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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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Tie1 controls angiopoietin function in vascular remodeling and inflammation

TL;DR: It is determined that both ANG1 and ANG2 binding to Tie2 increases Tie1-Tie2 interactions in a β1 integrin-dependent manner and that Tie1 regulates ANG-induced Tie2 trafficking in endothelial cells, which supports a model in which Tie1 directly interacts with Tie2 to promote ANG- induced vascular responses under noninflammatory conditions.
Journal Article

Two human FLT4 receptor tyrosine kinase isoforms with distinct carboxy terminal tails are produced by alternative processing of primary transcripts.

TL;DR: It is shown that these transcripts encode two polypeptides, FLT4s (short) and FLT41 (long), which are proteolytically processed in transfected cells and leukemia cells and which have different carboxy terminal tails.
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VEGF receptor 2/-3 heterodimers detected in situ by proximity ligation on angiogenic sprouts.

TL;DR: In this paper, the authors used in situ proximity ligation to detect receptor complexes in intact endothelial cells and found that both VEGFA and VEGFC potently induce formation of VEGFR2/-3 heterodimers.
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The mouse tie receptor tyrosine kinase gene: expression during embryonic angiogenesis.

TL;DR: The results suggest that the tie receptor tyrosine kinase is involved in angiogenesis and/or maintenance of endothelial cell functions.
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Activation of hypoxia-inducible factor-1 in bacillary angiomatosis: evidence for a role of hypoxia-inducible factor-1 in bacterial infections.

TL;DR: The data provide for the first time evidence that HIF-1 may play a role in bacterial infections, and reveal that a B henselae infection resulted in the activation of genes typical for the cellular response to hypoxia.