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Tek - TEK receptor tyrosine kinase (house mouse)

Gene
Symbol
Dates
  • Create:
    2016-09-14
  • Modify:
    2024-12-21
Description
Enables protein tyrosine kinase activity and signaling receptor activity. Involved in several processes, including circulatory system development; negative regulation of endothelial cell apoptotic process; and response to retinoic acid. Acts upstream of or within several processes, including positive regulation of macromolecule metabolic process; positive regulation of protein import into nucleus; and regulation of non-canonical NF-kappaB signal transduction. Located in perinuclear region of cytoplasm. Is expressed in several structures, including cardiovascular system; central nervous system; extraembryonic component; genitourinary system; and immune system. Human ortholog(s) of this gene implicated in arteriovenous malformation; multiple cutaneous and mucosal venous malformations; and renal Wilms' tumor. Orthologous to human TEK (TEK receptor tyrosine kinase).

1 Names and Identifiers

1.1 Synonyms

  • Cd202b
  • Hyk
  • STK1
  • Tie-2
  • Tie2
  • angiopoietin-1 receptor
  • endothelial tyrosine kinase
  • endothelial-specific receptor tyrosine kinase
  • p140 TEK
  • 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

1.2 Other Identifiers

1.2.1 Ensembl ID

1.2.2 Alliance Gene ID

1.2.3 Bgee Gene ID

1.2.4 Enzyme Commission (EC) Number

1.2.5 MGI ID

1.2.6 VEuPathDB ID

1.2.7 Wikidata

3 Proteins

3.1 Protein Function

Tyrosine-protein kinase that acts as a 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 pro-inflammatory plasma proteins and leukocytes from blood vessels. Required for normal angiogenesis and heart development during embryogenesis. Required for postnatal 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.

3.2 Protein 3D Structures

3.2.1 AlphaFold Structures

Highly accurate protein structure prediction with AlphaFold. Nature. 2021 Aug;596(7873):583-589. DOI:10.1038/s41586-021-03819-2. PMID:34265844; PMCID:PMC8371605

3.3 Protein Targets

4 Chemicals and Bioactivities

4.1 Tested Compounds

5 BioAssays

5.1 Small-Molecule BioAssays

5.2 RNAi BioAssays

6 Interactions and Pathways

6.1 Interactions

6.2 Pathways

7 Biochemical Reactions

8 Expression

9 Literature

9.1 Consolidated References

9.2 Gene-Chemical Co-Occurrences in Literature

9.3 Gene-Gene Co-Occurrences in Literature

9.4 Gene-Disease Co-Occurrences in Literature

10 Patents

10.1 Gene-Chemical Co-Occurrences in Patents

10.2 Gene-Gene Co-Occurrences in Patents

10.3 Gene-Disease Co-Occurrences in Patents

11 Classification

11.1 Gene Ontology: Biological Process

11.2 Gene Ontology: Cellular Component

11.3 Gene Ontology: Molecular Function

11.4 ChEMBL Target Tree

11.5 Enzyme Classification

12 Information Sources

  1. NCBI Gene
    LICENSE
    NCBI Website and Data Usage Policies and Disclaimers
    https://www.ncbi.nlm.nih.gov/home/about/policies/
  2. PubChem
  3. Alliance of Genome Resources
    LICENSE
    All annotations and data produced by Alliance members that are accessible from alliancegenome.org are distributed under a CC BY 4.0 license (https://creativecommons.org/licenses/by/4.0/).
    https://www.alliancegenome.org/privacy-warranty-licensing
  4. BioGRID
    LICENSE
    The MIT License (MIT); Copyright Mike Tyers Lab
    https://wiki.thebiogrid.org/doku.php/terms_and_conditions
  5. STRING: functional protein association networks
  6. Mouse Genome Informatics (MGI)
    LICENSE
    MGI data and annotations are licensed under a Creative Commons Attribution 4.0 International License (CC-BY).
    https://www.informatics.jax.org/mgihome/other/copyright.shtml
  7. NCBI Gene Expression Omnibus (GEO)
  8. Swiss Institute of Bioinformatics Bgee
    LICENSE
    Creative Commons Zero license (CC0)
    https://www.bgee.org/about/
  9. UniProt
    LICENSE
    We have chosen to apply the Creative Commons Attribution (CC BY 4.0, http://creativecommons.org/licenses/by/4.0/) License to all copyrightable parts of our databases.
    https://www.uniprot.org/help/license
  10. VEuPathDB: The Eukaryotic Pathogen, Vector and Host Informatics Resource
    LICENSE
    All data on VEuPathDB websites are provided freely for public use.
    https://veupathdb.org/veupathdb/app/static-content/about.html
  11. Wikidata
  12. ChEMBL
    LICENSE
    Access to the web interface of ChEMBL is made under the EBI's Terms of Use (http://www.ebi.ac.uk/Information/termsofuse.html). The ChEMBL data is made available on a Creative Commons Attribution-Share Alike 3.0 Unported License (http://creativecommons.org/licenses/by-sa/3.0/).
    http://www.ebi.ac.uk/Information/termsofuse.html
  13. Swiss Institute of Bioinformatics ENZYME
    LICENSE
    Copyrighted by the SIB Swiss Institute of Bioinformatics and distributed under the Creative Commons Attribution (CC BY 4.0) License (https://creativecommons.org/licenses/by/4.0/).
    https://enzyme.expasy.org/enzyme.get
    Enzyme Classification
    https://enzyme.expasy.org/
  14. Gene Ontology (GO)
    LICENSE
    Gene Ontology Consortium data and data products are licensed under the Creative Commons Attribution 4.0 Unported License (https://creativecommons.org/licenses/by/4.0/legalcode)
    http://geneontology.org/docs/go-citation-policy/
  15. AlphaFold DB
    LICENSE
    All of the data provided is freely available for both academic and commercial use under Creative Commons Attribution 4.0 (CC-BY 4.0) licence terms.
    https://alphafold.ebi.ac.uk/faq
  16. Rhea - annotated reactions database
    LICENSE
    Rhea has chosen to apply the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/). This means that you are free to copy, distribute, display and make commercial use of the database in all legislations, provided you credit (cite) Rhea.
    https://www.rhea-db.org/help/license-disclaimer
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