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GPR48-Induced keratinocyte proliferation occurs through HB-EGF mediated EGFR transactivation

  • Zhenlian Wang
  • , Chang Jin
  • , Hongxia Li
  • , Canxia Li
  • , Qiang Hou
  • , Mingyao Liu
  • , Xiang Da Eric Dong
  • , Li Li Tu*
  • *此作品的通讯作者
  • Wenzhou Medical University
  • Ministry of Health of the People's Republic of China
  • Texas A&M University
  • Columbia University

科研成果: 期刊稿件文章同行评审

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
584
18
DOI
出版状态已出版 - 9月 2010
已对外发布

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