共查询到20条相似文献,搜索用时 46 毫秒
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M C Birchenall-Roberts L A Falk J Kasper J Keller C R Faltynek F W Ruscetti 《The Journal of biological chemistry》1991,266(15):9617-9621
Transforming growth factor-beta 1 (TGF-beta 1) is a pleiotropic polypeptide hormone known to play an important role as a modulator of hematopoietic processes in human and murine cells. One of the characteristics of TGF-beta 1 is the ability to inhibit the growth of several cell types, including cells of the myeloid lineage. To study the mechanism by which TGF-beta 1 inhibits the growth of myeloid cells, we have used three murine myeloid cell lines, the parental interleukin-3-dependent 32D-123 cell line and two retrovirally infected interleukin-3-independent cell lines (32D-abl, 32D-src), all of which are growth inhibited by TGF-beta 1. Each of these oncogene-transfected cells expresses a greater number of TGF-beta 1 receptors than the parental cell line and responds to TGF-beta 1 with increased sensitivity; 32D and 32D-src cells are 2- and 58-fold more sensitive to TGF-beta 1 inhibition than the parental cell line (ED50 = 35 pM). Both 32D-abl- and 32D-src-transformed cell lines expressed higher levels of the 65- and 85-kDa TGF-beta 1 receptor species than did the parental cells. We observed a correlation between the greater sensitivity of 32D-src cells to TGF-beta 1 and the more rapid down-modulation and reappearance of cell surface TGF-beta 1 receptors on 32D-src cells. Thus, the level of TGF-beta 1 receptor expression and rate of reexpression both have a crucial regulatory effect on the functional activity of the TGF-beta 1 ligand. 相似文献
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Critical role of Smads and AP-1 complex in transforming growth factor-beta -dependent apoptosis 总被引:8,自引:0,他引:8
Yamamura Y Hua X Bergelson S Lodish HF 《The Journal of biological chemistry》2000,275(46):36295-36302
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S J Kim F Denhez K Y Kim J T Holt M B Sporn A B Roberts 《The Journal of biological chemistry》1989,264(32):19373-19378
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Autoinduction of transforming growth factor beta 1 is mediated by the AP-1 complex. 总被引:43,自引:9,他引:34 下载免费PDF全文
S J Kim P Angel R Lafyatis K Hattori K Y Kim M B Sporn M Karin A B Roberts 《Molecular and cellular biology》1990,10(4):1492-1497
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Structural and functional characterization of the transforming growth factor beta 3 promoter. A cAMP-responsive element regulates basal and induced transcription 总被引:18,自引:0,他引:18
R Lafyatis R Lechleider S J Kim S Jakowlew A B Roberts M B Sporn 《The Journal of biological chemistry》1990,265(31):19128-19136
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Finlay GA Thannickal VJ Fanburg BL Paulson KE 《The Journal of biological chemistry》2000,275(36):27650-27656
Transforming growth factor-beta (TGF-beta) is involved in multiple processes including cell growth and differentiation. In particular, TGF-beta has been implicated in the pathogenesis of fibrotic lung diseases. In this study, we examined regulation of the mitogen-activated protein kinase pathway by TGF-beta1 in primary human lung fibroblasts. TGF-beta1 treatment resulted in extracellular signal-regulated kinase (ERK) pathway activation in a delayed manner, with maximal activity at 16 h. ERK activation occurred concomitantly with the induction of activator protein-1 (AP-1) binding, a nuclear factor required for activation of multiple genes involved in fibrosis. AP-1 binding was dependent on ERK activation, since the MEK-1 (mitogen-activated protein kinase kinase) inhibitor PD98059 inhibited TGF-beta1-induced binding. Induction of the receptor tyrosine kinase-linked growth factor, basic fibroblast growth factor (bFGF) protein expression temporally paralleled the activation of ERK/AP-1. Induction of AP-1 by TGF-beta1-conditioned medium was observed at 2 h, similar to AP-1 induction in response to exogenous bFGF. Dependence of ERK/AP-1 activation on bFGF induction was demonstrated by inhibition of TGF-beta1-induced ERK/AP-1 activation when conditioned medium from TGF-beta1-treated cells was incubated with bFGF-neutralizing antibody. Together, these results demonstrate that TGF-beta1 regulates the autocrine induction of bFGF, resulting in activation of the ERK mitogen-activated protein kinase pathway and induction of AP-1 binding. 相似文献
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