DocumentCode :
1645577
Title :
The benefit of intrinsic disorder information in neural network prediction of calmodulin binding targets
Author :
O´Connor, Timothy R. ; Lawson, J. David ; Dunker, A. Keith
Author_Institution :
Sch. of Molecular Biosciences, Washington State Univ., Pullman, WA, USA
Volume :
1
fYear :
2002
fDate :
6/24/1905 12:00:00 AM
Firstpage :
296
Lastpage :
299
Abstract :
Calmodulin is an important calcium dependent signaling protein found in all eukaryotic cells. Binding calcium enables calmodulin to bind its targets: basic, amphipathic ∞-helices. Such binding regulates the activities of many proteins. Because calmodulin wraps completely around the target helix upon binding, it is hypothesized that disorder of a target helix is an important feature of this process. We have used several sequence derived features of calmodulin binding targets, including intrinsic order/disorder predictions, to construct neural networks based on permutations of three or more of these features. The resulting networks demonstrate that the addition of intrinsic order/disorder information always increases the performance of a given neural network predictor. The best predictor generated has a performance of 87.8% true positive prediction and 87.2% true negative prediction
Keywords :
backpropagation; biology computing; molecular biophysics; neural nets; proteins; Ca; amphipathic ∞-helices; calcium dependent signaling protein; calmodulin binding targets; eukaryotic cells; intrinsic disorder information; neural network prediction; true negative prediction; true positive prediction; Amino acids; Calcium; Cellular networks; Databases; Intelligent networks; Neural networks; Performance analysis; Proteins; Signal generators; Solvents;
fLanguage :
English
Publisher :
ieee
Conference_Titel :
Neural Networks, 2002. IJCNN '02. Proceedings of the 2002 International Joint Conference on
Conference_Location :
Honolulu, HI
ISSN :
1098-7576
Print_ISBN :
0-7803-7278-6
Type :
conf
DOI :
10.1109/IJCNN.2002.1005486
Filename :
1005486
Link To Document :
بازگشت