共查询到20条相似文献,搜索用时 15 毫秒
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O I Ornatsky D M Cox P Tangirala J J Andreucci Z A Quinn J L Wrana R Prywes Y T Yu J C McDermott 《Nucleic acids research》1999,27(13):2646-2654
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Identification of novel Smad binding proteins 总被引:5,自引:0,他引:5
Warner DR Roberts EA Greene RM Pisano MM 《Biochemical and biophysical research communications》2003,312(4):1185-1190
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Pan D Estévez-Salmerón LD Stroschein SL Zhu X He J Zhou S Luo K 《The Journal of biological chemistry》2005,280(16):15992-16001
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J D Brown M R DiChiara K R Anderson M A Gimbrone J N Topper 《The Journal of biological chemistry》1999,274(13):8797-8805
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GATA-dependent recruitment of MEF2 proteins to target promoters 总被引:38,自引:0,他引:38
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A dynamic role for HDAC7 in MEF2-mediated muscle differentiation 总被引:14,自引:0,他引:14
Dressel U Bailey PJ Wang SC Downes M Evans RM Muscat GE 《The Journal of biological chemistry》2001,276(20):17007-17013
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Hoffmann A Preobrazhenska O Wodarczyk C Medler Y Winkel A Shahab S Huylebroeck D Gross G Verschueren K 《The Journal of biological chemistry》2005,280(29):27271-27283
TAK1 (transforming growth factor-beta-activated kinase-1), a MAP3K with considerable sequence similarity to Raf-1 and MEKK-1, has been identified as a transforming growth factor-beta/bone morphogenetic protein (BMP)-activated cytosolic component of the MAPK pathways. In this investigation, the molecular interactions between TAK1 and Smad proteins were characterized as well as their influence on BMP-mediated mesenchymal cell differentiation along the osteogenic/chondrogenic pathway. In co-immunoprecipitations we found an interaction of TAK1 with all Smads tested, R-Smads Smads1-5, the co-Smad Smad4, and the inhibitory Smads (I-Smad6 and I-Smad7). Smad interaction with TAK1 takes place through their MH2 domain. This interaction is dependent on the presence of an active kinase domain in TAK1. TAK1 dramatically interferes with R-Smad transactivation in reporter assays and affects subcellular distribution of Smad proteins. Activated TAK1 also interferes with BMP-dependent osteogenic development in murine mesenchymal progenitor cells (C3H10T 1/2). A potential TAK1-mediated apoptosis process could be excluded for these cells. Both synergistic and interfering influences of TAK1 on BMP-mediated Smad-signaling have been reported previously. We suggest that TAK1 is a factor that is involved in the fine-tuning of BMP effects during osteogenic development. 相似文献
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Y Ono F Calhabeu J E Morgan T Katagiri H Amthor P S Zammit 《Cell death and differentiation》2011,18(2):222-234
Satellite cells are the resident stem cells of adult skeletal muscle, supplying myonuclei for homoeostasis, hypertrophy and repair. In this study, we have examined the role of bone morphogenetic protein (BMP) signalling in regulating satellite cell function. Activated satellite cells expressed BMP receptor type 1A (BMPR-1A/Alk-3) and contained phosphorylated Smad proteins, indicating that BMP signalling is operating during proliferation. Indeed, exogenous BMP4 stimulated satellite cell division and inhibited myogenic differentiation. Conversely, interfering with the interactions between BMPs and their receptors by the addition of either the BMP antagonist Noggin or soluble BMPR-1A fragments, induced precocious differentiation. Similarly, blockade of BMP signalling by siRNA-mediated knockdown of BMPR-1A, disruption of the intracellular pathway by either Smad5 or Smad4 knockdown or inhibition of Smad1/5/8 phosphorylation with Dorsomorphin, also caused premature myogenic differentiation. BMP signalling acted to inhibit the upregulation of genes associated with differentiation, in part, through regulating Id1. As satellite cells differentiated, Noggin levels increased to antagonise BMP signalling, since Noggin knockdown enhanced proliferation and impeded myoblast fusion into large multinucleated myotubes. Finally, interference of normal BMP signalling after muscle damage in vivo perturbed the regenerative process, and resulted in smaller regenerated myofibres. In conclusion, BMP signalling operates during routine satellite cell function to help coordinate the balance between proliferation and differentiation, before Noggin is activated to antagonise BMPs and facilitate terminal differentiation. 相似文献