Inhibition of the EGF-induced activation of phospholipase C-gamma 1 by a single chain antibody fragment
SCIE
SCOPUS
- Title
- Inhibition of the EGF-induced activation of phospholipase C-gamma 1 by a single chain antibody fragment
- Authors
- Yi, KS; Chung, JH; Lee, YH; Chung, HG; Kim, IJ; Suh, BC; Kim, E; Cocco, L; Ryu, SH; Suh, PG
- Date Issued
- 2001-11-29
- Publisher
- NATURE PUBLISHING GROUP
- Abstract
- Phospholipase C-gamma (PLC-gamma1) is known to play an essential role in various cellular responses, such as proliferation and tumorigenesis, and PLC-gamma1 -specific inhibitors are commonly employed to investigate the mechanism of the PLC-gamma1-mediated signaling pathway. In this study, we developed a single chain antibody fragment (scFv) as a blocker for PLC-gamma1 mediated signaling. scFv, designated F7-scFv, specifically bound to PLC-gammal with high affinity (K-d= 1.9 x 10(-8) M) in vitro. F7-scFv also bound to PLC-gamma1 in vivo and altered the distribution pattern of PLC-gamma1 from the cytoplasm to the intracellular aggregates, where F7-scFv was localized. Moreover, F7-scFv interrupted the EGF-induced translocation of PLC-gamma1 from the cytosol to the membrane ruffle and attenuated EGF-induced inositol phosphates generation and intracellular calcium mobilization. These results indicate that F7-scFv blocks EGF-induced PLC-gamma1 activation by causing sequestering of PLC-gamma1 into intracellular aggregates, and may therefore be useful in studies of the PLC-gamma1-mediated signaling pathway.
- Keywords
- PLC-gamma 1; single chain antibody (scFv); EGF; C ISOZYMES; INTRACELLULAR EXPRESSION; TYROSINE RESIDUES; ELEVATED CONTENT; SCFV FRAGMENT; DNA-SYNTHESIS; SH3 DOMAIN; GROWTH; RECEPTOR; CELLS
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/19298
- DOI
- 10.1038/sj.onc.1204959
- ISSN
- 0950-9232
- Article Type
- Article
- Citation
- ONCOGENE, vol. 20, no. 55, page. 7954 - 7964, 2001-11-29
- Files in This Item:
- There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.