@article {903,
	title = {Targeting Bacterial and Human Levodopa Decarboxylases for Improved Drug Treatment of Parkinson{\textquoteright}s Disease: Discovery and Characterization of New Inhibitors},
	journal = {European Journal of Pharmaceutical Sciences},
	year = {2025},
	month = {Jan-05-2025},
	pages = {107133},
	issn = {09280987},
	doi = {10.1016/j.ejps.2025.107133},
	url = {https://authors.elsevier.com/sd/article/S0928-0987(25)00132-0},
	author = {Reunanen, Saku and Ghemtio, Leo and Patel, Jayendrakumar Z. and Patel, Darshitkumar R. and Airavaara, Kerttu and Yli-Kauhaluoma, Jari and Jeltsch, Michael and Xhaard, Henri and Piepponen, Petteri and Tammela, P{\"a}ivi}
}
@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 {425,
	title = {A truncation allele in vascular endothelial growth factor c reveals distinct modes of signaling during lymphatic and vascular development.},
	journal = {Development},
	volume = {140},
	year = {2013},
	month = {2013 Apr},
	pages = {1497-506},
	abstract = {<p>Vascular endothelial growth factor C (Vegfc) is a secreted protein that guides lymphatic development in vertebrate embryos. However, its role during developmental angiogenesis is not well characterized. Here, we identify a mutation in zebrafish vegfc that severely affects lymphatic development and leads to angiogenesis defects on sensitized genetic backgrounds. The um18 mutation prematurely truncated Vegfc, blocking its secretion and paracrine activity but not its ability to activate its receptor Flt4. When expressed in endothelial cells, vegfc(um18) could not rescue lymphatic defects in mutant embryos, but induced ectopic blood vessel branching. Furthermore, vegfc-deficient endothelial cells did not efficiently contribute to tip cell positions in developing sprouts. Computational modeling together with assessment of endothelial cell dynamics by time-lapse analysis suggested that an autocrine Vegfc/Flt4 loop plays an important role in migratory persistence and filopodia stability during sprouting. Our results suggest that Vegfc acts in two distinct modes during development: as a paracrine factor secreted from arteries to guide closely associated lymphatic vasculature and as an autocrine factor to drive migratory persistence during angiogenesis.</p>},
	keywords = {Alleles, Animals, Animals, Genetically Modified, Autocrine Communication, Blood Vessels, Cell Movement, Codon, Nonsense, Embryo, Nonmammalian, Female, Lymphatic System, Mice, Mice, Knockout, Neovascularization, Physiologic, Paracrine Communication, Protein Isoforms, Signal Transduction, Vascular Endothelial Growth Factor C, Zebrafish, Zebrafish Proteins},
	issn = {1477-9129},
	doi = {10.1242/dev.084152},
	author = {Villefranc, Jacques A and Nicoli, Stefania and Bentley, Katie and Jeltsch, Michael and Zarkada, Georgia and Moore, John C and Gerhardt, Holger and Alitalo, Kari and Lawson, Nathan D}
}
@article {35,
	title = {The tyrosine kinase inhibitor cediranib blocks ligand-induced vascular endothelial growth factor receptor-3 activity and lymphangiogenesis},
	journal = {Cancer Res},
	volume = {68},
	year = {2008},
	month = {2008/Jun/},
	pages = {4754 - 62},
	abstract = {Solid tumors express a range of factors required to sustain their growth and promote their dissemination. Among these are vascular endothelial growth factor-A (VEGF-A), the key angiogenic stimulant, and VEGF-C, a primary mediator of lymphangiogenesis. Small molecule tyrosine kinase inhibitors offer the potential to inhibit more than one kinase and impede tumor growth by multiple mechanisms. However, their potency toward individual targets can vary. Cediranib (RECENTIN; AZD2171) is an inhibitor of VEGF signaling that has been shown in experimental models to prevent VEGF-A-induced angiogenesis and primary tumor growth, yet the effects of cediranib on VEGF receptor (VEGFR)-3-mediated endothelial cell function and lymphangiogenesis are unknown. To better understand the activity of cediranib against VEGFR-3 and its associated signaling events compared with its activity against VEGFR-2, we used the receptor-specific ligands VEGF-E and VEGF-C156S. In human endothelial cells, cediranib inhibited VEGF-E-induced phosphorylation of VEGFR-2 and VEGF-C156S-induced phosphorylation of VEGFR-3 at concentrations of </=1nmol/L and inhibited activation of downstream signaling molecules. Additionally, cediranib blocked VEGF-C156S-induced and VEGF-E-induced proliferation, survival, and migration of lymphatic and blood vascular endothelial cells. In vivo, cediranib (6 mg/kg/d) prevented angiogenesis and lymphangiogenesis induced by VEGF-E-expressing and VEGF-C156S-expressing adenoviruses, respectively. Cediranib (6 mg/kg/day) also blocked angiogenesis and lymphangiogenesis induced by adenoviruses expressing VEGF-A or VEGF-C and compromised the blood and lymphatic vasculatures of VEGF-C-expressing tumors. Cediranib may, therefore, be an effective means of preventing tumor progression, not only by inhibiting VEGFR-2 activity and angiogenesis, but also by concomitantly inhibiting VEGFR-3 activity and lymphangiogenesis.},
	url = {http://view.ncbi.nlm.nih.gov/pubmed/18559522},
	author = {Heckman, Caroline A and Holopainen, Tanja and Wirzenius, Maria and Keskitalo, Salla and Jeltsch, Michael and Yl{\"a}-Herttuala, Seppo and Wedge, Stephen R and J{\"u}rgensmeier, Juliane M and Alitalo, Kari}
}
