共查询到20条相似文献,搜索用时 46 毫秒
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Functional antagonism between c-Jun and MyoD proteins: a direct physical association. 总被引:63,自引:0,他引:63
E Bengal L Ransone R Scharfmann V J Dwarki S J Tapscott H Weintraub I M Verma 《Cell》1992,68(3):507-519
The product of the proto-oncogene Jun inhibits myogenesis. Constitutive expression of Jun in myoblasts interferes with the expression and the function of MyoD protein. In transient transfection assays Jun inhibits transactivation of the MyoD promoter, the muscle creatine kinase enhancer, and a reporter gene linked to MyoD DNA-binding sites. Conversely, MyoD suppresses the transactivation by Jun of genes linked to an AP-1 site. We demonstrate that both in vivo and in vitro MyoD and Jun proteins physically interact. Mutational analysis suggests that this interaction occurs via the leucine zipper domain of Jun and the helix-loop-helix region of MyoD. 相似文献
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The gibbon ape leukemia virus (GALV) contains enhancer activity within its long terminal repeat. In the GALV Seato strain this activity resides in a 48-base-pair (bp) repeated element. We demonstrate the existence of a cellular protein which binds in this region of the Seato strain. A sensitive method for enriching protein-DNA complexes from crude extracts coupled with exonuclease and DNase footprint analysis revealed the specific binding of this protein to a 21-bp region within each repeated element. A 22-bp oligonucleotide fragment defined solely by the 21-bp footprint binds a protein in vitro and displays enhancer activity in vivo, suggesting that this protein is a major determinant of GALV enhancer activity. The protein is present in three cell lines which are positive for enhancer activity and is not detected in Jurkat cells, which are negative for enhancer activity. Only GALV long-terminal-repeat variants which support high levels of enhancer activity in vivo compete with this protein for specific binding in vitro, suggesting a potential role for the protein in determining enhancer activity. This protein binding is not inhibited by competition with heterologous retroviral enhancers, demonstrating that it is not a ubiquitous retroviral enhancer binding protein. 相似文献
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Adjacent DNA sequences modulate Sox9 transcriptional activation at paired Sox sites in three chondrocyte-specific enhancer elements 下载免费PDF全文
Bridgewater LC Walker MD Miller GC Ellison TA Holsinger LD Potter JL Jackson TL Chen RK Winkel VL Zhang Z McKinney S de Crombrugghe B 《Nucleic acids research》2003,31(5):1541-1553
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Transcriptional activation of the human papillomavirus-16 P97 promoter by an 88-nucleotide enhancer containing distinct cell-dependent and AP-1-responsive modules 总被引:17,自引:0,他引:17
T P Cripe A Alderborn R D Anderson S Parkkinen P Bergman T H Haugen U Pettersson L P Turek 《The New biologist》1990,2(5):450-463
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Yoshioka Y Nguyen TT Fujiwara S Matsuda R Valadez-Graham V Zurita M Yamaguchi M 《Genesis (New York, N.Y. : 2000)》2012,50(8):599-611
The Drosophila Jun N-terminal kinase (JNK) gene basket (bsk) promoter contains a DNA replication-related element (DRE)-like sequence, raising the possibility of regulation by the DNA replication-related element-binding factor (DREF). Chromatin immunoprecipitation assays with anti-DREF IgG showed the bsk gene promoter region to be effectively amplified. Luciferase transient expression assays revealed the DRE-like sequence to be important for bsk gene promoter activity, and knockdown of DREF decreased the bsk mRNA level and the bsk gene promoter activity. Furthermore, knockdown of DREF in the notum compartment of wing discs by pannier-GAL4 and UAS-DREFIR resulted in a split thorax phenotype. Monitoring of JNK activity in the wing disc by LacZ expression in a puckered (puc)-LacZ enhancer trap line revealed the reduction in DREF knockdown clones. These findings indicate that DREF is involved in regulation of Drosophila thorax development via actions on the JNK pathway. 相似文献
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Characterization of a cell type-specific enhancer found in the human papilloma virus type 18 genome. 总被引:24,自引:3,他引:21 下载免费PDF全文
We have previously isolated long-range acting enhancer elements from the HeLa genome by functional selection. In this report, the structural and functional characteristics of one (GA1) of the enhancers are reported. By cloning various restriction fragments and by deletion mutagenesis, the activity of GA1 was located in a 230-bp region. The nucleotide sequence of GA1 and genomic Southern blot analysis indicated that GA1 is derived from human papilloma virus (HPV) 18 DNA that had been integrated into the HeLa genome. The enhancer is located in the non-coding region of the HPV 18 genome. The HPV 18 enhancer consists of two functional domains, both of which have full enhancer activity in HeLa cells. The enhancer does not contain enhancer core sequences but contains several blocks of potential Z-DNA sequence. Like SV40 and polyoma virus enhancers, the activity of the HPV 18 enhancer was repressed by adenovirus E1a products. The HPV 18 enhancer shows a narrow cell type specificity: it is active in some cervical carcinoma cell lines, but inactive in all non-cervical cells except for one neuroblastoma cell line. These results suggest that the HPV 18 enhancer plays an important role in regulation of the viral genes. 相似文献