共查询到20条相似文献,搜索用时 31 毫秒
1.
2.
3.
Laderoute KR Mendonca HL Calaoagan JM Knapp AM Giaccia AJ Stork PJ 《The Journal of biological chemistry》1999,274(18):12890-12897
4.
5.
6.
7.
8.
Uchida T Rossignol F Matthay MA Mounier R Couette S Clottes E Clerici C 《The Journal of biological chemistry》2004,279(15):14871-14878
9.
10.
11.
12.
Modulation of collagen and MMP-1 gene expression in fibroblasts by the immunosuppressive drug rapamycin. A direct role as an antifibrotic agent? 总被引:1,自引:0,他引:1
Poulalhon N Farge D Roos N Tacheau C Neuzillet C Michel L Mauviel A Verrecchia F 《The Journal of biological chemistry》2006,281(44):33045-33052
13.
Bowles DK Graier WF Sturek M 《Biochemical and biophysical research communications》2001,284(5):1134-1139
The c-jun gene is a major regulator of proliferative and stress responses of both normal and transformed cells. In general, during immortalization/transformation c-jun cooperates with oncogenic signals rather than acting as an oncogene itself. Here we report a novel example of this cooperation, the requirement for c-jun to sustain expression of the matrix metalloproteinase-2 (MMP-2) gene in cells immortalized by SV40 large T-antigen (TAg). MMP-2 encodes a type IV collagenase that is secreted by cells within normal and tumor microenvironments. We used wild-type and c-jun null primary and TAg-immortalized mouse embryonic fibroblasts (mEFs) to investigate the importance of c-jun for the regulation of this activity, and observed that c-jun is essential for MMP-2 expression in immortalized but not primary mEFs. This finding directly demonstrates a cooperative interaction of c-jun with an oncogene, and suggests that TAg dependent immortalization/transformation may require other c-Jun/AP-1-dependent genes. 相似文献
14.
Hossain MA Bouton CM Pevsner J Laterra J 《The Journal of biological chemistry》2000,275(36):27874-27882
15.
16.
17.
18.
19.
20.
Hypoxia-induced bFGF gene expression is mediated through the JNK signal transduction pathway 总被引:7,自引:0,他引:7
Although the synthesis of angiogenic factors in hypoxic regions of solid tumors is recognized as one of the critical steps in tumor growth and metastasis, the signal transduction pathway involved in hypoxic induction of basic fibroblast growth factor (bFGF) gene expression is still obscure. In the study described here, we investigated the intracellular responses to hypoxia and the mechanisms triggering the initiation of angiogenic activity in drug-resistant human breast carcinoma MCF-7/ADR cells. Northern blots showed an increase in the level of c-jun, c-fos, and bFGF mRNA during hypoxia. Gel mobility-shift analysis of nuclear extracts from hypoxia-exposed cells showed an increase in AP-1 binding activity. In addition, hypoxic treatment strongly activated c-Jun N-terminal kinase 1 (JNK1), leading to phosphorylation and activation of c-Jun. Expression of a dominant negative mutant of JNK1 suppressed hypoxia-induced JNK1 activation as well as bFGF gene expression. Taken together, hypoxia-induced bFGF gene expression is mediated through the stress-activated protein kinase (SAPK) signal transduction pathway. 相似文献