pulposus progenitor cells, from the intervertebral disc, which upon activation by Angiopoietin-1 starts to multiply and differentiate.

Defects in TEK are associated with inherited venous malformations; the TEK signaling pathway appears to be critical for endothelial cell-smooth muscle cell communication in venous morphogenesis.

In cancer patients, TEK (Tie2) is expressed in a subpopulation of monocytes that home in on the tumor and are essential for the formation of new blood vessels there.

Interactions

TEK tyrosine kinase has been shown to interact with:

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Text from Wikipedia, CC BY-SA 4.0 · Source article