Ligand-induced changes in membrane-bound acetylcholine receptor observed by ethidium fluorescence. 1. Equilibrium studies

Biochemistry ◽  
1979 ◽  
Vol 18 (10) ◽  
pp. 1884-1890 ◽  
Author(s):  
Michael Schimerlik ◽  
Ulrich Quast ◽  
Michael A. Raftery
Biochemistry ◽  
1977 ◽  
Vol 16 (4) ◽  
pp. 684-692 ◽  
Author(s):  
James E. Bulger ◽  
Juian-Juian L. Fu ◽  
Ellen F. Hindy ◽  
Richard L. Silberstein ◽  
George P. Hess

1980 ◽  
Vol 2 ◽  
pp. 257-267 ◽  
Author(s):  
Y.P. Tan ◽  
W. Stender ◽  
A.L. Harvey ◽  
B. Soria ◽  
F.J. Barrantes

Biochemistry ◽  
1978 ◽  
Vol 17 (12) ◽  
pp. 2405-2414 ◽  
Author(s):  
U. Quast ◽  
M. Schimerlik ◽  
T. Lee ◽  
V. Witzemann ◽  
S. Blanchard ◽  
...  

1997 ◽  
Vol 129 (3) ◽  
pp. 225-232 ◽  
Author(s):  
Yoshihiro Tani ◽  
Kyoshi Saito ◽  
Atsuko Tsuneyoshi ◽  
Masahiro Imoto ◽  
Tomochika Ohno

Blood ◽  
2008 ◽  
Vol 111 (1) ◽  
pp. 260-270 ◽  
Author(s):  
Jui-Hung Yen ◽  
Tanzilya Khayrullina ◽  
Doina Ganea

Following antigen acquisition and maturation, dendritic cells (DCs) disengage from the extracellular matrix, cross basement membranes, and travel to draining lymph nodes to activate T cells. CCR7 expression is necessary but not sufficient for the directional migration of DCs. Prostaglandin E2 (PGE2), present in inflammatory sites, induces DC migration, presumably by enacting a migration-permissive gene expression program. Since regulation of DC migration is highly important for their use in vaccination and therapy, we examined the PGE2-induced changes in the expression of metalloproteinases (MMPs). Our results indicate that PGE2 significantly up-regulates MMP-9 expression, induces both secreted and membrane-bound MMP-9, and that in turn, DC-derived MMP-9 is essential for DC chemotaxis in response to the CCR7 ligand CCL19, Matrigel migration, and in vivo migration in both wild-type and MMP-9–deficient hosts. We conclude that DCs matured within inflammatory sites require both CCR7 and PGE2-induced MMP-9 for their directional migration to draining lymph nodes.


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