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
Role of Ets factors in the activity and endothelial cell specificity of the mouse Tie gene promoter
Kristiina Iljin,Antoinise Dube,Sirpa Kontusaari,Jaana Korhonen,Isto Lahtinen,Peter Oettgen,Kari Alitalo +6 more
TL;DR: The properties of the Tie promoter suggest that Tie promoter activity is controlled by endothelial cell Ets factors and that it has potential for use in vectors for endothelialcell‐specific gene expression.
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Subcellular location of an abundant substrate (p36) for tyrosine-specific protein kinases.
TL;DR: It is concluded that at least a substantial fraction of p36 is located on the cytoplasmic aspect of the plasma membrane, where it could be well situated to serve as a substrate for several identified tyrosine-specific kinases.
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Cardiac lymphatics in health and disease.
Ebba Brakenhielm,Kari Alitalo +1 more
TL;DR: The physiological role of the lymphatic system in the heart in the maintenance of cardiac health is discussed and alterations in lymphatic structure and function that occur in cardiovascular pathology, including atherosclerosis and myocardial infarction are described.
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Vascular endothelial growth factor-C gene therapy restores lymphatic flow across incision wounds
Anne Saaristo,Tuomas Tammela,Jari Timonen,Seppo Ylä-Herttuala,Erkki Tukiainen,Sirpa Asko-Seljavaara,Kari Alitalo +6 more
TL;DR: It is demonstrated that vascular endothelial growth factor C (VEGF‐C) gene transfer can be used to reconstruct a lymphatic vessel network severed by incision of skin flaps and provides new tools to promote vascular perfusion and to reduce tissue edema in skin and muscle flaps.
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Proteolytic activation defines distinct lymphangiogenic mechanisms for VEGFC and VEGFD
Hung Bui,David Enis,Marius R. Robciuc,Harri Nurmi,Jennifer L. Cohen,Mei Chen,Yiqing Yang,Veerpal Dhillon,Kathy Johnson,Hong Zhang,Robert B. Kirkpatrick,Elizabeth A. Traxler,Andrey Anisimov,Kari Alitalo,Mark L. Kahn +14 more
TL;DR: It is shown that an ADAMTS3-CCBE1 complex can form independently of VEGFR3 and is required to convert VEGFC, but not VEGFD, into an active ligand, revealing that lymphangiogenesis is regulated by two distinct proteolytic mechanisms of ligand activation.