TEK tyrosine kinase

Angiopoietin-1 receptor also known as CD202B (cluster of differentiation 202B) is a protein that in humans is encoded by the TEK gene.[5][6] Also known as TIE2, it is an angiopoietin receptor.

TEK
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesTEK, CD202B, TIE-2, TIE2, VMCM, VMCM1, TEK tyrosine kinase, TEK receptor tyrosine kinase, GLC3E
External IDsOMIM: 600221; MGI: 98664; HomoloGene: 397; GeneCards: TEK; OMA:TEK - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_000459
NM_001290077
NM_001290078
NM_001375475
NM_001375476

NM_001290549
NM_001290551
NM_013690

RefSeq (protein)

NP_000450
NP_001277006
NP_001277007
NP_001362404
NP_001362405

NP_001277478
NP_001277480
NP_038718

Location (UCSC)Chr 9: 27.11 – 27.23 MbChr 4: 94.63 – 94.76 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

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.)[7]

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.[8] The ligand for the receptor is angiopoietin-1.[7] 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.[9][10]

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.[7]

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.[11]

Interactions

TEK tyrosine kinase has been shown to interact with:

See also

References

Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.