K
Kari Alitalo
Researcher at University of Helsinki
Publications - 844
Citations - 122462
Kari Alitalo is an academic researcher from University of Helsinki. The author has contributed to research in topics: Angiogenesis & Vascular endothelial growth factor C. The author has an hindex of 174, co-authored 817 publications receiving 114231 citations. Previous affiliations of Kari Alitalo include Mount Sinai Hospital, Toronto & Cornell University.
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Journal ArticleDOI
The mechanisms of ornithine decarboxylase deregulation in c-Ha-ras oncogene-transformed NIH 3T3 cells.
TL;DR: ODC deregulation at multiple levels in the ras-oncogene-transformed cells is suggested, suggesting that labile proteins may be involved in the regulation of both the stability and translatability of the ODC mRNA.
Journal ArticleDOI
Endothelial cells genetically selected from differentiating mouse embryonic stem cells incorporate at sites of neovascularization in vivo.
Sandrine Marchetti,Clotilde Gimond,Kristiina Iljin,Christine Bourcier,Kari Alitalo,Jacques Pouysségur,Gilles Pagès +6 more
TL;DR: Results suggest that application of endothelial lineage selection to differentiating ES cells may become a useful approach for future pro-angiogenic and endothelial cell replacement therapies.
Journal ArticleDOI
Lymphangiogenesis guidance by paracrine and pericellular factors.
TL;DR: This review describes several of these cues and how they are integrated for the generation of functional lymphatic vessel networks and their role in the pathogenesis of several human diseases.
Journal ArticleDOI
Targeting Lymphatic Vessel Activation and CCL21 Production by Vascular Endothelial Growth Factor Receptor-3 Inhibition Has Novel Immunomodulatory and Antiarteriosclerotic Effects in Cardiac Allografts
Antti I. Nykänen,Henrik Sandelin,Rainer Krebs,Mikko A. I. Keränen,Raimo Tuuminen,Terhi Karpanen,Yan Wu,Bronislaw Pytowski,Petri Koskinen,Seppo Ylä-Herttuala,Kari Alitalo,Karl B. Lemström +11 more
TL;DR: Results show that VEGFR-3 participates in immune cell traffic from peripheral tissues to secondary lymphoid organs by regulating allograft lymphatic vessel CCL21 production and suggest VEG FR-3 inhibition as a novel lymphatic vessels–targeted immunomodulatory therapy for cardiac allografted rejection and arteriosclerosis.
Journal ArticleDOI
Tyrosine phosphorylation of CD45 phosphotyrosine phosphatase by p50csk kinase creates a binding site for p56lck tyrosine kinase and activates the phosphatase.
Matti Autero,Juha Saharinen,Tiina Pessa-Morikawa,M Soula-Rothhut,Christina Oetken,M Gassmann,Mathias Bergman,Kari Alitalo,Paul Burn,Carl G. Gahmberg +9 more
TL;DR: It is reported that CD45 was phosphorylated by p50csk on two tyrosine residues, one of them identified as Tyr-1193, and phosphorylation increased upon treatment with PTPase inhibitors, indicating that this tyosine is a target for a constitutively active PTK.