Predicting Binding Affinity Based on Docking Measures for Spinocerebellar Ataxia: A Study

2017 ◽  
pp. 33-43
Author(s):  
P. R. Asha ◽  
M. S. Vijaya
Keyword(s):  
Binding Affinity ◽  
Spinocerebellar Ataxia

Antiproliferative and antiviral effects of mutated IFN-alpha with increased IFN receptor binding affinity

2011 ◽  
Vol 49 (01) ◽  
Author(s):  
MF Sprinzl ◽  
L Bührer ◽  
D Strand ◽  
G Schreiber ◽  
PR Galle ◽  
...  
Keyword(s):  
Binding Affinity ◽  
Receptor Binding ◽  
Receptor Binding Affinity ◽  
Ifn Alpha ◽  
Antiviral Effects

Enhancement of Plasminogen Binding to U937 Cells and Fibrin by Complestatin

1997 ◽  
Vol 77 (01) ◽  
pp. 137-142 ◽  
Author(s):  
Kiyoshi Tachikawa ◽  
Keiji Hasurni ◽  
Akira Endo
Keyword(s):  
Binding Site ◽  
Binding Affinity ◽  
Blood Cells ◽  
Aminocaproic Acid ◽  
U937 Cells ◽  
Biochemical Basis ◽  
Equilibrium Binding ◽  
Pharmacological Stimulation ◽  
Endogenous Fibrinolysis ◽  
Stimulation Of

SummaryPlasminogen binds to endothelial and blood cells as well as to fibrin, where the zymogen is efficiently activated and protected from inhibition by α2-antiplasmin. In the present study we have found that complestatin, a peptide-like metabolite of a streptomyces, enhances binding of plasminogen to cells and fibrin. Complestatin, at concentrations ranging from 1 to 5 μM, doubled 125I-plasminogen binding to U937 cells both in the absence and presence of lipoprotein(a), a putative physiological competitor of plasminogen. The binding of 125I-plasminogen in the presence of complestatin was abolished by e-aminocaproic acid, suggesting that the lysine binding site(s) of the plasminogen molecule are involved in the binding. Equilibrium binding analyses indicated that complestatin increased the maximum binding of 125I-plasminogen to U937 cells without affecting the binding affinity. Complestatin was also effective in increasing 125I-plasminogen binding to fibrin, causing 2-fold elevation of the binding at ~1 μM. Along with the potentiation of plasminogen binding, complestatin enhanced plasmin formation, and thereby increased fibrinolysis. These results would provide a biochemical basis for a pharmacological stimulation of endogenous fibrinolysis through a promotion of plasminogen binding to cells and fibrin.

Mitochondrial impairment in patients with spinocerebellar ataxia type 3

2004 ◽  
Vol 31 (S 1) ◽  
Author(s):  
L Schöls ◽  
J Andrich ◽  
H Przuntek ◽  
K Müller ◽  
J Zange
Keyword(s):  
Spinocerebellar Ataxia ◽  
Spinocerebellar Ataxia Type ◽  
Spinocerebellar Ataxia Type 3 ◽  
Mitochondrial Impairment ◽  
Type 3

Eye hand coordination in spinocerebellar ataxia type 17

2006 ◽  
Vol 37 (01) ◽  
Author(s):  
P Trillenberg ◽  
A Sprenger ◽  
A Hiller ◽  
C Klein ◽  
G Weinberger ◽  
...  
Keyword(s):  
Spinocerebellar Ataxia ◽  
Spinocerebellar Ataxia Type ◽  
Hand Coordination ◽  
Spinocerebellar Ataxia Type 17

Eye movement abnormalities in spinocerebellar ataxia type 17

2006 ◽  
Vol 33 (S 1) ◽  
Author(s):  
J. Hübner ◽  
A. Sprenger ◽  
J. Hagenah ◽  
C. Klein ◽  
H. Rambold ◽  
...  
Keyword(s):  
Eye Movement ◽  
Spinocerebellar Ataxia ◽  
Spinocerebellar Ataxia Type ◽  
Spinocerebellar Ataxia Type 17
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