Journal
FEBS LETTERS
Volume 584, Issue 18, Pages 4057-4062Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2010.08.028
Keywords
GPR48; Keratinocyte; Cell proliferation; EGFR; HB-EGF
Funding
- Program for New Century Excellent Talents in University [NCET-06-0538]
- National Natural Science Foundation of China [30771067]
- Zhejiang Provincial Natural Science Foundation of China [Z206842, Y2100280]
- Wenzhou Science & Technology Project [Y20090098]
- School of Ophthalmology and Optometry, Wenzhou Medical College [YNKT090312]
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GPR48 can mediate keratinocyte proliferation and migration. Our investigations showed that AG1478, an inhibitor of EGFR tyrosine kinase, could block GPR48-mediated cellular processes. AG1478 treatment of Gpr48(+/+) cells also decreased phosphorylation of EGFR, ERK and STAT3. Subsequent screening using conditioned media immunodepleted of EGFR ligands identified HB-EGF as the ligand responsible for phosphorylation of EGFR, ERK and STAT3. HB-EGF was reduced in Gpr48 (/) cell culture medium, but its addition restored the phosphorylation of EGFR, ERK, STAT3, as well as cell proliferation. Confirmation that GPR48 mediates EGFR signaling pathway through HB-EGF was subsequently performed using an inhibitor of HB-EGF. (c) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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