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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Tie endothelial cell-specific receptor tyrosine kinase is upregulated in the vasculature of arteriovenous malformations.
TL;DR: The significant upregulation of VEGF and Tie in AVMs may indicate some ongoing angiogenesis, possibly contributing to the slow growth and maintenance of the AVM, and could be of potential use in the therapeutic targeting of these lesions.
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Counteracting age-related VEGF signaling insufficiency promotes healthy aging and extends life span
Myriam Grunewald,Saran Kumar,Husni Sharife,Evgenia Volinsky,A. Gileles-Hillel,A. Gileles-Hillel,Tamar Licht,Anna Permyakova,Liad Hinden,Shahar Azar,Y. Friedmann,P. Kupetz,R. Tzuberi,Andrey Anisimov,Kari Alitalo,M. Horwitz,S. Leebhoff,Oleksiy-Zakhar Khoma,Ruslan Hlushchuk,Valentin Djonov,Rinat Abramovitch,Joseph Tam,Eli Keshet +22 more
TL;DR: In this article, the authors show that vascular endothelial growth factor (VEGF) signaling insufficiency, which is caused by increased production of decoy receptors, may drive physiological aging across multiple organ systems, and suggest that modulating this pathway may result in increased mammalian life span and improved overall health.
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How do angiopoietins Tie in with vascular endothelial growth factors
TL;DR: In this article, the authors discuss the other pathways where progress is made for drug development, in particular the angiopoietin (Ang)-Tie receptor pathway, and reveal that Tie2 utilizes a unique signaling mechanism at endothelial cell-cell junctions.
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Akt/Protein Kinase B Is Required for Lymphatic Network Formation, Remodeling, and Valve Development
Fei Zhou,Zai Chang,Luqing Zhang,Young-Kwon Hong,Bin Shen,Bo Wang,Fan Zhang,Guangming Lu,Denis Tvorogov,Kari Alitalo,Brian A. Hemmings,Zhongzhou Yang,Yulong He +12 more
TL;DR: The results indicate that despite the compensatory roles of other Akt isoforms, Akt1 is more critically required during lymphatic development.
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NOTUM from Apc-mutant cells biases clonal competition to initiate cancer.
Dustin J. Flanagan,Nalle Pentinmikko,Kalle Luopajärvi,Nicky J. Willis,Kathryn Gilroy,Alexander Raven,Lynn McGarry,Johanna Englund,Anna Taylor Webb,Sandra Scharaw,Nadia Nasreddin,Michael C. Hodder,Rachel A. Ridgway,Emma Minnee,Nathalie Sphyris,Ella Gilchrist,Arafath Kaja Najumudeen,Béatrice Romagnolo,Christine Perret,Ann C. Williams,Hans Clevers,Hans Clevers,Pirjo Nummela,Marianne Lähde,Kari Alitalo,Ville Hietakangas,Ann Hedley,William C. Clark,Colin Nixon,Kristina Kirschner,E. Yvonne Jones,Ari Ristimäki,Simon J. Leedham,Paul V. Fish,Paul V. Fish,Jean-Paul Vincent,Pekka Katajisto,Pekka Katajisto,Owen J. Sansom,Owen J. Sansom +39 more
TL;DR: In this article, the authors investigated how Apc-mutant cells gain a clonal advantage over wild-type counterparts to achieve fixation and identified Notum as a key mediator during the early stages of mutation fixation that can be targeted to restore wild type cell competitiveness and provide preventative strategies for people at a high risk of developing colorectal cancer.