R
Rakesh K. Jain
Researcher at Harvard University
Publications - 1528
Citations - 198912
Rakesh K. Jain is an academic researcher from Harvard University. The author has contributed to research in topics: Angiogenesis & Cancer. The author has an hindex of 200, co-authored 1467 publications receiving 177727 citations. Previous affiliations of Rakesh K. Jain include Government Medical College, Thiruvananthapuram & University of Oslo.
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An update on natural occurrence and biological activity of chromones.
TL;DR: This comprehensive review describes the current status and knowledge of natural occurrence, and biological activities of chromones and recent advances made over the last decade are critically discussed.
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Chemotaxis of a Ralstonia sp. SJ98 toward different nitroaromatic compounds and their degradation.
TL;DR: This is the first report which shows the chemotaxis of a microorganism toward different NACs and their subsequent degradation, and indicates a correlation between chemotactic and biodegradation of Nacs.
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Blockade of VEGFR2 and not VEGFR1 can limit diet-induced fat tissue expansion: role of local versus bone marrow-derived endothelial cells.
Joshua Tam,Dan G. Duda,Jean Yannis Perentes,Jean Yannis Perentes,Rehan Quadri,Dai Fukumura,Rakesh K. Jain +6 more
TL;DR: Formation of new vessels in fat tissues during DIO is largely due to angiogenesis rather than de novo vasculogenesis, and antiangiogenic treatment by blockade of VEGFR2 but not VEG FR1 may limit adipose tissue expansion.
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Decorin inhibits endothelial migration and tube-like structure formation: role of thrombospondin-1.
Catharina de Lange Davies,Robert J. Melder,Lance L. Munn,Carla Mouta-Carreira,Rakesh K. Jain,Yves Boucher +5 more
TL;DR: It is suggested that decorin alone or in combination with TSP-1 interferes with the activation of endothelial cell receptors by ECM molecules, thus blocking intracellular signals that induce cytoskeletal reorganization, migration, and TLS formation.
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Leukocyte-endothelial adhesion and angiogenesis in tumors
TL;DR: A molecular link may partially explain why the overall leukocyte-endothelial interaction is often low and heterogeneous in angiogenic tumor vessels and why activated lymphocytes adhere nonuniformly to tumor vessels when injected into the tumor's blood supply.