摘要
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.
| 源语言 | 英语 |
|---|---|
| 页(从-至) | 4057-4062 |
| 页数 | 6 |
| 期刊 | FEBS Letters |
| 卷 | 584 |
| 期 | 18 |
| DOI | |
| 出版状态 | 已出版 - 9月 2010 |
| 已对外发布 | 是 |
指纹
探究 'GPR48-Induced keratinocyte proliferation occurs through HB-EGF mediated EGFR transactivation' 的科研主题。它们共同构成独一无二的指纹。引用此
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