1000 resultados para 09091510 CTD-157


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利用在束γ谱学技术,通过反应144Sm(16O,3n)研究了157Yb的高自旋态,其中16O束流的能量为90MeV.采用门套BGO(AC)HPGe探测器进行了长时间的γ-γ-t符合测量.基于γ-γ符合关系、γ射线的各向异性度和DCO系数的测量结果,首次建立了157Yb的高自旋能级纲图.围绕157Yb的能级纲图着重讨论了此核的形状共存和Vi13/2能带随着角动量增加的结构演变,另外还比较了N=87同中子素链的Vi13/2转动带结构的系统性.

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利用在束γ谱学方法 ,通过反应1 4 4 Sm( 1 6O ,3n) 1 57Yb研究了1 57Yb的激发态能级结构 .实验中使用的1 6O束流能量为 90MeV .基于实验得到的γ γ符合关系、γ射线的各向异性度和DCO系数 ,建议了1 57Yb的高自旋能级纲图 .1 57Yb的能级纲图主要由两串跃迁性质明显不同的级联能级组成 ,它们分别对应于νi1 3 2 转动带和单粒子激发态 .着重讨论了1 57Yb的形状共存和νi1 3 2 转动带随角动量的结构演化 .

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用蒸发中子反应产生~(157)Tb和~(153)Er,收集活性样品,作x, #gamma# 单谱及符合谱测量,对~(157)Yb和~(153)Er的(EC+#beta#~+)衰变进行了研究,给出了~(157)Yb及~(153)Er的衰变纲图,其中~(157)Yb的衰变纲图包括25条新#gamma#射线,分析~(157)Yb的衰变纲图,~(153)Er的衰变纲图包括15条#gamma#射线,并指定出~(153)Er半衰变期值,该值与文献给出值符合得很好。指定了~(153)Er的衰变纲图中能级状况

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利用142Nd(16O,5n)153Er和147Sm(16O,6n)157Yb反应并藉助与氦喷嘴快速带传输装置和x(γ) γt-符合测量技术首次建立了153Er和157Yb的(EC/β+)衰变能级纲图。 对153Er的(EC/β+)衰变纲图的分析,得到结果有, 1) 辨认了256.7KeV和634.2KeV的二条低位能级分别为d3/2和d5/2的单质子态。因此,153H0的基态 的形状为球形。在同位素链Ho(Z=67)上,随着中子数的增加,奇质量数Ho核的基态核形状由球形过渡到变形发生在中子数86和88之间。 2) 位于1700.1KeV能级为三粒子态,具有[(πh11/2 νh9/2)1+ νf7/2] , , 的结构特征。 经对157Yb的(EC/β+)衰变纲图分析,得到结果有, 1) 发现了建立在157Tm基态上的Kπ= 转动带的带头部分。用可变转动惯量的三轴行变粒子转子模型对157Tm的转动能谱的计算结果表明,157Tm的基态Kπ= 转动带所对应的形变是三轴形变,相应的形变参数为ε2=0.23,ε4=0.01,γ=35°。给出了随着中子数的增加,奇质量数Tm(Z=69)核的基态核形状由球形过渡到非球形发生在中子数86和88之间。 2) 辨认了一条位于激发能为3502KeV的同质异能态,其寿命>40ns。

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BRCA1 has been implicated in numerous DNA repair pathways that maintain genome integrity, however the function responsible for its tumor suppressor activity in breast cancer remains obscure. To identify the most highly conserved of the many BRCA1 functions, we screened the evolutionarily distant eukaryote Saccharomyces cerevisiae for mutants that suppressed the G1 checkpoint arrest and lethality induced following heterologous BRCA1 expression. A genome-wide screen in the diploid deletion collection combined with a screen of ionizing radiation sensitive gene deletions identified mutants that permit growth in the presence of BRCA1. These genes delineate a metabolic mRNA pathway that temporally links transcription elongation (SPT4, SPT5, CTK1, DEF1) to nucleopore-mediated mRNA export (ASM4, MLP1, MLP2, NUP2, NUP53, NUP120, NUP133, NUP170, NUP188, POM34) and cytoplasmic mRNA decay at P-bodies (CCR4, DHH1). Strikingly, BRCA1 interacted with the phosphorylated RNA polymerase II (RNAPII) carboxy terminal domain (P-CTD), phosphorylated in the pattern specified by the CTDK-I kinase, to induce DEF1-dependent cleavage and accumulation of a RNAPII fragment containing the P-CTD. Significantly, breast cancer associated BRCT domain defects in BRCA1 that suppressed P-CTD cleavage and lethality in yeast also suppressed the physical interaction of BRCA1 with human SPT5 in breast epithelial cells, thus confirming SPT5 as a relevant target of BRCA1 interaction. Furthermore, enhanced P-CTD cleavage was observed in both yeast and human breast cells following UV-irradiation indicating a conserved eukaryotic damage response. Moreover, P-CTD cleavage in breast epithelial cells was BRCA1-dependent since damage-induced P-CTD cleavage was only observed in the mutant BRCA1 cell line HCC1937 following ectopic expression of wild type BRCA1. Finally, BRCA1, SPT5 and hyperphosphorylated RPB1 form a complex that was rapidly degraded following MMS treatment in wild type but not BRCA1 mutant breast cells. These results extend the mechanistic links between BRCA1 and transcriptional consequences in response to DNA damage and suggest an important role for RNAPII P-CTD cleavage in BRCA1-mediated cancer suppression.

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Au f. 157, souscription rubriquée du 20 novembre 1384: "Explicit summa dictaminis magistri Petri de Vineis. Qui scripsit scribat, semper cum Domini vivat. Ffinito (sic) libro, referamus gratia Christo. Ffuit (sic) scriptum presens opus et completum, die qua computabatur vicesima mensis novembris, anno a Nativitate Domini M°CCC° octuagesimo quarto". Tout le ms. est de la même main.

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La phosphorylation du domaine C-terminal de l’ARN polymérase II permet à ce complexe protéique d’exécuter la transcription des gènes, en plus de coupler à la transcription des événements moléculaires comme la maturation des ARNm. Mes résultats montrent que même si cette phosphorylation suit un patron similaire à l’ensemble des gènes, il existe des exceptions pouvant être dues à des mécanismes alternatifs de phosphorylation du CTD. Le présent ouvrage s’intéresse également au rôle qu’occupe la variante d’histone H2A.Z dans l’organisation de la chromatine. Des études précédentes on montré que le positionnement de certains nucléosomes le long de l’ADN serait influencé par H2A.Z et aurait une influence sur la capacité de transcrire les gènes. Par une approche génomique utilisant les puces à ADN, j’ai cartographié l’impact de la délétion de H2A.Z sur la structure des nucléosomes. Enfin, des résultats intéressants sur la dynamique d’incorporation de H2A.Z à la chromatine ont été obtenus.