scholarly journals Improved Angiostatic Activity of Dasatinib by Modulation with Hydrophobic Chains

2015 ◽  
Vol 6 (3) ◽  
pp. 313-317 ◽  
Author(s):  
Emilia Păunescu ◽  
Catherine M. Clavel ◽  
Patrycja Nowak-Sliwinska ◽  
Arjan W. Griffioen ◽  
Paul J. Dyson
Keyword(s):  
2006 ◽  
Vol 45 (3) ◽  
pp. e147
Author(s):  
Mary Jo Mulligan-Kehoe ◽  
Mary C. Drinane ◽  
Livia Casciola-Rosen ◽  
Laura K. Hummers ◽  
Amy E. Hall ◽  
...  

2008 ◽  
Vol 123 (9) ◽  
pp. 2195-2203 ◽  
Author(s):  
Meghan C. Brown ◽  
Izabela Staniszewska ◽  
Luis Del Valle ◽  
George P. Tuszynski ◽  
Cezary Marcinkiewicz

1993 ◽  
Vol 46 (4) ◽  
pp. 569-579 ◽  
Author(s):  
YUKIMASA NOZAKI ◽  
TSUNEAKI HIDA ◽  
SFFIGEMI IINUMA ◽  
TAKAFUMI ISHII ◽  
KATSUICHI SUDO ◽  
...  
Keyword(s):  

2005 ◽  
Vol 19 (12) ◽  
pp. 1713-1715 ◽  
Author(s):  
Luca Primo ◽  
Chiara Ferrandi ◽  
Cristina Roca ◽  
Serena Marchiò ◽  
Laura Di Blasio ◽  
...  

2003 ◽  
Vol 197 (11) ◽  
pp. 1537-1549 ◽  
Author(s):  
Laura Lasagni ◽  
Michela Francalanci ◽  
Francesco Annunziato ◽  
Elena Lazzeri ◽  
Stefano Giannini ◽  
...  

The chemokines CXCL9/Mig, CXCL10/IP-10, and CXCL11/I-TAC regulate lymphocyte chemotaxis, mediate vascular pericyte proliferation, and act as angiostatic agents, thus inhibiting tumor growth. These multiple activities are apparently mediated by a unique G protein–coupled receptor, termed CXCR3. The chemokine CXCL4/PF4 shares several activities with CXCL9, CXCL10, and CXCL11, including a powerful angiostatic effect, but its specific receptor is still unknown. Here, we describe a distinct, previously unrecognized receptor named CXCR3-B, derived from an alternative splicing of the CXCR3 gene that mediates the angiostatic activity of CXCR3 ligands and also acts as functional receptor for CXCL4. Human microvascular endothelial cell line-1 (HMEC-1), transfected with either the known CXCR3 (renamed CXCR3-A) or CXCR3-B, bound CXCL9, CXCL10, and CXCL11, whereas CXCL4 showed high affinity only for CXCR3-B. Overexpression of CXCR3-A induced an increase of survival, whereas overexpression of CXCR3-B dramatically reduced DNA synthesis and up-regulated apoptotic HMEC-1 death through activation of distinct signal transduction pathways. Remarkably, primary cultures of human microvascular endothelial cells, whose growth is inhibited by CXCL9, CXCL10, CXCL11, and CXCL4, expressed CXCR3-B, but not CXCR3-A. Finally, monoclonal antibodies raised to selectively recognize CXCR3-B reacted with endothelial cells from neoplastic tissues, providing evidence that CXCR3-B is also expressed in vivo and may account for the angiostatic effects of CXC chemokines.


1999 ◽  
Vol 15 (5) ◽  
pp. 413-423 ◽  
Author(s):  
LORETTA G. McNATT ◽  
LORI WEIMER ◽  
JOHN YANNI ◽  
ABBOT F. CLARK

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