共查询到20条相似文献,搜索用时 421 毫秒
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Two new homologs of human (h) TAFII30, dTAFII16 and dTAFII24 were revealed inDrosophila melanogaster. The proteins are encoded by neighboring genes and bind with the TATA-binding protein and other dTAFII proteins involved in TFIID. Only dTAFII24 interacts with GCN5 histone acetyltransferase (HAT), which is the first demonstration of the TAFII-GCN5-HAT complex inD. melanogaster. The two proteins have both common and individual location sites on polytene chromosomes. Possibly, the functions of dTAFII16 and dTAFII24 are similar but not identical. 相似文献
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Joseph E. Klebba Brian J. Galletta Jonathan Nye Karen M. Plevock Daniel W. Buster Natalie A. Hollingsworth Kevin C. Slep Nasser M. Rusan Gregory C. Rogers 《The Journal of cell biology》2015,208(4):401-414
Plk4 (Polo-like kinase 4) and its binding partner Asterless (Asl) are essential, conserved centriole assembly factors that induce centriole amplification when overexpressed. Previous studies found that Asl acts as a scaffolding protein; its N terminus binds Plk4’s tandem Polo box cassette (PB1-PB2) and targets Plk4 to centrioles to initiate centriole duplication. However, how Asl overexpression drives centriole amplification is unknown. In this paper, we investigated the Asl–Plk4 interaction in Drosophila melanogaster cells. Surprisingly, the N-terminal region of Asl is not required for centriole duplication, but a previously unidentified Plk4-binding domain in the C terminus is required. Mechanistic analyses of the different Asl regions revealed that they act uniquely during the cell cycle: the Asl N terminus promotes Plk4 homodimerization and autophosphorylation during interphase, whereas the Asl C terminus stabilizes Plk4 during mitosis. Therefore, Asl affects Plk4 in multiple ways to regulate centriole duplication. Asl not only targets Plk4 to centrioles but also modulates Plk4 stability and activity, explaining the ability of overexpressed Asl to drive centriole amplification. 相似文献
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Takeshi Sekiguchi Torahiko Nakashima Toshiro Hayashida Akio Kuraoka Shuichi Hashimoto Nobuo Tsuchida Yosaburo Shibata Tony Hunter Takeharu Nishimoto 《Experimental cell research》1995,218(2)
A temperature-sensitive (ts) mutant of the BHK21 cell line derived from golden hamsters, tsBN462 has a mutation in the gene encoding the largest subunit of the TFIID complex, TAFII250/p230/CCG1, and arrests in the G1 phase at the nonpermissive temperature, 39.5°C. We found that tsBN462 cells underwent apoptosis following growth arrest at 39.5°C, suggesting a role for CCG1 as a repressor of apoptosis. By electron microscopic observation, tsBN462 cells at 39.5°C showed characteristic features of apoptosis. Apoptosis was not suppressed by expression of Bc1-2 or the adenovirus E1B 19 kDa protein. Cell death was suppressed completely by expression of wild-type CCG1 and partially by wild-type p53, a growth suppressor protein. Cell cycle arrest induced by p53 may help survival of tsBN462 cells at 39.5°C. Apoptosis was accelerated in SV40 large T antigen-transformed tsBN462 cells at 39.5°C where SV40 large T antigen formed a complex with p53, implying that the apoptosis of tsBN462 cells at 39.5°C occurred in a p53-independent manner. Our results suggest that CCG1/TAFII250 is required for the expression of factors regulating apoptosis. 相似文献
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A highly conserved domain of TFIID displays species specificity in vivo 总被引:22,自引:0,他引:22
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EWS, but Not EWS-FLI-1, Is Associated with Both TFIID and RNA Polymerase II: Interactions between Two Members of the TET Family, EWS and hTAFII68, and Subunits of TFIID and RNA Polymerase II Complexes 总被引:6,自引:2,他引:4 下载免费PDF全文
Anne Bertolotti Thomas Melot Joël Acker Marc Vigneron Olivier Delattre Laszlo Tora 《Molecular and cellular biology》1998,18(3):1489-1497
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The Gcn4p Activation Domain Interacts Specifically In Vitro with RNA Polymerase II Holoenzyme, TFIID, and the Adap-Gcn5p Coactivator Complex 总被引:10,自引:8,他引:2 下载免费PDF全文
Connie M. Drysdale Belinda M. Jackson Richard McVeigh Edward R. Klebanow Yu Bai Tetsuro Kokubo Mark Swanson Yoshihiro Nakatani P. Anthony Weil Alan G. Hinnebusch 《Molecular and cellular biology》1998,18(3):1711-1724