共查询到20条相似文献,搜索用时 31 毫秒
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Serum response element binding protein (SRE BP) is a novel binding factor present in nuclear extracts of avian and NIH 3T3 fibroblasts which specifically binds to the cfos SRE within a region overlapping and immediately 3' to the CArG box. Site-directed mutagenesis combined with transfection experiments in NIH 3T3 cells showed that binding of both serum response factor (SRF) and SRE BP is necessary for maximal serum induction of the SRE. In this study, we have combined size fractionation of the SRE BP DNA binding activity with C/EBPbeta antibodies to demonstrate that homodimers and heterodimers of p35C/EBPbeta (a transactivator) and p20C/EBPbeta (a repressor) contribute to the SRE BP complex in NIH 3T3 cells. Transactivation of the SRE by p35C/EBPbeta is dependent on SRF binding but not ternary complex factor (TCF) formation. Both p35C/EBPbeta and p20C/EBPbeta bind to SRF in vitro via a carboxy-terminal domain that probably does not include the leucine zipper. Moreover, SRE mutants which retain responsiveness to the TCF-independent signaling pathway bind SRE BP in vitro with affinities that are nearly identical to that of the wild-type SRE, whereas mutant SRE.M, which is not responsive to the TCF-independent pathway, has a nearly 10-fold lower affinity for SRE BP. We propose that C/EBPbeta may play a role in conjunction with SRF in the TCF-independent signaling pathway for SRE activation. 相似文献
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Raymond Poon Saeid Amini Nik Jessica Ahn Laura Slade Benjamin A Alman 《BMC cell biology》2009,10(1):38-10
Background
β-catenin and transforming growth factor β signaling are activated in fibroblasts during wound healing. Both signaling pathways positively regulate fibroblast proliferation during this reparative process, and the effect of transforming growth factor β is partially mediated by β-catenin. Other cellular processes, such as cell motility and the induction of extracellular matrix contraction, also play important roles during wound repair. We examined the function of β-catenin and its interaction with transforming growth factor β in cell motility and the induction of collagen lattice contraction. 相似文献7.
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Lisa?L?Maduzia Andrew?F?Roberts Huang?Wang Xia?Lin Lena?J?Chin Cole?M?Zimmerman Stephen?Cohen Xin-Hua?Feng Richard?W?Padgett
Background
In C. elegans there are two well-defined TGFβ-like signaling pathways. The Sma/Mab pathway affects body size morphogenesis, male tail development and spicule formation while the Daf pathway regulates entry into and exit out of the dauer state. To identify additional factors that modulate TGFβ signaling in the Sma/Mab pathway, we have undertaken a genetic screen for small animals and have identified kin-29. 相似文献10.
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Gudrun Valdimarsdottir Marie-José Goumans Fumiko Itoh Susumu Itoh Carl-Henrik Heldin Peter ten Dijke 《BMC cell biology》2006,7(1):16-11
Background
In endothelial cells (EC), transforming growth factor-β (TGF-β) can bind to and transduce signals through ALK1 and ALK5. The TGF-β/ALK5 and TGF-β/ALK1 pathways have opposite effects on EC behaviour. Besides differential receptor binding, the duration of TGF-β signaling is an important specificity determinant for signaling responses. TGF-β/ALK1-induced Smad1/5 phosphorylation in ECs occurs transiently. 相似文献15.
Ranjan P Boss JM 《Apoptosis : an international journal on programmed cell death》2006,11(10):1837-1849
The CCAAT enhancer binding protein-β (C/EBPβ) is a critical regulator of many cellular processes. Exposure of C/EBPβ-deficient
fibroblasts to tumor necrosis factor-α (TNF) resulted in their death due to apoptosis. While, the expression of Bad, Bcl-2,
Bcl-x, CAS, and hILP/XIAP, as well as the nuclear translocation of NF-κB was normal in C/EBPβ-deficient cells, induction of
manganous superoxide dismutase (MnSOD) gene did not occur. Ectopic expression of C/EBPβ in C/EBPβ–deficient fibroblasts prevented
TNF-induced apoptosis. C/EBPβ complemented cells were able to induce MnSOD in response to TNF, ruling out the possibilities
that C/EBPβ could render protection by regulating early apoptotic gene expression and/or NF-κB p65 expression. Moreover, C/EBPβ-deficient
cells stably transfected with an MnSOD expression vector bypassed the requirement of C/EBPβ in protection against TNF-induced
cell death, suggesting that C/EBPβ protects TNF-induced apoptotic cell death through its role in activating MnSOD expression.
Mechanistically, C/EBPβ was required for induced NF-κB p65 binding to MnSOD’s intronic TNF response element and indispensable
for histone acetylation of the element in response to TNF. These results suggest a role for C/EBPβ in MnSOD regulation through
remodeling of local chromatin structure.
This work was supported by a grant from the National Institutes of Health, CA96810. 相似文献
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