The Role of Epidermal Growth Factor (EGF) and Its Receptor in Mucosal Protection, Adaptation to Injury, and Ulcer Healing: Involvement of EGF-R Signal Transduction Pathways

1998 ◽  
Vol 27 ◽  
pp. S12-S20 ◽  
Author(s):  
Andrzej S. Tarnawski ◽  
Michael K. Jones
Keyword(s):  
Signal Transduction ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Ulcer Healing ◽  
Signal Transduction Pathways ◽  
Mucosal Protection ◽  
Epidermal Growth

Interaction of Growth Hormone-Releasing Factor and Somatostatin on Ulcer Healing and Mucosal Growth in Rats: Role of Gastrin and Epidermal Growth Factor

Digestion ◽  
1988 ◽  
Vol 41 (3) ◽  
pp. 121-128 ◽  
Author(s):  
S.J. Konturek ◽  
T. Brzozowski ◽  
A. Dembinski ◽  
Z. Warzecha ◽  
P.K. Konturek ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Ulcer Healing ◽  
Growth Hormone Releasing Factor ◽  
Epidermal Growth ◽  
Mucosal Growth

scholarly journals Endosomal Signaling of Epidermal Growth Factor Receptor Stimulates Signal Transduction Pathways Leading to Cell Survival

2002 ◽  
Vol 22 (20) ◽  
pp. 7279-7290 ◽  
Author(s):  
Yi Wang ◽  
Steven Pennock ◽  
Xinmei Chen ◽  
Zhixiang Wang
Keyword(s):  
Signal Transduction ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Egf Receptor ◽  
Kinase Inhibitor ◽  
Nucleation Site ◽  
Signal Transduction Pathways ◽  
Egfr Signaling ◽  
Endosomal Signaling ◽  
Epidermal Growth

ABSTRACT In spite of intensified efforts to understand cell signaling from endosomes, there is no direct evidence demonstrating that endosomal signaling is sufficient to activate signal transduction pathways and no evidence to demonstrate that endosomal signaling is able to produce a biological outcome. The lack of breakthrough is due in part to the lack of means to generate endosomal signals without plasma membrane signaling. In this paper, we report the establishment of a system to specifically activate epidermal growth factor (EGF) receptor (EGFR) when it endocytoses into endosomes. We treated cells with EGF in the presence of AG-1478, a specific EGFR tyrosine kinase inhibitor, and monensin, which blocks the recycling of EGFR. This treatment led to the internalization of nonactivated EGF-EGFR complexes into endosomes. The endosome-associated EGFR was then activated by removing AG-1478 and monensin. During this procedure we did not observe any surface EGFR phosphorylation. We also achieved specific activation of endosome-associated EGFR without using monensin. By using this system, we provided original evidence demonstrating that (i) the endosome can serve as a nucleation site for the formation of signaling complexes, (ii) endosomal EGFR signaling is sufficient to activate the major signaling pathways leading to cell proliferation and survival, and (iii) endosomal EGFR signaling is sufficient to suppress apoptosis induced by serum withdrawal.

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