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Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/27881

Title: Prediction of Regulatory Molecules for Enhancement of EGFR Overexpression Triggered by Signal Peptide of Ribonuclease 3
Authors: Hao-Teng Chang;Chung-Hsiao Chao;Yu-Fong Lin;Louis J. Tseng;Tun-Wen Pai;Tsan-Huang Shih;Margaret Dah-Tsyr Chang;Pei-Wen Tsai
Contributors: NTOU:Department of Computer Science and Engineering
Keywords: EGFR;phage display;ribonuclease 3;signal peptide
Date: 2010-02
Issue Date: 2011-10-21T02:34:19Z
Publisher: 2010 IEEE International Conference on Complex, Intelligent and Software Intensive Systems
Abstract: Abstract:Ribonuclease 3 (RNase3) is a member of the human RNaseA superfamily. It is led by a 27-residue signal peptide and secreted into body fluid to eliminate the infection of microbial pathogens in innate immune systems. The signal peptide of RNase3 (RNase3sp) not only directs protein secretion via endoplasmic reticulum (ER) and Golgi apparatus, but also its N-terminal 17 amino acid residues (RNase3sp1-17) induces the overexpression of epidermal growth factor receptor (EGFR). In this study, phage display technology was employed to screen the phage peptides which interacted with RNase3sp1-17. The peptide sequences were efficiently analyzed by proposed similarity search systems to retrieve potential candidates which possessed consensus residues conserved with the phage peptides. The retrieved potential candidates were subsequently input into the STRING database for discovering the interaction relationship among the candidates and EGFR. Finally, four potential RNase3sp1-17 interacting candidates, Notch1, GATA2, CBL, and RPX were selected, and the interaction network centered by Notch1 was generated. According to the interaction network and our 3 hypotheses, we attempt to solve the signaling pathway of EGFR overexpression triggered by RNase3sp1-17 by molecular biological experiments.
Relation: pp.672-676
URI: http://ntour.ntou.edu.tw/handle/987654321/27881
Appears in Collections:[資訊工程學系] 演講及研討會

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