@inbook {503,
	title = {The TIE Receptor Family},
	booktitle = {Receptor Tyrosine Kinases: Family and Subfamilies},
	year = {2015},
	pages = {743-775},
	publisher = {Springer International Publishing},
	organization = {Springer International Publishing},
	chapter = {16},
	keywords = {ANG, Angiopoietin, ANGPT, Endothelial cell, Lymphatic vessel, Neovascularization, TIE1, TIE2, Vascular dysfunction},
	issn = {978-3-319-11888-8},
	doi = {10.1007/978-3-319-11888-8_16},
	url = {https://link.springer.com/content/pdf/10.1007\%2F978-3-319-11888-8_16.pdf},
	author = {Saharinen, Pipsa and Jeltsch, Michael and Santoyo, MayteM. and Lepp{\"a}nen, Veli-Matti and Alitalo, Kari},
	editor = {Wheeler, Deric L. and Yarden, Yosef}
}
@article {445,
	title = {Receptor Tyrosine Kinase-Mediated Angiogenesis},
	journal = {Cold Spring Harbor Perspectives in Biology},
	volume = {5},
	year = {2013},
	month = {2013},
	abstract = {The endothelial cell is the essential cell type forming the inner layer of the vasculature. Two families of receptor tyrosine kinases (RTKs) are almost completely endothelial cell specific: the vascular endothelial growth factor (VEGF) receptors (VEGFR1-3) and the Tie receptors (Tie1 and Tie2). Both are key players governing the generation of blood and lymphatic vessels during embryonic development. Because the growth of new blood and lymphatic vessels (or the lack thereof) is a central element in many diseases, the VEGF and the Tie receptors provide attractive therapeutic targets in various diseases. Indeed, several drugs directed to these RTK signaling pathways are already on the market, whereas many are in clinical trials. Here we review the VEGFR and Tie families, their involvement in developmental and pathological angiogenesis, and the different possibilities for targeting them to either block or enhance angiogenesis and lymphangiogenesis.},
	isbn = {, 1943-0264},
	doi = {10.1101/cshperspect.a009183},
	url = {http://cshperspectives.cshlp.org/content/5/9/a009183},
	author = {Jeltsch, Michael and Lepp{\"a}nen, Veli-Matti and Saharinen, Pipsa and Alitalo, Kari}
}
@article {39,
	title = {Claudin-like protein 24 interacts with the VEGFR-2 and VEGFR-3 pathways and regulates lymphatic vessel development},
	journal = {Genes Dev},
	volume = {24},
	year = {2010},
	month = {2010/May/},
	pages = {875 - 80},
	abstract = {The Claudin-like protein of 24 kDa (CLP24) is a hypoxia-regulated transmembrane protein of unknown function. We show here that clp24 knockdown in Danio rerio and Xenopus laevis results in defective lymphatic development. Targeted disruption of Clp24 in mice led to enlarged lymphatic vessels having an abnormal smooth muscle cell coating. We also show that the Clp24(-/-) phenotype was further aggravated in the Vegfr2(+/LacZ) or Vegfr3(+/LacZ) backgrounds and that CLP24 interacts with vascular endothelial growth factor receptor-2 (VEGFR-2) and VEGFR-3 and attenuates the transcription factor CREB phosphorylation via these receptors. Our results indicate that CLP24 is a novel regulator of VEGFR-2 and VEGFR-3 signaling pathways and of normal lymphatic vessel structure.},
	url = {http://view.ncbi.nlm.nih.gov/pubmed/20439428},
	author = {Saharinen, Pipsa and Helotera, Hanna and Miettinen, Juho and Norrmen, Camilla and D{\textquoteright}Amico, Gabriela and Jeltsch, Michael and Langenberg, Tobias and Vandevelde, Wouter and Ny, Annelii and Dewerchin, Mieke and Carmeliet, Peter and Alitalo, Kari}
}
