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Identifying target sites for cooperatively binding factors. 总被引:15,自引:0,他引:15
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Pinte S Stankovic-Valentin N Deltour S Rood BR Guérardel C Leprince D 《The Journal of biological chemistry》2004,279(37):38313-38324
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The fragile X mental retardation protein binds specifically to its mRNA via a purine quartet motif 总被引:30,自引:0,他引:30
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Schaeffer C Bardoni B Mandel JL Ehresmann B Ehresmann C Moine H 《The EMBO journal》2001,20(17):4803-4813
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Identification of a nuclear factor that binds to a conserved sequence of the I-A beta gene 总被引:8,自引:0,他引:8
A Celada M Shiga M Imagawa J Kop R A Maki 《Journal of immunology (Baltimore, Md. : 1950)》1988,140(11):3995-4002
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A full genome sequence of the episomal form of Cotesia plutellae bracovirus (CpBV) suggests 11 BEN family genes. This study analyzed their expression and physiological function in the viral host, Plutella xylostella. All 11 BEN family genes were expressed during entire parasitization period of P. xylostella larvae. In addition, these BEN family genes were expressed in fat body, gut, epidermis, and hemocytes in final larval instar of parasitized P. xylostella. The 11 BEN family genes were transiently expressed in nonparasitized larvae by injection of each viral segment containing its corresponding BEN family gene. The transient expression of BEN family genes significantly suppressed hemocyte nodule formation in response to bacterial challenge. Subsequent injection of double-stranded RNA specific to each BEN family gene suppressed the expression of the BEN family gene and rescued the immunosuppression. These results indicate that 11 BEN family genes are expressed in larvae parasitized by C. plutellae and play crucial role in inducing immunosuppression. Homologous BEN family genes were found in other bracoviral genomes. We propose BEN domain-containing genes as a new functional gene family in polydnaviruses. 相似文献
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J. E. Skonier M. A. Bowen A. Aruffo J. Bajorath 《Protein science : a publication of the Protein Society》1997,6(8):1768-1770
CD6 and its ligand activated leukocyte cell adhesion molecule (ALCAM, CD166) have been detected on various immune cells and in the brain. CD6-ligand interactions have been implicated in the regulation of T cell function. ALCAM shares the same extracellular domain organization and significant sequence homology with the chicken neural adhesion molecule BEN. Although ALCAM's CD6 binding site is only partially conserved in BEN, CD6 specifically binds BEN, albeit with approximately 10-fold lower avidity than ALCAM. Differences in binding avidity are not detected when ALCAM and BEN fusion proteins containing the full-length extracellular regions are tested. Homotypic interactions between full-length forms are likely to account for these observations. The identified cross-species interaction between CD6 and BEN suggests that CD6-ligand interactions are highly conserved. 相似文献
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