期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 371, 期 2, 页码 304-308出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2008.04.063
关键词
lung cancer cells; MAP kinases; ERK1/2 kinases; AP-1; c-jun
资金
- NCI NIH HHS [R01 CA078282, R01 CA078282-09, R01 CA105005, CA87282, CA105005] Funding Source: Medline
- NHLBI NIH HHS [R01 HL066109, R01 HL066109-04, R01 HL066109-05A1, HL66109] Funding Source: Medline
- NIEHS NIH HHS [R01 ES011863-05, R01 ES011863, ES11863] Funding Source: Medline
Fra-1 as an integral part of AP-1 (Jun/Fos) drives transcriptional programs involved in several physiologic and pathologic processes. It is also critical for tumor cell motility and metastasis. We have previously shown that two critical elements of Fra-1 promoter, the Upstream TPA response element (TRE) and the serum response element (SRE), are necessary for its induction in response to phorbol esters in human pulmonary epithelial cell lines. Here, we have investigated the roles of various MAP kinases in regulating Fra-1 expression in response to TPA. Using pharmacologic and genetic tools, we demonstrate a prominent role for ERK1/2, but not JNK1/2 and p38, signaling in the TPA-induced activation of specific transcription factors that bind to the AP1 site and the SRE. Inhibition of ERK1/2 pathway suppresses Elk1 activation, and c-Jun and Fra-2 recruitment to the promoter. Published by Elsevier Inc.
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